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Surgery_Schwartz_5602 | Surgery_Schwartz | approach, have failed one or more attempts at catheter ablation, or are poor candidates for catheter ablation.243 At our institution, relative indications for surgical ablation in patients with permanent AF that were not included in the consensus statement are (a) a contraindica-tion to long term anticoagulation for patients at high risk for stroke (CHADS2 score ≥2) and (b) a history of stroke while on therapeutic anticoagulation. Since the consensus statement was released, a multicenter, randomized, controlled trial of surgical ablation in patients undergoing mitral valve surgery showed a significant improvement in freedom from atrial fibrillation in patients receiving surgical ablation (63% vs. 29%, P <0.001).250 Controversially, this trial did not show a difference between left atrial and biatrial ablation; this may have been due to techni-cal issues with the operations.251 The STS has recently released guidelines for surgical ablation that give a Class I Level A rec-ommendation | Surgery_Schwartz. approach, have failed one or more attempts at catheter ablation, or are poor candidates for catheter ablation.243 At our institution, relative indications for surgical ablation in patients with permanent AF that were not included in the consensus statement are (a) a contraindica-tion to long term anticoagulation for patients at high risk for stroke (CHADS2 score ≥2) and (b) a history of stroke while on therapeutic anticoagulation. Since the consensus statement was released, a multicenter, randomized, controlled trial of surgical ablation in patients undergoing mitral valve surgery showed a significant improvement in freedom from atrial fibrillation in patients receiving surgical ablation (63% vs. 29%, P <0.001).250 Controversially, this trial did not show a difference between left atrial and biatrial ablation; this may have been due to techni-cal issues with the operations.251 The STS has recently released guidelines for surgical ablation that give a Class I Level A rec-ommendation |
Surgery_Schwartz_5603 | Surgery_Schwartz | and biatrial ablation; this may have been due to techni-cal issues with the operations.251 The STS has recently released guidelines for surgical ablation that give a Class I Level A rec-ommendation for concomitant surgical ablation at the time of mitral valve surgery and a Class I Level B-NR recommendation for concomitant surgical ablation at the time of AVR, CABG, or AVR-CABG.252The Cox-Maze IV Procedure. The first successful operation for atrial fibrillation, the Cox-Maze procedure, was introduced clinically in 1987 by James Cox. The procedure involved the completion of a maze-like pattern of surgical incisions across both the right and left atrial that were designed to interrupt the multiple macroreentrant circuits thought to be responsible for AF, while still allowing propagation of the sinus impulse, restoring atrioventricular synchrony, and preserving atrial trans-port function. While effective at eliminating AF and reducing the risk of thromboembolism, it was not widely | Surgery_Schwartz. and biatrial ablation; this may have been due to techni-cal issues with the operations.251 The STS has recently released guidelines for surgical ablation that give a Class I Level A rec-ommendation for concomitant surgical ablation at the time of mitral valve surgery and a Class I Level B-NR recommendation for concomitant surgical ablation at the time of AVR, CABG, or AVR-CABG.252The Cox-Maze IV Procedure. The first successful operation for atrial fibrillation, the Cox-Maze procedure, was introduced clinically in 1987 by James Cox. The procedure involved the completion of a maze-like pattern of surgical incisions across both the right and left atrial that were designed to interrupt the multiple macroreentrant circuits thought to be responsible for AF, while still allowing propagation of the sinus impulse, restoring atrioventricular synchrony, and preserving atrial trans-port function. While effective at eliminating AF and reducing the risk of thromboembolism, it was not widely |
Surgery_Schwartz_5604 | Surgery_Schwartz | of the sinus impulse, restoring atrioventricular synchrony, and preserving atrial trans-port function. While effective at eliminating AF and reducing the risk of thromboembolism, it was not widely performed because it was technically difficult and significantly prolonged time on cardiopulmonary bypass. In 2002, the Cox-Maze IV, was introduced. The Cox-Maze IV uses a combination of bipo-lar radiofrequency (RF) ablation and cryoablation to effectively replace the majority of incisions that comprise the Cox-Maze III while significantly shortening cross-clamp time and reducing operative complexity.The Cox-Maze IV is performed on cardiopulmonary bypass through either a median sternotomy, often in combina-tion with other cardiac surgery or a right minithoracotomy.253,254 In most cases, the right atrial lesion set performed on the beat-ing heart, whereas the left atrial lesions are performed during cardioplegic arrest (Fig. 21-15).Results from the Cox-Maze IV procedure have been excellent. | Surgery_Schwartz. of the sinus impulse, restoring atrioventricular synchrony, and preserving atrial trans-port function. While effective at eliminating AF and reducing the risk of thromboembolism, it was not widely performed because it was technically difficult and significantly prolonged time on cardiopulmonary bypass. In 2002, the Cox-Maze IV, was introduced. The Cox-Maze IV uses a combination of bipo-lar radiofrequency (RF) ablation and cryoablation to effectively replace the majority of incisions that comprise the Cox-Maze III while significantly shortening cross-clamp time and reducing operative complexity.The Cox-Maze IV is performed on cardiopulmonary bypass through either a median sternotomy, often in combina-tion with other cardiac surgery or a right minithoracotomy.253,254 In most cases, the right atrial lesion set performed on the beat-ing heart, whereas the left atrial lesions are performed during cardioplegic arrest (Fig. 21-15).Results from the Cox-Maze IV procedure have been excellent. |
Surgery_Schwartz_5605 | Surgery_Schwartz | atrial lesion set performed on the beat-ing heart, whereas the left atrial lesions are performed during cardioplegic arrest (Fig. 21-15).Results from the Cox-Maze IV procedure have been excellent. The Washington University group reported a series of 576 consecutive patients in 2015, demonstrating free-dom from atrial tachyarrhythmias in 92% of patients at 1 year and 73% of patients at 5 years postoperatively.255 Additionally, freedom from atrial tachyarrhythmias and antiarrhythmic drugs was 81% at 1 year and 61% at 5 years. A recent propensity-matched analysis showed that the addition of the Cox-Maze IV procedure to a routine cardiac surgery did not significantly increase postoperative morbidity or mortality and was associ-ated with improved late survival compared with patients with untreated AF and a similar survival to patients without a his-tory of AF.256 A propensity analysis has shown that results are similar between the traditional “cut-and-sew” maze (Cox-Maze III) and the | Surgery_Schwartz. atrial lesion set performed on the beat-ing heart, whereas the left atrial lesions are performed during cardioplegic arrest (Fig. 21-15).Results from the Cox-Maze IV procedure have been excellent. The Washington University group reported a series of 576 consecutive patients in 2015, demonstrating free-dom from atrial tachyarrhythmias in 92% of patients at 1 year and 73% of patients at 5 years postoperatively.255 Additionally, freedom from atrial tachyarrhythmias and antiarrhythmic drugs was 81% at 1 year and 61% at 5 years. A recent propensity-matched analysis showed that the addition of the Cox-Maze IV procedure to a routine cardiac surgery did not significantly increase postoperative morbidity or mortality and was associ-ated with improved late survival compared with patients with untreated AF and a similar survival to patients without a his-tory of AF.256 A propensity analysis has shown that results are similar between the traditional “cut-and-sew” maze (Cox-Maze III) and the |
Surgery_Schwartz_5606 | Surgery_Schwartz | untreated AF and a similar survival to patients without a his-tory of AF.256 A propensity analysis has shown that results are similar between the traditional “cut-and-sew” maze (Cox-Maze III) and the Cox-Maze IV.257 This procedure is often successful in patients who are poor candidates for catheter-based ablation, such as those with large left atria and patients with long-standing persistent AF.The combination of surgical management of the left atrial appendage (LAA) and restoration of normal sinus rhythm after the Cox-Maze procedure significantly reduces stroke risk. It is our practice to stop warfarin at 3 months postoperatively in patients who are in normal sinus rhythm and without another indication for anticoagulation, regardless of CHA2DS2-VASc score. With this approach, the stroke rate following the Cox-Maze procedure off anticoagulation has been remarkably low (annual risk = 0.2%).258 In contrast, in one report the annual rate of intracranial hemorrhage in anticoagulated | Surgery_Schwartz. untreated AF and a similar survival to patients without a his-tory of AF.256 A propensity analysis has shown that results are similar between the traditional “cut-and-sew” maze (Cox-Maze III) and the Cox-Maze IV.257 This procedure is often successful in patients who are poor candidates for catheter-based ablation, such as those with large left atria and patients with long-standing persistent AF.The combination of surgical management of the left atrial appendage (LAA) and restoration of normal sinus rhythm after the Cox-Maze procedure significantly reduces stroke risk. It is our practice to stop warfarin at 3 months postoperatively in patients who are in normal sinus rhythm and without another indication for anticoagulation, regardless of CHA2DS2-VASc score. With this approach, the stroke rate following the Cox-Maze procedure off anticoagulation has been remarkably low (annual risk = 0.2%).258 In contrast, in one report the annual rate of intracranial hemorrhage in anticoagulated |
Surgery_Schwartz_5607 | Surgery_Schwartz | rate following the Cox-Maze procedure off anticoagulation has been remarkably low (annual risk = 0.2%).258 In contrast, in one report the annual rate of intracranial hemorrhage in anticoagulated patients with AF was 0.9% per year, and the overall rate of major bleeding complications was 2.3% per year.259Left Atrial Lesion Sets. Some surgeons perform more lim-ited ablation procedures, such as isolated pulmonary vein isola-tion or lesion sets that are limited to the left side of the heart. This is done in order to further reduce the complexity of the pro-cedure and takes advantage of the fact that in most patients AF 7Brunicardi_Ch21_p0801-p0852.indd 83801/03/19 5:32 PM 839ACQUIRED HEART DISEASECHAPTER 21Figure 21-15. The Cox-Maze IV Lesion Set. A. The left atrial lesion set is comprised of right and left pulmonary vein isolation, connecting lesions between the left and right superior and inferior pulmonary veins, a lesion from the left atrial appendage excision site to the | Surgery_Schwartz. rate following the Cox-Maze procedure off anticoagulation has been remarkably low (annual risk = 0.2%).258 In contrast, in one report the annual rate of intracranial hemorrhage in anticoagulated patients with AF was 0.9% per year, and the overall rate of major bleeding complications was 2.3% per year.259Left Atrial Lesion Sets. Some surgeons perform more lim-ited ablation procedures, such as isolated pulmonary vein isola-tion or lesion sets that are limited to the left side of the heart. This is done in order to further reduce the complexity of the pro-cedure and takes advantage of the fact that in most patients AF 7Brunicardi_Ch21_p0801-p0852.indd 83801/03/19 5:32 PM 839ACQUIRED HEART DISEASECHAPTER 21Figure 21-15. The Cox-Maze IV Lesion Set. A. The left atrial lesion set is comprised of right and left pulmonary vein isolation, connecting lesions between the left and right superior and inferior pulmonary veins, a lesion from the left atrial appendage excision site to the |
Surgery_Schwartz_5608 | Surgery_Schwartz | comprised of right and left pulmonary vein isolation, connecting lesions between the left and right superior and inferior pulmonary veins, a lesion from the left atrial appendage excision site to the pulmonary vein, and a lesion to the mitral valve annulus. B. The right atrial lesion set consists of lines of ablation along the superior and inferior vena cavae, the free wall of the right atrium, and down to the tricuspid valve annulus. (Reproduced with permission from Weimar T, Bailey MS, Watanabe Y, et al: The Cox-maze IV procedure for lone atrial fibrillation: a single center experience in 100 consecutive patients, J Interv Card Electrophysiol. 2011 Jun;31(1):47-54.)ABoriginates from the pulmonary veins and posterior left atrium. However, there is seldom justification for limited lesion sets in experienced hands.While there is a high degree of variability in both the techniques and energy sources that have been attempted for left-sided atrial lesion sets, these procedures have all | Surgery_Schwartz. comprised of right and left pulmonary vein isolation, connecting lesions between the left and right superior and inferior pulmonary veins, a lesion from the left atrial appendage excision site to the pulmonary vein, and a lesion to the mitral valve annulus. B. The right atrial lesion set consists of lines of ablation along the superior and inferior vena cavae, the free wall of the right atrium, and down to the tricuspid valve annulus. (Reproduced with permission from Weimar T, Bailey MS, Watanabe Y, et al: The Cox-maze IV procedure for lone atrial fibrillation: a single center experience in 100 consecutive patients, J Interv Card Electrophysiol. 2011 Jun;31(1):47-54.)ABoriginates from the pulmonary veins and posterior left atrium. However, there is seldom justification for limited lesion sets in experienced hands.While there is a high degree of variability in both the techniques and energy sources that have been attempted for left-sided atrial lesion sets, these procedures have all |
Surgery_Schwartz_5609 | Surgery_Schwartz | sets in experienced hands.While there is a high degree of variability in both the techniques and energy sources that have been attempted for left-sided atrial lesion sets, these procedures have all incorpo-rated some subset of the left atrial lesion set of the Cox-Maze procedure. Pulmonary vein isolation is ubiquitously performed, and the LAA is often excised. Results differ greatly between series, including the recent CTSNet multicenter trial,250 but a meta-analysis of the published literature by Ad and colleagues revealed that a biatrial lesion set resulted in a significantly higher late freedom from AF compared with a left atrial lesion set alone (87% vs. 73%, P = 0.05).260 These results are not sur-prising, as our intraoperative mapping experience with such patients showed a distinct region of stable dominant frequency in the left atrium only 30% of the time.261 The dominant fre-quency was located in the right atrium 12% of the time and moved during the recording period in almost | Surgery_Schwartz. sets in experienced hands.While there is a high degree of variability in both the techniques and energy sources that have been attempted for left-sided atrial lesion sets, these procedures have all incorpo-rated some subset of the left atrial lesion set of the Cox-Maze procedure. Pulmonary vein isolation is ubiquitously performed, and the LAA is often excised. Results differ greatly between series, including the recent CTSNet multicenter trial,250 but a meta-analysis of the published literature by Ad and colleagues revealed that a biatrial lesion set resulted in a significantly higher late freedom from AF compared with a left atrial lesion set alone (87% vs. 73%, P = 0.05).260 These results are not sur-prising, as our intraoperative mapping experience with such patients showed a distinct region of stable dominant frequency in the left atrium only 30% of the time.261 The dominant fre-quency was located in the right atrium 12% of the time and moved during the recording period in almost |
Surgery_Schwartz_5610 | Surgery_Schwartz | region of stable dominant frequency in the left atrium only 30% of the time.261 The dominant fre-quency was located in the right atrium 12% of the time and moved during the recording period in almost half of all patients. It must also be kept in mind that recurrent right atrial flutter is a known complication of performing only the left atrial lesions. When it does occur, atrial flutter can be treated with catheter-based ablation; however, recurrent left atrial flutter can be very difficult to ablate.Pulmonary Vein Isolation. Pulmonary vein isolation (PVI) is an attractive therapeutic option because it can be performed off of cardiopulmonary bypass (CPB) through small or thora-coscopic incisions. The results of PVI have been variable and highly dependent on patient selection since outcomes are con-sistently worse in patients with longstanding persistent AF. In a study from Edgerton et al, only 56% of patients were free from AF at 6 months (35% off antiarrhythmic drugs), and with | Surgery_Schwartz. region of stable dominant frequency in the left atrium only 30% of the time.261 The dominant fre-quency was located in the right atrium 12% of the time and moved during the recording period in almost half of all patients. It must also be kept in mind that recurrent right atrial flutter is a known complication of performing only the left atrial lesions. When it does occur, atrial flutter can be treated with catheter-based ablation; however, recurrent left atrial flutter can be very difficult to ablate.Pulmonary Vein Isolation. Pulmonary vein isolation (PVI) is an attractive therapeutic option because it can be performed off of cardiopulmonary bypass (CPB) through small or thora-coscopic incisions. The results of PVI have been variable and highly dependent on patient selection since outcomes are con-sistently worse in patients with longstanding persistent AF. In a study from Edgerton et al, only 56% of patients were free from AF at 6 months (35% off antiarrhythmic drugs), and with |
Surgery_Schwartz_5611 | Surgery_Schwartz | are con-sistently worse in patients with longstanding persistent AF. In a study from Edgerton et al, only 56% of patients were free from AF at 6 months (35% off antiarrhythmic drugs), and with concomitant procedures, the success rate of PVI has been even lower.262 Several devices are available to close the LAA at the time of PVI. These include staplers and epicardial clips that can be placed without the need for CPB.263While surgical PVI has had poorer results than a Cox-Maze procedure, it has had superior results to catheter-based PVI. The Atrial Fibrillation Catheter Ablation Versus Surgi-cal Ablation Treatment (FAST) Trial, which was a two cen-ter, randomized clinical trial, compared catheter-based ablation to thoracoscopic PVI in patients with antiarrhythmic drug-refractory AF and either left atrial dilatation and hypertension or failed prior catheter-ablation.264 This study demonstrated that the 12-month freedom from AF and antiarrhythmic drugs was 37% for the catheter ablation | Surgery_Schwartz. are con-sistently worse in patients with longstanding persistent AF. In a study from Edgerton et al, only 56% of patients were free from AF at 6 months (35% off antiarrhythmic drugs), and with concomitant procedures, the success rate of PVI has been even lower.262 Several devices are available to close the LAA at the time of PVI. These include staplers and epicardial clips that can be placed without the need for CPB.263While surgical PVI has had poorer results than a Cox-Maze procedure, it has had superior results to catheter-based PVI. The Atrial Fibrillation Catheter Ablation Versus Surgi-cal Ablation Treatment (FAST) Trial, which was a two cen-ter, randomized clinical trial, compared catheter-based ablation to thoracoscopic PVI in patients with antiarrhythmic drug-refractory AF and either left atrial dilatation and hypertension or failed prior catheter-ablation.264 This study demonstrated that the 12-month freedom from AF and antiarrhythmic drugs was 37% for the catheter ablation |
Surgery_Schwartz_5612 | Surgery_Schwartz | left atrial dilatation and hypertension or failed prior catheter-ablation.264 This study demonstrated that the 12-month freedom from AF and antiarrhythmic drugs was 37% for the catheter ablation group and 66% for the PVI group (P = 0.002).264SURGERY FOR PERICARDIAL DISEASEAcute PericarditisPericarditis is characterized by infiltration of the cellular and fibrous pericardium by inflammatory cells. The exact incidence and prevalence of pericarditis is unknown, but it is estimated that pericarditis is found in approximately 1% of autopsies and accounts for up to 5% of presentations of nonischemic chest pain.265,266 The etiologies of acute pericarditis are diverse and may result from primary pericardial disorders or occur sec-ondary to a systemic illness.267 In developed countries, 80% to 90% of cases are now considered idiopathic or related to a viral pathogen, but nonviral infection, autoimmune diseases, myocardial infarction, radiation, malignancy, endocrinopathy, myocarditis, aortic | Surgery_Schwartz. left atrial dilatation and hypertension or failed prior catheter-ablation.264 This study demonstrated that the 12-month freedom from AF and antiarrhythmic drugs was 37% for the catheter ablation group and 66% for the PVI group (P = 0.002).264SURGERY FOR PERICARDIAL DISEASEAcute PericarditisPericarditis is characterized by infiltration of the cellular and fibrous pericardium by inflammatory cells. The exact incidence and prevalence of pericarditis is unknown, but it is estimated that pericarditis is found in approximately 1% of autopsies and accounts for up to 5% of presentations of nonischemic chest pain.265,266 The etiologies of acute pericarditis are diverse and may result from primary pericardial disorders or occur sec-ondary to a systemic illness.267 In developed countries, 80% to 90% of cases are now considered idiopathic or related to a viral pathogen, but nonviral infection, autoimmune diseases, myocardial infarction, radiation, malignancy, endocrinopathy, myocarditis, aortic |
Surgery_Schwartz_5613 | Surgery_Schwartz | of cases are now considered idiopathic or related to a viral pathogen, but nonviral infection, autoimmune diseases, myocardial infarction, radiation, malignancy, endocrinopathy, myocarditis, aortic dissection, uremia, trauma, pharmacologi-cal side effects, and previous cardiothoracic surgery must be included in the differential diagnosis. The relative incidences of peri-infarction pericarditis, which was once common, and post-cardiac injury syndrome have been dramatically reduced with the advent of thrombolytics and coronary angioplasty.267Clinical Presentation and Diagnosis. Diagnosis of acute pericarditis typically requires the identification of at least two of four cardinal features (Table 21-14). The presentation may be confused with several more common cardiopulmonary condi-tions, particularly myocardial infarction, making a careful his-tory and physical critical. Patients with pericarditis classically complain of sudden onset, retrosternal pain that may be pleuritic in nature. | Surgery_Schwartz. of cases are now considered idiopathic or related to a viral pathogen, but nonviral infection, autoimmune diseases, myocardial infarction, radiation, malignancy, endocrinopathy, myocarditis, aortic dissection, uremia, trauma, pharmacologi-cal side effects, and previous cardiothoracic surgery must be included in the differential diagnosis. The relative incidences of peri-infarction pericarditis, which was once common, and post-cardiac injury syndrome have been dramatically reduced with the advent of thrombolytics and coronary angioplasty.267Clinical Presentation and Diagnosis. Diagnosis of acute pericarditis typically requires the identification of at least two of four cardinal features (Table 21-14). The presentation may be confused with several more common cardiopulmonary condi-tions, particularly myocardial infarction, making a careful his-tory and physical critical. Patients with pericarditis classically complain of sudden onset, retrosternal pain that may be pleuritic in nature. |
Surgery_Schwartz_5614 | Surgery_Schwartz | myocardial infarction, making a careful his-tory and physical critical. Patients with pericarditis classically complain of sudden onset, retrosternal pain that may be pleuritic in nature. The pain may also be positional, with alleviation of pain when the patient is upright and leaning forward. Pain from pericarditis is typically sharp or stabbing, as opposed to the dull pain or pressure that is common with angina, and it typically does not crescendo. While both conditions cause pain that often radiates to the neck, arms, and shoulders, pericarditis pain may Brunicardi_Ch21_p0801-p0852.indd 83901/03/19 5:32 PM 840SPECIFIC CONSIDERATIONSPART IIuniquely radiate to the trapezius ridge due to innervation from the phrenic nerve.268-269The presence of a pericardial friction rub is pathogno-monic for pericarditis, but it tends to vary in intensity over time and may be absent in 15% to 65% of patients.265,268 As such, the sensitivity of this physical finding is dependent on the fre-quency | Surgery_Schwartz. myocardial infarction, making a careful his-tory and physical critical. Patients with pericarditis classically complain of sudden onset, retrosternal pain that may be pleuritic in nature. The pain may also be positional, with alleviation of pain when the patient is upright and leaning forward. Pain from pericarditis is typically sharp or stabbing, as opposed to the dull pain or pressure that is common with angina, and it typically does not crescendo. While both conditions cause pain that often radiates to the neck, arms, and shoulders, pericarditis pain may Brunicardi_Ch21_p0801-p0852.indd 83901/03/19 5:32 PM 840SPECIFIC CONSIDERATIONSPART IIuniquely radiate to the trapezius ridge due to innervation from the phrenic nerve.268-269The presence of a pericardial friction rub is pathogno-monic for pericarditis, but it tends to vary in intensity over time and may be absent in 15% to 65% of patients.265,268 As such, the sensitivity of this physical finding is dependent on the fre-quency |
Surgery_Schwartz_5615 | Surgery_Schwartz | for pericarditis, but it tends to vary in intensity over time and may be absent in 15% to 65% of patients.265,268 As such, the sensitivity of this physical finding is dependent on the fre-quency and quality of auscultation. A pericardial friction rub is best heard at the left lower sternal border and is typically described as a high-pitched scratchy or squeaky sound with a triphasic cadence corresponding to the movement of the heart during atrial systole, ventricular systole, and early ventricular diastole. However, it may be monophasic or biphasic in up to 50% of patients.Electrocardiogram changes typically progress through four stages representing global subepicardial myocarditis and subsequent recovery. Pericarditis patients may have concave ST deflections with diffuse changes, spanning the leads of multiple coronary artery distributions, but ST segment abnormalities are absent in 20% to 40% of patients.270,271 Acute pericarditis should not result in the development of infarct | Surgery_Schwartz. for pericarditis, but it tends to vary in intensity over time and may be absent in 15% to 65% of patients.265,268 As such, the sensitivity of this physical finding is dependent on the fre-quency and quality of auscultation. A pericardial friction rub is best heard at the left lower sternal border and is typically described as a high-pitched scratchy or squeaky sound with a triphasic cadence corresponding to the movement of the heart during atrial systole, ventricular systole, and early ventricular diastole. However, it may be monophasic or biphasic in up to 50% of patients.Electrocardiogram changes typically progress through four stages representing global subepicardial myocarditis and subsequent recovery. Pericarditis patients may have concave ST deflections with diffuse changes, spanning the leads of multiple coronary artery distributions, but ST segment abnormalities are absent in 20% to 40% of patients.270,271 Acute pericarditis should not result in the development of infarct |
Surgery_Schwartz_5616 | Surgery_Schwartz | the leads of multiple coronary artery distributions, but ST segment abnormalities are absent in 20% to 40% of patients.270,271 Acute pericarditis should not result in the development of infarct patterns, such as Q waves or loss of R waves, and T-wave inversions from pericarditis tend to result later in the disease process after the ST segment has returned to baseline.Echocardiography is routinely performed in the evaluation of acute pericarditis. Its role is primarily to assess for a pericar-dial effusion. However, in a patient who can be demonstrated to have previously had normal cardiac function, it may be used to exclude segmental wall motion abnormalities that may suggest ischemia.The remaining workup should attempt to determine the underlying cause of the pericarditis and should be directed by the history and physical. Most inflammatory markers and labo-ratory tests are nonspecific, but C-reactive protein may be useful in predicting recurrence risks and in guiding the duration of | Surgery_Schwartz. the leads of multiple coronary artery distributions, but ST segment abnormalities are absent in 20% to 40% of patients.270,271 Acute pericarditis should not result in the development of infarct patterns, such as Q waves or loss of R waves, and T-wave inversions from pericarditis tend to result later in the disease process after the ST segment has returned to baseline.Echocardiography is routinely performed in the evaluation of acute pericarditis. Its role is primarily to assess for a pericar-dial effusion. However, in a patient who can be demonstrated to have previously had normal cardiac function, it may be used to exclude segmental wall motion abnormalities that may suggest ischemia.The remaining workup should attempt to determine the underlying cause of the pericarditis and should be directed by the history and physical. Most inflammatory markers and labo-ratory tests are nonspecific, but C-reactive protein may be useful in predicting recurrence risks and in guiding the duration of |
Surgery_Schwartz_5617 | Surgery_Schwartz | by the history and physical. Most inflammatory markers and labo-ratory tests are nonspecific, but C-reactive protein may be useful in predicting recurrence risks and in guiding the duration of anti-inflammatory medications.272 Rarely, other imaging modalities, such as CT scanning, pericardial biopsies, or pericardiocentesis may aid in diagnosis.Treatment. The preferred treatment depends on the underly-ing cause of the pericarditis. The disease usually follows a self-limited and benign course and can be successfully treated with a short course of nonsteroidal anti-inflammatory agents (NSAIDs). The addition of colchicine may be beneficial.273 Some patients may require judicious use of steroids or IV anti-biotics. In cases of purulent pyogenic pericarditis, surgical exploration and drainage are occasionally necessary. Rarely, accumulation of fluid in the pericardium may lead to tampon-ade, requiring prompt evacuation of the pericardial space. While pericardiocentesis will typically | Surgery_Schwartz. by the history and physical. Most inflammatory markers and labo-ratory tests are nonspecific, but C-reactive protein may be useful in predicting recurrence risks and in guiding the duration of anti-inflammatory medications.272 Rarely, other imaging modalities, such as CT scanning, pericardial biopsies, or pericardiocentesis may aid in diagnosis.Treatment. The preferred treatment depends on the underly-ing cause of the pericarditis. The disease usually follows a self-limited and benign course and can be successfully treated with a short course of nonsteroidal anti-inflammatory agents (NSAIDs). The addition of colchicine may be beneficial.273 Some patients may require judicious use of steroids or IV anti-biotics. In cases of purulent pyogenic pericarditis, surgical exploration and drainage are occasionally necessary. Rarely, accumulation of fluid in the pericardium may lead to tampon-ade, requiring prompt evacuation of the pericardial space. While pericardiocentesis will typically |
Surgery_Schwartz_5618 | Surgery_Schwartz | are occasionally necessary. Rarely, accumulation of fluid in the pericardium may lead to tampon-ade, requiring prompt evacuation of the pericardial space. While pericardiocentesis will typically suffice, surgical drain-age may be required for thick, viscous, or clotted fluid or in patients with significant scarring from previous operations. More commonly, surgical intervention is required to manage recurrent disease.8Table 21-14Features of acute pericarditis• Pleuritic and positional, retrosternal chest pain• Pericardial friction rub• EKG changes: diffuse ST elevation and PR depression• Pericardial effusionEKG = Electrocardiogram.Relapsing PericarditisAs many as one-third of patients with acute pericarditis will develop at least one episode of relapse.267 While many of these patients can be treated medically during their initial relapse and do not experience further episodes, a subset of patients experi-ence chronic relapsing pericarditis that can significantly impact their quality of | Surgery_Schwartz. are occasionally necessary. Rarely, accumulation of fluid in the pericardium may lead to tampon-ade, requiring prompt evacuation of the pericardial space. While pericardiocentesis will typically suffice, surgical drain-age may be required for thick, viscous, or clotted fluid or in patients with significant scarring from previous operations. More commonly, surgical intervention is required to manage recurrent disease.8Table 21-14Features of acute pericarditis• Pleuritic and positional, retrosternal chest pain• Pericardial friction rub• EKG changes: diffuse ST elevation and PR depression• Pericardial effusionEKG = Electrocardiogram.Relapsing PericarditisAs many as one-third of patients with acute pericarditis will develop at least one episode of relapse.267 While many of these patients can be treated medically during their initial relapse and do not experience further episodes, a subset of patients experi-ence chronic relapsing pericarditis that can significantly impact their quality of |
Surgery_Schwartz_5619 | Surgery_Schwartz | treated medically during their initial relapse and do not experience further episodes, a subset of patients experi-ence chronic relapsing pericarditis that can significantly impact their quality of life. Recurrence may develop either from the original etiology or from an autoimmune process that occurs as a consequence of damage from the initial episode. Relapsing pericarditis normally responds to a longer course of NSAIDS ± colchicine. While steroids may induce rapid symptomatic response, their use should be limited to patients who have mul-tiple relapses and are unresponsive to first-line agents, as several studies have suggested that steroid administration may favor relapse.273,274Pericardiectomy may be considered a last resort treatment in patients with relapsing pericarditis who are severely symp-tomatic despite optimal medical management, are unable to tol-erate steroids, or have recurrence with tamponade. Evidence for this approach is lacking, as few studies have described | Surgery_Schwartz. treated medically during their initial relapse and do not experience further episodes, a subset of patients experi-ence chronic relapsing pericarditis that can significantly impact their quality of life. Recurrence may develop either from the original etiology or from an autoimmune process that occurs as a consequence of damage from the initial episode. Relapsing pericarditis normally responds to a longer course of NSAIDS ± colchicine. While steroids may induce rapid symptomatic response, their use should be limited to patients who have mul-tiple relapses and are unresponsive to first-line agents, as several studies have suggested that steroid administration may favor relapse.273,274Pericardiectomy may be considered a last resort treatment in patients with relapsing pericarditis who are severely symp-tomatic despite optimal medical management, are unable to tol-erate steroids, or have recurrence with tamponade. Evidence for this approach is lacking, as few studies have described |
Surgery_Schwartz_5620 | Surgery_Schwartz | are severely symp-tomatic despite optimal medical management, are unable to tol-erate steroids, or have recurrence with tamponade. Evidence for this approach is lacking, as few studies have described pericar-diectomy in this population.275-277 The largest study and the only one to compare surgical treatment with medical management for patients with persistent relapsing pericarditis was a report of 184 patients from the Mayo Clinic.276 About 58 patients were identi-fied as having undergone a pericardiectomy after failed medi-cal treatment, whereas the remainder were treated with medical management only. Compared to medical treatment only, peri-cardiectomy resulted in significantly fewer relapses (8.6% vs. 28.6%, P = 0.009) at long term follow-up, as well as a nonsig-nificant trend towards less medication and corticosteroid usage. Of note, 80% of patients in the pericardiectomy group who had relapses reported significant improvements in their symptoms and had fewer relapses than before | Surgery_Schwartz. are severely symp-tomatic despite optimal medical management, are unable to tol-erate steroids, or have recurrence with tamponade. Evidence for this approach is lacking, as few studies have described pericar-diectomy in this population.275-277 The largest study and the only one to compare surgical treatment with medical management for patients with persistent relapsing pericarditis was a report of 184 patients from the Mayo Clinic.276 About 58 patients were identi-fied as having undergone a pericardiectomy after failed medi-cal treatment, whereas the remainder were treated with medical management only. Compared to medical treatment only, peri-cardiectomy resulted in significantly fewer relapses (8.6% vs. 28.6%, P = 0.009) at long term follow-up, as well as a nonsig-nificant trend towards less medication and corticosteroid usage. Of note, 80% of patients in the pericardiectomy group who had relapses reported significant improvements in their symptoms and had fewer relapses than before |
Surgery_Schwartz_5621 | Surgery_Schwartz | less medication and corticosteroid usage. Of note, 80% of patients in the pericardiectomy group who had relapses reported significant improvements in their symptoms and had fewer relapses than before pericardiectomy. No periop-erative deaths were observed, and only two patients (3%) had major complications. Hence, at experienced centers pericardi-ectomy may be a safe and viable option in select patients with relapsing pericarditis.Chronic Constrictive PericarditisEtiology, Pathology, and Pathophysiology. Constrictive pericarditis can occur after any pericardial disease process but remains a rare outcome of recurrent pericarditis. It results when chronic pericardial scarring and fibrosis cause adhesion of the visceral and parietal layers and resultant obliteration of the pericardial space. While the pericardium is often grossly thickened with either focal or diffuse calcification in chronic disease, constriction may occur with normal pericardial thick-ness in approximately 20% of | Surgery_Schwartz. less medication and corticosteroid usage. Of note, 80% of patients in the pericardiectomy group who had relapses reported significant improvements in their symptoms and had fewer relapses than before pericardiectomy. No periop-erative deaths were observed, and only two patients (3%) had major complications. Hence, at experienced centers pericardi-ectomy may be a safe and viable option in select patients with relapsing pericarditis.Chronic Constrictive PericarditisEtiology, Pathology, and Pathophysiology. Constrictive pericarditis can occur after any pericardial disease process but remains a rare outcome of recurrent pericarditis. It results when chronic pericardial scarring and fibrosis cause adhesion of the visceral and parietal layers and resultant obliteration of the pericardial space. While the pericardium is often grossly thickened with either focal or diffuse calcification in chronic disease, constriction may occur with normal pericardial thick-ness in approximately 20% of |
Surgery_Schwartz_5622 | Surgery_Schwartz | While the pericardium is often grossly thickened with either focal or diffuse calcification in chronic disease, constriction may occur with normal pericardial thick-ness in approximately 20% of cases.267,278 In developed nations, idiopathic causes and cardiac surgery (accounting for almost 40% of cases in some series) are the predominant underlying eti-ologies, followed by mediastinal radiation, pyogenic infections (i.e., Staphylococcus), and other miscellaneous causes. Tuber-culosis is an additional common cause in immunosuppressed patients and in developing or underdeveloped countries.Clinically, pericardial constriction limits diastolic filling of the ventricles and mimics right heart failure since the right-sided chambers are more affected by a rise in filling pressures. Subsequent increases in central venous pressure result in the progressive development of hepatomegaly, ascites, peripheral edema, abdominal pain, dyspnea on exertion, anorexia, and nausea (in part due to hepatic | Surgery_Schwartz. While the pericardium is often grossly thickened with either focal or diffuse calcification in chronic disease, constriction may occur with normal pericardial thick-ness in approximately 20% of cases.267,278 In developed nations, idiopathic causes and cardiac surgery (accounting for almost 40% of cases in some series) are the predominant underlying eti-ologies, followed by mediastinal radiation, pyogenic infections (i.e., Staphylococcus), and other miscellaneous causes. Tuber-culosis is an additional common cause in immunosuppressed patients and in developing or underdeveloped countries.Clinically, pericardial constriction limits diastolic filling of the ventricles and mimics right heart failure since the right-sided chambers are more affected by a rise in filling pressures. Subsequent increases in central venous pressure result in the progressive development of hepatomegaly, ascites, peripheral edema, abdominal pain, dyspnea on exertion, anorexia, and nausea (in part due to hepatic |
Surgery_Schwartz_5623 | Surgery_Schwartz | in central venous pressure result in the progressive development of hepatomegaly, ascites, peripheral edema, abdominal pain, dyspnea on exertion, anorexia, and nausea (in part due to hepatic and bowel congestion). In many patients, these symptoms develop insidiously over a course Brunicardi_Ch21_p0801-p0852.indd 84001/03/19 5:32 PM 841ACQUIRED HEART DISEASECHAPTER 21of years. Since many of these symptoms are similar to those seen in patients with restrictive cardiomyopathy, the distinc-tion between the two entities is difficult, but it remains critical because the treatment is completely different for restriction. The primary difference is that restrictive cardiomyopathy is defined by a nondilated ventricle with a rigid myocardium that causes a significant decrease in myocardial compliance, which is not seen in constrictive pericarditis.Clinical and Diagnostic Findings. Classic physical exam findings include jugular venous distention with Kussmaul’s sign, diminished cardiac apical | Surgery_Schwartz. in central venous pressure result in the progressive development of hepatomegaly, ascites, peripheral edema, abdominal pain, dyspnea on exertion, anorexia, and nausea (in part due to hepatic and bowel congestion). In many patients, these symptoms develop insidiously over a course Brunicardi_Ch21_p0801-p0852.indd 84001/03/19 5:32 PM 841ACQUIRED HEART DISEASECHAPTER 21of years. Since many of these symptoms are similar to those seen in patients with restrictive cardiomyopathy, the distinc-tion between the two entities is difficult, but it remains critical because the treatment is completely different for restriction. The primary difference is that restrictive cardiomyopathy is defined by a nondilated ventricle with a rigid myocardium that causes a significant decrease in myocardial compliance, which is not seen in constrictive pericarditis.Clinical and Diagnostic Findings. Classic physical exam findings include jugular venous distention with Kussmaul’s sign, diminished cardiac apical |
Surgery_Schwartz_5624 | Surgery_Schwartz | which is not seen in constrictive pericarditis.Clinical and Diagnostic Findings. Classic physical exam findings include jugular venous distention with Kussmaul’s sign, diminished cardiac apical impulses, peripheral edema, ascites, pulsatile liver, a pericardial knock, and, in advanced disease, signs of liver dysfunction, such as jaundice or cachexia. The “pericardial knock” is an early diastolic sound that reflects a sudden impediment to ventricular filling, similar to an S3 but of higher pitch.Several findings are characteristic on noninvasive and invasive testing. CVP is often elevated 15 to 20 mmHg or higher. ECG commonly demonstrates nonspecific low voltage QRS complexes and isolated repolarization abnormalities. Chest X-ray may demonstrate calcification of the pericardium, which is highly suggestive of constrictive pericarditis in patients with heart failure, but this is present in only 25% of cases.274 Cardiac CT or MRI (cMRI) typically demonstrate increased pericardial | Surgery_Schwartz. which is not seen in constrictive pericarditis.Clinical and Diagnostic Findings. Classic physical exam findings include jugular venous distention with Kussmaul’s sign, diminished cardiac apical impulses, peripheral edema, ascites, pulsatile liver, a pericardial knock, and, in advanced disease, signs of liver dysfunction, such as jaundice or cachexia. The “pericardial knock” is an early diastolic sound that reflects a sudden impediment to ventricular filling, similar to an S3 but of higher pitch.Several findings are characteristic on noninvasive and invasive testing. CVP is often elevated 15 to 20 mmHg or higher. ECG commonly demonstrates nonspecific low voltage QRS complexes and isolated repolarization abnormalities. Chest X-ray may demonstrate calcification of the pericardium, which is highly suggestive of constrictive pericarditis in patients with heart failure, but this is present in only 25% of cases.274 Cardiac CT or MRI (cMRI) typically demonstrate increased pericardial |
Surgery_Schwartz_5625 | Surgery_Schwartz | is highly suggestive of constrictive pericarditis in patients with heart failure, but this is present in only 25% of cases.274 Cardiac CT or MRI (cMRI) typically demonstrate increased pericardial thickness (>4 mm) and calcification, dilation of the inferior vena cava, deformed ventricular contours, and flattening or leftward shift of the ventricular septum. Pericardial adhesions may also be seen on tagged cine MRI studies.As discussed, it is most important to distinguish peri-cardial constriction from restrictive cardiomyopathy, which is best done with either echocardiography or right heart catheter-ization. Findings favoring constriction on echocardiography include respiratory variation of ventricular septal motion and mitral inflow velocity, preserved or increased mitral annulus early diastolic filling velocity, and increased hepatic vein flow reversal with expiration.267,274 Cardiac catheterization will show increased atrial pressures, equalization of end-diastolic pressure and | Surgery_Schwartz. is highly suggestive of constrictive pericarditis in patients with heart failure, but this is present in only 25% of cases.274 Cardiac CT or MRI (cMRI) typically demonstrate increased pericardial thickness (>4 mm) and calcification, dilation of the inferior vena cava, deformed ventricular contours, and flattening or leftward shift of the ventricular septum. Pericardial adhesions may also be seen on tagged cine MRI studies.As discussed, it is most important to distinguish peri-cardial constriction from restrictive cardiomyopathy, which is best done with either echocardiography or right heart catheter-ization. Findings favoring constriction on echocardiography include respiratory variation of ventricular septal motion and mitral inflow velocity, preserved or increased mitral annulus early diastolic filling velocity, and increased hepatic vein flow reversal with expiration.267,274 Cardiac catheterization will show increased atrial pressures, equalization of end-diastolic pressure and |
Surgery_Schwartz_5626 | Surgery_Schwartz | diastolic filling velocity, and increased hepatic vein flow reversal with expiration.267,274 Cardiac catheterization will show increased atrial pressures, equalization of end-diastolic pressure and early ventricular diastolic filling with a subsequent plateau, called the “square-root sign.” Additional findings upon cath-eterization that would favor constriction include respiratory variation in ventricular filling and increased ventricular inter-dependence, manifest as a discordant change in the total area of the LV and RV systolic pressure curve with respiration.Surgical Treatment. Transient constrictive pericarditis may occur weeks to months after an initial injury and follows a self-limiting course of weeks to a few months. These patients are best treated with medical therapy alone. They often lack calci-fication of their pericardium, and the degree of late gadolinium enhancement of the pericardium on cardiac MRI has shown promise in predicting which patients may have resolution of | Surgery_Schwartz. diastolic filling velocity, and increased hepatic vein flow reversal with expiration.267,274 Cardiac catheterization will show increased atrial pressures, equalization of end-diastolic pressure and early ventricular diastolic filling with a subsequent plateau, called the “square-root sign.” Additional findings upon cath-eterization that would favor constriction include respiratory variation in ventricular filling and increased ventricular inter-dependence, manifest as a discordant change in the total area of the LV and RV systolic pressure curve with respiration.Surgical Treatment. Transient constrictive pericarditis may occur weeks to months after an initial injury and follows a self-limiting course of weeks to a few months. These patients are best treated with medical therapy alone. They often lack calci-fication of their pericardium, and the degree of late gadolinium enhancement of the pericardium on cardiac MRI has shown promise in predicting which patients may have resolution of |
Surgery_Schwartz_5627 | Surgery_Schwartz | often lack calci-fication of their pericardium, and the degree of late gadolinium enhancement of the pericardium on cardiac MRI has shown promise in predicting which patients may have resolution of the process.279 Still, there is no ideal way to distinguish these patients from those who will develop chronic constrictive peri-carditis, which is permanent. Therefore, if a newly diagnosed patient is hemodynamically stable, it is recommended that con-servative management is attempted for 2 to 3 months prior to performing a pericardiectomy.278 Surgical therapy should not be delayed indefinitely, however, as results are improved when the operation is performed earlier in the course of the disease. A series of 938 patients undergoing pericardiectomy reported by the Mayo Clinic, 355 of whom underwent pericardiec-tomy for constrictive pericarditis, showed significantly lower survival in patients with constrictive pericarditis compared with patients with effusive/relapsing pericarditis.280 | Surgery_Schwartz. often lack calci-fication of their pericardium, and the degree of late gadolinium enhancement of the pericardium on cardiac MRI has shown promise in predicting which patients may have resolution of the process.279 Still, there is no ideal way to distinguish these patients from those who will develop chronic constrictive peri-carditis, which is permanent. Therefore, if a newly diagnosed patient is hemodynamically stable, it is recommended that con-servative management is attempted for 2 to 3 months prior to performing a pericardiectomy.278 Surgical therapy should not be delayed indefinitely, however, as results are improved when the operation is performed earlier in the course of the disease. A series of 938 patients undergoing pericardiectomy reported by the Mayo Clinic, 355 of whom underwent pericardiec-tomy for constrictive pericarditis, showed significantly lower survival in patients with constrictive pericarditis compared with patients with effusive/relapsing pericarditis.280 |
Surgery_Schwartz_5628 | Surgery_Schwartz | pericardiec-tomy for constrictive pericarditis, showed significantly lower survival in patients with constrictive pericarditis compared with patients with effusive/relapsing pericarditis.280 Patients with left ventricular systolic dysfunction or right ventricular dilata-tion are at increased risk of early mortality.281 Additional fac-tors that predict adverse long-term outcomes include older age and prior ionizing radiation, as well as cardiopulmonary and renal dysfunction.274,281 Surgery should therefore be approached cautiously in patients with advanced, “end-stage” constrictive pericarditis, mixed constrictive-restrictive disease (often from radiation), and significant myocardial or renal dysfunction, as those patients are at increased risk from surgery and may not experience improvement of symptoms.In order to minimize recurrence following pericardiec-tomy, complete pericardial resection is desirable. This is typi-cally performed through either a median sternotomy or left | Surgery_Schwartz. pericardiec-tomy for constrictive pericarditis, showed significantly lower survival in patients with constrictive pericarditis compared with patients with effusive/relapsing pericarditis.280 Patients with left ventricular systolic dysfunction or right ventricular dilata-tion are at increased risk of early mortality.281 Additional fac-tors that predict adverse long-term outcomes include older age and prior ionizing radiation, as well as cardiopulmonary and renal dysfunction.274,281 Surgery should therefore be approached cautiously in patients with advanced, “end-stage” constrictive pericarditis, mixed constrictive-restrictive disease (often from radiation), and significant myocardial or renal dysfunction, as those patients are at increased risk from surgery and may not experience improvement of symptoms.In order to minimize recurrence following pericardiec-tomy, complete pericardial resection is desirable. This is typi-cally performed through either a median sternotomy or left |
Surgery_Schwartz_5629 | Surgery_Schwartz | of symptoms.In order to minimize recurrence following pericardiec-tomy, complete pericardial resection is desirable. This is typi-cally performed through either a median sternotomy or left anterolateral thoracotomy while on cardiopulmonary bypass. Radical pericardiectomy involves wide resection of the con-stricting pericardium from the anterior surface of the heart between the phrenic nerves and the diaphragmatic surface. Decortication of the right atrium and vena cavae is not univer-sally performed, but doing so improves the risk of persistent disease or relapse.282,283The extent of myocardial involvement may also affect long-term outcomes, and, thus, the depth of decortication is an important consideration.282 Even when an adequate pericardi-ectomy is performed, epicardial sclerosis can cause persistent hemodynamic instability or a delayed response to surgery. Scle-rotic epicardium is often thin and nearly transparent, but in cases of severe chronic constrictive pericarditis it can | Surgery_Schwartz. of symptoms.In order to minimize recurrence following pericardiec-tomy, complete pericardial resection is desirable. This is typi-cally performed through either a median sternotomy or left anterolateral thoracotomy while on cardiopulmonary bypass. Radical pericardiectomy involves wide resection of the con-stricting pericardium from the anterior surface of the heart between the phrenic nerves and the diaphragmatic surface. Decortication of the right atrium and vena cavae is not univer-sally performed, but doing so improves the risk of persistent disease or relapse.282,283The extent of myocardial involvement may also affect long-term outcomes, and, thus, the depth of decortication is an important consideration.282 Even when an adequate pericardi-ectomy is performed, epicardial sclerosis can cause persistent hemodynamic instability or a delayed response to surgery. Scle-rotic epicardium is often thin and nearly transparent, but in cases of severe chronic constrictive pericarditis it can |
Surgery_Schwartz_5630 | Surgery_Schwartz | cause persistent hemodynamic instability or a delayed response to surgery. Scle-rotic epicardium is often thin and nearly transparent, but in cases of severe chronic constrictive pericarditis it can be difficult to remove it without injury to the heart.Surgical Results. While most patients experience significant improvement in their symptoms following pericardiectomy, symptomatic relief may take several months. Since there is a significant perioperative morbidity and mortality, pericardiec-tomy is best performed by experienced surgeons at high-volume centers. Between 1970 and 1985, the operative mortality was reported to be 12%, but a lower mortality of approximately 4% to 8% was noted between 1977 and 2006 at several experienced centers.278,283-287Long-term survival is in part determined by etiology of the disease. In a report from the Cleveland Clinic, 7-year survival rates following pericardiectomy for idiopathic, postsurgical, and radiation-induced constrictive pericarditis were | Surgery_Schwartz. cause persistent hemodynamic instability or a delayed response to surgery. Scle-rotic epicardium is often thin and nearly transparent, but in cases of severe chronic constrictive pericarditis it can be difficult to remove it without injury to the heart.Surgical Results. While most patients experience significant improvement in their symptoms following pericardiectomy, symptomatic relief may take several months. Since there is a significant perioperative morbidity and mortality, pericardiec-tomy is best performed by experienced surgeons at high-volume centers. Between 1970 and 1985, the operative mortality was reported to be 12%, but a lower mortality of approximately 4% to 8% was noted between 1977 and 2006 at several experienced centers.278,283-287Long-term survival is in part determined by etiology of the disease. In a report from the Cleveland Clinic, 7-year survival rates following pericardiectomy for idiopathic, postsurgical, and radiation-induced constrictive pericarditis were |
Surgery_Schwartz_5631 | Surgery_Schwartz | by etiology of the disease. In a report from the Cleveland Clinic, 7-year survival rates following pericardiectomy for idiopathic, postsurgical, and radiation-induced constrictive pericarditis were 88%, 66%, and 27%, respectively.284 Results are worst for radiation-induced disease because ionizing radiation is often associated with myo-cardial injury as well as pericardial disease.Despite the risks, many patients experience significant benefits from surgical treatment. In one large series, 83% of patients were reported to be free of symptoms at last follow-up.287 This is in agreement with other studies that have shown a signif-icant improvement in NYHA functional status from class III/IV preoperatively to class I/II following pericardiectomy in >95% of patients.283,285-287CARDIAC NEOPLASMSOverview and General Clinical FeaturesCardiac neoplasms are rare, with an incidence ranging from 0.001% to 0.3% in autopsy studies and a 0.15% incidence in major echocardiographic series.288,289 In | Surgery_Schwartz. by etiology of the disease. In a report from the Cleveland Clinic, 7-year survival rates following pericardiectomy for idiopathic, postsurgical, and radiation-induced constrictive pericarditis were 88%, 66%, and 27%, respectively.284 Results are worst for radiation-induced disease because ionizing radiation is often associated with myo-cardial injury as well as pericardial disease.Despite the risks, many patients experience significant benefits from surgical treatment. In one large series, 83% of patients were reported to be free of symptoms at last follow-up.287 This is in agreement with other studies that have shown a signif-icant improvement in NYHA functional status from class III/IV preoperatively to class I/II following pericardiectomy in >95% of patients.283,285-287CARDIAC NEOPLASMSOverview and General Clinical FeaturesCardiac neoplasms are rare, with an incidence ranging from 0.001% to 0.3% in autopsy studies and a 0.15% incidence in major echocardiographic series.288,289 In |
Surgery_Schwartz_5632 | Surgery_Schwartz | and General Clinical FeaturesCardiac neoplasms are rare, with an incidence ranging from 0.001% to 0.3% in autopsy studies and a 0.15% incidence in major echocardiographic series.288,289 In one large autopsy series, 99.2% of cardiac tumors were metastatic in origin; however, Brunicardi_Ch21_p0801-p0852.indd 84101/03/19 5:32 PM 842SPECIFIC CONSIDERATIONSPART IIthese patients almost never present for surgical management as they usually have fatal diffuse metastatic disease.290 As a result, a majority of surgical series describe management of primary cardiac neoplasms. Benign cardiac tumors are most common and account for 75% of primary neoplasms. Approximately 50% of benign cardiac tumors are myxomas, with the remainder being papillary fibroelastomas, lipomas, rhabdomyomas, fibro-mas, hemangiomas, teratomas, lymphangiomas, and others, in order of decreasing frequency. Most malignant primary cardiac tumors are sarcomas (angiosarcoma, rhabdomyosarcoma, fibro-sarcoma, leiomyosarcoma, | Surgery_Schwartz. and General Clinical FeaturesCardiac neoplasms are rare, with an incidence ranging from 0.001% to 0.3% in autopsy studies and a 0.15% incidence in major echocardiographic series.288,289 In one large autopsy series, 99.2% of cardiac tumors were metastatic in origin; however, Brunicardi_Ch21_p0801-p0852.indd 84101/03/19 5:32 PM 842SPECIFIC CONSIDERATIONSPART IIthese patients almost never present for surgical management as they usually have fatal diffuse metastatic disease.290 As a result, a majority of surgical series describe management of primary cardiac neoplasms. Benign cardiac tumors are most common and account for 75% of primary neoplasms. Approximately 50% of benign cardiac tumors are myxomas, with the remainder being papillary fibroelastomas, lipomas, rhabdomyomas, fibro-mas, hemangiomas, teratomas, lymphangiomas, and others, in order of decreasing frequency. Most malignant primary cardiac tumors are sarcomas (angiosarcoma, rhabdomyosarcoma, fibro-sarcoma, leiomyosarcoma, |
Surgery_Schwartz_5633 | Surgery_Schwartz | hemangiomas, teratomas, lymphangiomas, and others, in order of decreasing frequency. Most malignant primary cardiac tumors are sarcomas (angiosarcoma, rhabdomyosarcoma, fibro-sarcoma, leiomyosarcoma, and liposarcoma), with a small inci-dence of malignant lymphomas.Clinical Presentation. The clinical presentation of cardiac neoplasms varies greatly depending on the location of the tumor, as well as its size, rate of growth, invasiveness, and fri-ability. While as many as 10% of patients are asymptomatic, most manifest some combination of symptoms from the classic triad resulting from blood flow obstruction, tumor embolization, and constitutional symptoms.291,292 Systemic manifestations of disease include fever, myalgias, chills, night sweats, weight loss, and fatigue and occur in up to one-third of patients.Obstruction of cardiac blood flow accounts for the major-ity of presenting symptoms.292 When the tumor is located in the left atrium, symptoms tend to mimic mitral valve disease | Surgery_Schwartz. hemangiomas, teratomas, lymphangiomas, and others, in order of decreasing frequency. Most malignant primary cardiac tumors are sarcomas (angiosarcoma, rhabdomyosarcoma, fibro-sarcoma, leiomyosarcoma, and liposarcoma), with a small inci-dence of malignant lymphomas.Clinical Presentation. The clinical presentation of cardiac neoplasms varies greatly depending on the location of the tumor, as well as its size, rate of growth, invasiveness, and fri-ability. While as many as 10% of patients are asymptomatic, most manifest some combination of symptoms from the classic triad resulting from blood flow obstruction, tumor embolization, and constitutional symptoms.291,292 Systemic manifestations of disease include fever, myalgias, chills, night sweats, weight loss, and fatigue and occur in up to one-third of patients.Obstruction of cardiac blood flow accounts for the major-ity of presenting symptoms.292 When the tumor is located in the left atrium, symptoms tend to mimic mitral valve disease |
Surgery_Schwartz_5634 | Surgery_Schwartz | one-third of patients.Obstruction of cardiac blood flow accounts for the major-ity of presenting symptoms.292 When the tumor is located in the left atrium, symptoms tend to mimic mitral valve disease with dyspnea and pulmonary edema; although more severe presenta-tions with syncopal episodes, hypotension, and sudden cardiac death have been reported from temporary valve orifice occlu-sion. When the tumor is located in the right atrium, symptoms may mimic right heart failure and include hepatomegaly, asci-tes, and peripheral edema. Outflow tract obstruction is rare but may be caused by large ventricular tumors.293Tumor lysis and embolization may also lead to neurologic presentations such as stroke, retinal artery occlusion, or cere-bral aneurysms, particularly in the case of pedunculated tumors and those with frond-like projections.294 Embolic tumor cells are able to lodge and penetrate distant vessel walls via subintimal growth, which leads to weakening of the arterial wall and | Surgery_Schwartz. one-third of patients.Obstruction of cardiac blood flow accounts for the major-ity of presenting symptoms.292 When the tumor is located in the left atrium, symptoms tend to mimic mitral valve disease with dyspnea and pulmonary edema; although more severe presenta-tions with syncopal episodes, hypotension, and sudden cardiac death have been reported from temporary valve orifice occlu-sion. When the tumor is located in the right atrium, symptoms may mimic right heart failure and include hepatomegaly, asci-tes, and peripheral edema. Outflow tract obstruction is rare but may be caused by large ventricular tumors.293Tumor lysis and embolization may also lead to neurologic presentations such as stroke, retinal artery occlusion, or cere-bral aneurysms, particularly in the case of pedunculated tumors and those with frond-like projections.294 Embolic tumor cells are able to lodge and penetrate distant vessel walls via subintimal growth, which leads to weakening of the arterial wall and |
Surgery_Schwartz_5635 | Surgery_Schwartz | tumors and those with frond-like projections.294 Embolic tumor cells are able to lodge and penetrate distant vessel walls via subintimal growth, which leads to weakening of the arterial wall and sub-sequent aneurysm formation. This has been documented as late as 5 years after successful primary myxoma resection.295 Alter-natively, embolic implants may metastasize and create space occupying lesions. While rare, myxomatous tumor emboli have also been identified in the coronary arteries, common iliac and femoral arteries, kidney, spleen, pancreas, and liver.294Certain clinical features may be helpful in distinguishing benign from malignant primary cardiac tumors.292 Malignant tumors, primarily sarcomas, do not demonstrate a gender pref-erence and tend to present after the fourth decade of life. They are often multifocal within the right atrium, and intramyocardial invasion can lead to refractory congestive heart failure, arrhyth-mias, hemopericardium, and ischemia. Conversely, benign | Surgery_Schwartz. tumors and those with frond-like projections.294 Embolic tumor cells are able to lodge and penetrate distant vessel walls via subintimal growth, which leads to weakening of the arterial wall and sub-sequent aneurysm formation. This has been documented as late as 5 years after successful primary myxoma resection.295 Alter-natively, embolic implants may metastasize and create space occupying lesions. While rare, myxomatous tumor emboli have also been identified in the coronary arteries, common iliac and femoral arteries, kidney, spleen, pancreas, and liver.294Certain clinical features may be helpful in distinguishing benign from malignant primary cardiac tumors.292 Malignant tumors, primarily sarcomas, do not demonstrate a gender pref-erence and tend to present after the fourth decade of life. They are often multifocal within the right atrium, and intramyocardial invasion can lead to refractory congestive heart failure, arrhyth-mias, hemopericardium, and ischemia. Conversely, benign |
Surgery_Schwartz_5636 | Surgery_Schwartz | life. They are often multifocal within the right atrium, and intramyocardial invasion can lead to refractory congestive heart failure, arrhyth-mias, hemopericardium, and ischemia. Conversely, benign tumors, primarily myxomas, are typically unifocal in the left atrium, have a 3:1 female preference, and occur in younger patients. Arrhythmias and pericardial effusions are very rare in this population.Diagnosis and Characterization of Cardiac Masses. Trans-thoracic echocardiography is the mainstay imaging technique for the detection of cardiac tumors.292 However, echocardiogra-phy is limited by dependence on an acoustic window, subopti-mal visualization of extracardiac extension, and poor soft-tissue visualization. TEE is generally only beneficial for small local-ized tumors due to its limited field of view. cMRI is therefore the current standard for delineating the anatomical extent of the tumor and assessing the paracardiac space and great vessels. Advantages of cMRI over CT scans | Surgery_Schwartz. life. They are often multifocal within the right atrium, and intramyocardial invasion can lead to refractory congestive heart failure, arrhyth-mias, hemopericardium, and ischemia. Conversely, benign tumors, primarily myxomas, are typically unifocal in the left atrium, have a 3:1 female preference, and occur in younger patients. Arrhythmias and pericardial effusions are very rare in this population.Diagnosis and Characterization of Cardiac Masses. Trans-thoracic echocardiography is the mainstay imaging technique for the detection of cardiac tumors.292 However, echocardiogra-phy is limited by dependence on an acoustic window, subopti-mal visualization of extracardiac extension, and poor soft-tissue visualization. TEE is generally only beneficial for small local-ized tumors due to its limited field of view. cMRI is therefore the current standard for delineating the anatomical extent of the tumor and assessing the paracardiac space and great vessels. Advantages of cMRI over CT scans |
Surgery_Schwartz_5637 | Surgery_Schwartz | field of view. cMRI is therefore the current standard for delineating the anatomical extent of the tumor and assessing the paracardiac space and great vessels. Advantages of cMRI over CT scans include better soft-tissue evaluation without the need for iodinated contrast and no expo-sure to ionizing radiation.It is important in the initial workup to distinguish a cardiac tumor from an intracardiac thrombus, which may be common in the atria of patients with AF and can mimic echocardiographic features of atrial myxomas. This determination is critical, as an atrial thrombus may be expected to resolve with anticoagula-tion, whereas a tumor requires surgical intervention. Moreover, anticoagulation can potentially increase the risk of peripheral embolization in patients with cardiac tumors. Delayed enhance-ment cMRI is the best modality to separate these two entities. cMRI may show vascularization, areas of necrosis, hemorrhage, or calcification in cardiac tumors that are not present in | Surgery_Schwartz. field of view. cMRI is therefore the current standard for delineating the anatomical extent of the tumor and assessing the paracardiac space and great vessels. Advantages of cMRI over CT scans include better soft-tissue evaluation without the need for iodinated contrast and no expo-sure to ionizing radiation.It is important in the initial workup to distinguish a cardiac tumor from an intracardiac thrombus, which may be common in the atria of patients with AF and can mimic echocardiographic features of atrial myxomas. This determination is critical, as an atrial thrombus may be expected to resolve with anticoagula-tion, whereas a tumor requires surgical intervention. Moreover, anticoagulation can potentially increase the risk of peripheral embolization in patients with cardiac tumors. Delayed enhance-ment cMRI is the best modality to separate these two entities. cMRI may show vascularization, areas of necrosis, hemorrhage, or calcification in cardiac tumors that are not present in |
Surgery_Schwartz_5638 | Surgery_Schwartz | Delayed enhance-ment cMRI is the best modality to separate these two entities. cMRI may show vascularization, areas of necrosis, hemorrhage, or calcification in cardiac tumors that are not present in thrombi.MyxomaPathology and Genetics. Cardiac myxomas are the most common cardiac tumor and are characterized by several distinguishing features. About 75% of the time, they arise from the interatrial septum near the fossa ovalis in the left atrium.296 Most others will develop in the right atrium, but, less commonly, they can arise from valvular surfaces and the walls of other cardiac chambers. Macroscopically, these tumors are pedunculated with a gelatinous consistency, and the surface may be smooth (65%), villous, or friable.291 Size varies greatly with these tumors and ranges from 1 to 15 cm in diameter. Internally, myxomas are heterogeneous and often contain hemorrhage, cysts, necrosis, or calcification. Histologically, these tumors contain cells that arise from a multipotent | Surgery_Schwartz. Delayed enhance-ment cMRI is the best modality to separate these two entities. cMRI may show vascularization, areas of necrosis, hemorrhage, or calcification in cardiac tumors that are not present in thrombi.MyxomaPathology and Genetics. Cardiac myxomas are the most common cardiac tumor and are characterized by several distinguishing features. About 75% of the time, they arise from the interatrial septum near the fossa ovalis in the left atrium.296 Most others will develop in the right atrium, but, less commonly, they can arise from valvular surfaces and the walls of other cardiac chambers. Macroscopically, these tumors are pedunculated with a gelatinous consistency, and the surface may be smooth (65%), villous, or friable.291 Size varies greatly with these tumors and ranges from 1 to 15 cm in diameter. Internally, myxomas are heterogeneous and often contain hemorrhage, cysts, necrosis, or calcification. Histologically, these tumors contain cells that arise from a multipotent |
Surgery_Schwartz_5639 | Surgery_Schwartz | 1 to 15 cm in diameter. Internally, myxomas are heterogeneous and often contain hemorrhage, cysts, necrosis, or calcification. Histologically, these tumors contain cells that arise from a multipotent mesenchyme and are contained within a mucopolysaccharide stroma.297While the majority of myxomas occur spontaneously with the highest incidence in women aged 40 to 60 years old, approx-imately 7% of cases are familial as part of Carney complex.291 Carney complex is an autosomal dominant disorder character-ized by two or more of the following conditions: atrial and extra-cardiac myxomas, schwannomas, cutaneous lentiginosis, spotty pigmentation, myxoid fibroadenomas of the breast, endocrine overactivity (pituitary adenomas or primary adrenal hyperplasia with Cushing’s syndrome), and testicular tumors. Compared to sporadic myxomas, those that occur as part of Carney complex are more commonly found in the right atrium (37% vs. 18%) or one of the ventricles (25% vs. 0%), more often | Surgery_Schwartz. 1 to 15 cm in diameter. Internally, myxomas are heterogeneous and often contain hemorrhage, cysts, necrosis, or calcification. Histologically, these tumors contain cells that arise from a multipotent mesenchyme and are contained within a mucopolysaccharide stroma.297While the majority of myxomas occur spontaneously with the highest incidence in women aged 40 to 60 years old, approx-imately 7% of cases are familial as part of Carney complex.291 Carney complex is an autosomal dominant disorder character-ized by two or more of the following conditions: atrial and extra-cardiac myxomas, schwannomas, cutaneous lentiginosis, spotty pigmentation, myxoid fibroadenomas of the breast, endocrine overactivity (pituitary adenomas or primary adrenal hyperplasia with Cushing’s syndrome), and testicular tumors. Compared to sporadic myxomas, those that occur as part of Carney complex are more commonly found in the right atrium (37% vs. 18%) or one of the ventricles (25% vs. 0%), more often |
Surgery_Schwartz_5640 | Surgery_Schwartz | testicular tumors. Compared to sporadic myxomas, those that occur as part of Carney complex are more commonly found in the right atrium (37% vs. 18%) or one of the ventricles (25% vs. 0%), more often multicentric (33% vs. 6%) and more likely to recur (20% vs. 3%).296 They also present earlier at an average age of 24 years old (range 4–48 years).Pathophysiology. Larger tumors are more likely to be asso-ciated with cardiovascular symptoms from obstruction, and embolic symptoms tend to occur from organized thrombi pres-ent on friable or villous tumors (Fig. 21-16). The relative fre-quencies of symptoms was illustrated by a series of 112 patients who reported cardiovascular symptoms (67%), most commonly resembling mitral valve obstruction; systemic embolization (29%); neurologic deficits (20%); and constitutional symptoms (34%).291 Similar incidences of symptoms have been reported in other large studies.Treatment. Cardiac myxomas should be promptly excised after diagnosis due to the | Surgery_Schwartz. testicular tumors. Compared to sporadic myxomas, those that occur as part of Carney complex are more commonly found in the right atrium (37% vs. 18%) or one of the ventricles (25% vs. 0%), more often multicentric (33% vs. 6%) and more likely to recur (20% vs. 3%).296 They also present earlier at an average age of 24 years old (range 4–48 years).Pathophysiology. Larger tumors are more likely to be asso-ciated with cardiovascular symptoms from obstruction, and embolic symptoms tend to occur from organized thrombi pres-ent on friable or villous tumors (Fig. 21-16). The relative fre-quencies of symptoms was illustrated by a series of 112 patients who reported cardiovascular symptoms (67%), most commonly resembling mitral valve obstruction; systemic embolization (29%); neurologic deficits (20%); and constitutional symptoms (34%).291 Similar incidences of symptoms have been reported in other large studies.Treatment. Cardiac myxomas should be promptly excised after diagnosis due to the |
Surgery_Schwartz_5641 | Surgery_Schwartz | (20%); and constitutional symptoms (34%).291 Similar incidences of symptoms have been reported in other large studies.Treatment. Cardiac myxomas should be promptly excised after diagnosis due to the significant risk of embolization and cardiovascular complications, including sudden death. Resec-tion may be performed through either a median sternotomy or 9Brunicardi_Ch21_p0801-p0852.indd 84201/03/19 5:32 PM 843ACQUIRED HEART DISEASECHAPTER 21Figure 21-16. Massive left atrial myxoma. A. Intraoperative echocardiogram of a large left atrial mass, diagnosed preoperatively as a left atrial myxoma. The mass can be seen prolapsing through the mitral valve orifice causing intermittent symptoms of mitral stenosis. B. The resected specimen. The neck of the mass that was obstructing the mitral orifice is clearly delineated.a minimally invasive right thoracotomy while on cardiopulmo-nary bypass. Care is taken not to manipulate the tumor before cross clamping of the aorta in order to avoid | Surgery_Schwartz. (20%); and constitutional symptoms (34%).291 Similar incidences of symptoms have been reported in other large studies.Treatment. Cardiac myxomas should be promptly excised after diagnosis due to the significant risk of embolization and cardiovascular complications, including sudden death. Resec-tion may be performed through either a median sternotomy or 9Brunicardi_Ch21_p0801-p0852.indd 84201/03/19 5:32 PM 843ACQUIRED HEART DISEASECHAPTER 21Figure 21-16. Massive left atrial myxoma. A. Intraoperative echocardiogram of a large left atrial mass, diagnosed preoperatively as a left atrial myxoma. The mass can be seen prolapsing through the mitral valve orifice causing intermittent symptoms of mitral stenosis. B. The resected specimen. The neck of the mass that was obstructing the mitral orifice is clearly delineated.a minimally invasive right thoracotomy while on cardiopulmo-nary bypass. Care is taken not to manipulate the tumor before cross clamping of the aorta in order to avoid |
Surgery_Schwartz_5642 | Surgery_Schwartz | orifice is clearly delineated.a minimally invasive right thoracotomy while on cardiopulmo-nary bypass. Care is taken not to manipulate the tumor before cross clamping of the aorta in order to avoid embolization. Left atrial tumors may be approached through a standard left atriotomy.298 Exposure of large tumors attached to the interatrial septum may be facilitated by an additional parallel incision in the right atrium, but this is rarely necessary. An ideal resection encompasses both the tumor and a portion of the cardiac wall or interatrial septum to which it is attached. In order to prevent recurrence, a full thickness excision of the attachment site is preferred, but partial thickness excisions and cryoablation of the base have been performed with good late results.298 The defect created in the atrial septum can either be repaired primarily or with a small patch. Finally, patients with valvular involvement may require additional valvular reconstruction or replacement, and rare cases | Surgery_Schwartz. orifice is clearly delineated.a minimally invasive right thoracotomy while on cardiopulmo-nary bypass. Care is taken not to manipulate the tumor before cross clamping of the aorta in order to avoid embolization. Left atrial tumors may be approached through a standard left atriotomy.298 Exposure of large tumors attached to the interatrial septum may be facilitated by an additional parallel incision in the right atrium, but this is rarely necessary. An ideal resection encompasses both the tumor and a portion of the cardiac wall or interatrial septum to which it is attached. In order to prevent recurrence, a full thickness excision of the attachment site is preferred, but partial thickness excisions and cryoablation of the base have been performed with good late results.298 The defect created in the atrial septum can either be repaired primarily or with a small patch. Finally, patients with valvular involvement may require additional valvular reconstruction or replacement, and rare cases |
Surgery_Schwartz_5643 | Surgery_Schwartz | in the atrial septum can either be repaired primarily or with a small patch. Finally, patients with valvular involvement may require additional valvular reconstruction or replacement, and rare cases of cardiac autotransplantation (with atrial recon-struction) or transplantation have been reported as strategies for complex cases of recurrent atrial myxoma.299,300Shortand long-term results following excision are excellent for benign cardiac myxomas. Operative mortality is low, and the probability of disease-free survival at 20 years has been reported to be as high as 92% for benign, sporadic myxomas.291,298 Risk of recurrence is significantly higher for familial cases. Other risk factors for recurrence include younger age, smaller tumor mass, and ventricular tumor location.301Other Benign Cardiac TumorsThere are several benign cardiac tumors apart from myxomas that are infrequent but have distinct pathophysiologic features.292 Papillary fibroelastomas are the second most common primary | Surgery_Schwartz. in the atrial septum can either be repaired primarily or with a small patch. Finally, patients with valvular involvement may require additional valvular reconstruction or replacement, and rare cases of cardiac autotransplantation (with atrial recon-struction) or transplantation have been reported as strategies for complex cases of recurrent atrial myxoma.299,300Shortand long-term results following excision are excellent for benign cardiac myxomas. Operative mortality is low, and the probability of disease-free survival at 20 years has been reported to be as high as 92% for benign, sporadic myxomas.291,298 Risk of recurrence is significantly higher for familial cases. Other risk factors for recurrence include younger age, smaller tumor mass, and ventricular tumor location.301Other Benign Cardiac TumorsThere are several benign cardiac tumors apart from myxomas that are infrequent but have distinct pathophysiologic features.292 Papillary fibroelastomas are the second most common primary |
Surgery_Schwartz_5644 | Surgery_Schwartz | TumorsThere are several benign cardiac tumors apart from myxomas that are infrequent but have distinct pathophysiologic features.292 Papillary fibroelastomas are the second most common primary cardiac tumor, representing approximately 8% of all cases. These tumors typically occur in more elderly patients; are small (<1 cm in diameter) sessile, pedunculated masses that arise from the mitral or aortic valves; and frequently result in embo-lization. Fibroelastomas can almost always be resected with preservation of the native valve leaflets, and cryoablation of the valve leaflet after resection can help prevent recurrence. Lipomas are encapsulated tumors that usually arise from the epicardium and remain asymptomatic in most patients. Heman-giomas, which may arise from any cardiac structure, including the pericardium, account for 2% of benign cardiac tumors, and atrioventricular node tumors, which often lead to sudden cardiac death from heart block and ventricular fibrillation, are | Surgery_Schwartz. TumorsThere are several benign cardiac tumors apart from myxomas that are infrequent but have distinct pathophysiologic features.292 Papillary fibroelastomas are the second most common primary cardiac tumor, representing approximately 8% of all cases. These tumors typically occur in more elderly patients; are small (<1 cm in diameter) sessile, pedunculated masses that arise from the mitral or aortic valves; and frequently result in embo-lization. Fibroelastomas can almost always be resected with preservation of the native valve leaflets, and cryoablation of the valve leaflet after resection can help prevent recurrence. Lipomas are encapsulated tumors that usually arise from the epicardium and remain asymptomatic in most patients. Heman-giomas, which may arise from any cardiac structure, including the pericardium, account for 2% of benign cardiac tumors, and atrioventricular node tumors, which often lead to sudden cardiac death from heart block and ventricular fibrillation, are |
Surgery_Schwartz_5645 | Surgery_Schwartz | including the pericardium, account for 2% of benign cardiac tumors, and atrioventricular node tumors, which often lead to sudden cardiac death from heart block and ventricular fibrillation, are exceedingly rare.In children, rhabdomyomas are the most common pri-mary cardiac tumor, whereas fibromas are the most commonly resected cardiac tumor. Rhabdomyomas are myocardial hamar-tomas that are often multicentric in the ventricles. About 50% of cases are associated with tuberous sclerosis, and while resection is occasionally necessary, most disappear spontaneously. Fibro-mas are congenital lesions that one-third of the time are found in children younger than 1-year old. These tumors, conversely, are ordinarily solitary lesions found in the inner interventricu-lar septum, and they may present with heart failure, cyanosis, arrhythmias, syncopal episodes, chest pain, or sudden cardiac death.Malignant Cardiac TumorsPrimary cardiac malignancies are very rare, but when they occur they tend to | Surgery_Schwartz. including the pericardium, account for 2% of benign cardiac tumors, and atrioventricular node tumors, which often lead to sudden cardiac death from heart block and ventricular fibrillation, are exceedingly rare.In children, rhabdomyomas are the most common pri-mary cardiac tumor, whereas fibromas are the most commonly resected cardiac tumor. Rhabdomyomas are myocardial hamar-tomas that are often multicentric in the ventricles. About 50% of cases are associated with tuberous sclerosis, and while resection is occasionally necessary, most disappear spontaneously. Fibro-mas are congenital lesions that one-third of the time are found in children younger than 1-year old. These tumors, conversely, are ordinarily solitary lesions found in the inner interventricu-lar septum, and they may present with heart failure, cyanosis, arrhythmias, syncopal episodes, chest pain, or sudden cardiac death.Malignant Cardiac TumorsPrimary cardiac malignancies are very rare, but when they occur they tend to |
Surgery_Schwartz_5646 | Surgery_Schwartz | with heart failure, cyanosis, arrhythmias, syncopal episodes, chest pain, or sudden cardiac death.Malignant Cardiac TumorsPrimary cardiac malignancies are very rare, but when they occur they tend to have a right-sided predominance and frequently demonstrate extracardiac extension and involvement.292,302 Malignant cardiac tumors include intimal sarcoma, angiosar-coma, osteosarcoma, leiomyosarcoma, rhabdomyosarcoma, liposarcoma, and primary cardiac lymphomas. Intimal sarcoma is the most common subtype.303 Angiosarcomas are aggressive, rapidly invading adjacent structures, and 47% to 89% of patients present with lung, liver, or brain metastases by the time of diag-nosis. Leiomyosarcomas are sessile masses with a mucous appearance that are typically found in the posterior wall of the left atrium. Rhabdomyosarcomas are bulky (>10 cm in diam-eter) tumors that usually occur in children and do not have a predilection for any particular chamber. They frequently invade nearby cardiac structures | Surgery_Schwartz. with heart failure, cyanosis, arrhythmias, syncopal episodes, chest pain, or sudden cardiac death.Malignant Cardiac TumorsPrimary cardiac malignancies are very rare, but when they occur they tend to have a right-sided predominance and frequently demonstrate extracardiac extension and involvement.292,302 Malignant cardiac tumors include intimal sarcoma, angiosar-coma, osteosarcoma, leiomyosarcoma, rhabdomyosarcoma, liposarcoma, and primary cardiac lymphomas. Intimal sarcoma is the most common subtype.303 Angiosarcomas are aggressive, rapidly invading adjacent structures, and 47% to 89% of patients present with lung, liver, or brain metastases by the time of diag-nosis. Leiomyosarcomas are sessile masses with a mucous appearance that are typically found in the posterior wall of the left atrium. Rhabdomyosarcomas are bulky (>10 cm in diam-eter) tumors that usually occur in children and do not have a predilection for any particular chamber. They frequently invade nearby cardiac structures |
Surgery_Schwartz_5647 | Surgery_Schwartz | Rhabdomyosarcomas are bulky (>10 cm in diam-eter) tumors that usually occur in children and do not have a predilection for any particular chamber. They frequently invade nearby cardiac structures and are multicentric in 60% of cases. Finally, while not as frequent as secondary cardiac lymphomas, primary cardiac lymphomas are increasing in frequency due to lymphoproliferative disorders caused by Epstein-Barr virus in immunosuppressed patients. The absence of necrotic foci in lymphomas can be used to differentiate these tumors from car-diac sarcomas.Metastatic Cardiac TumorsCardiac metastases have been found in approximately 10% of autopsies performed for malignant disease.292 Secondary cardiac tumors, unlike primary tumors, are therefore relatively common. They may arise from direct extension of mediastinal tumors, hematological spread, intracavitary extension from the inferior vena cava or lymphatic extension, although the latter is the most common mechanism.While they can occur with | Surgery_Schwartz. Rhabdomyosarcomas are bulky (>10 cm in diam-eter) tumors that usually occur in children and do not have a predilection for any particular chamber. They frequently invade nearby cardiac structures and are multicentric in 60% of cases. Finally, while not as frequent as secondary cardiac lymphomas, primary cardiac lymphomas are increasing in frequency due to lymphoproliferative disorders caused by Epstein-Barr virus in immunosuppressed patients. The absence of necrotic foci in lymphomas can be used to differentiate these tumors from car-diac sarcomas.Metastatic Cardiac TumorsCardiac metastases have been found in approximately 10% of autopsies performed for malignant disease.292 Secondary cardiac tumors, unlike primary tumors, are therefore relatively common. They may arise from direct extension of mediastinal tumors, hematological spread, intracavitary extension from the inferior vena cava or lymphatic extension, although the latter is the most common mechanism.While they can occur with |
Surgery_Schwartz_5648 | Surgery_Schwartz | of mediastinal tumors, hematological spread, intracavitary extension from the inferior vena cava or lymphatic extension, although the latter is the most common mechanism.While they can occur with most any primary tumor, they are generally observed late in the course of disease. Malignant melanomas have a high potential for cardiac involvement, but Brunicardi_Ch21_p0801-p0852.indd 84301/03/19 5:32 PM 844SPECIFIC CONSIDERATIONSPART IIother soft tissue tumors such as lung cancer, breast cancer, sarcomas, renal carcinoma, esophageal cancer, hepatocellu-lar carcinoma, and thyroid cancer may all progress to cardiac involvement. Cardiac metastases may also develop from leuke-mia and lymphoma in 25% to 40% of cases.304Metastatic cardiac tumors are typically found in random locations, excluding the valvular tissue where lymphatics are absent, and they may be multifocal or diffusely extend along the epicardial surface. Signs of malignant cardiac involvement in cancer patients include | Surgery_Schwartz. of mediastinal tumors, hematological spread, intracavitary extension from the inferior vena cava or lymphatic extension, although the latter is the most common mechanism.While they can occur with most any primary tumor, they are generally observed late in the course of disease. Malignant melanomas have a high potential for cardiac involvement, but Brunicardi_Ch21_p0801-p0852.indd 84301/03/19 5:32 PM 844SPECIFIC CONSIDERATIONSPART IIother soft tissue tumors such as lung cancer, breast cancer, sarcomas, renal carcinoma, esophageal cancer, hepatocellu-lar carcinoma, and thyroid cancer may all progress to cardiac involvement. Cardiac metastases may also develop from leuke-mia and lymphoma in 25% to 40% of cases.304Metastatic cardiac tumors are typically found in random locations, excluding the valvular tissue where lymphatics are absent, and they may be multifocal or diffusely extend along the epicardial surface. Signs of malignant cardiac involvement in cancer patients include |
Surgery_Schwartz_5649 | Surgery_Schwartz | the valvular tissue where lymphatics are absent, and they may be multifocal or diffusely extend along the epicardial surface. Signs of malignant cardiac involvement in cancer patients include pericardial effusion or tamponade, tachyarrhythmias, and heart failure symptoms. Workup is simi-lar to other cardiac tumors. Treatment is generally with com-bined chemotherapy and radiation and is rarely effective.REFERENCESEntries highlighted in bright blue are key references. 1. Task Force for the Diagnosis and Management of Syncope; European Society of Cardiology (ESC); European Heart Rhythm Association (EHRA); et al. Guidelines for the diag-nosis and management of syncope (version 2009). Eur Heart J. 2009;30(21):2631-2671. 2. Braunwald E, Bonow RO. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 9th ed. Philadel-phia: Saunders; 2012. 3. New York Heart Association. Diseases of the Heart and Blood Vessels: Nomenclature and Criteria for Diagnosis, 6th ed. Boston: Little, | Surgery_Schwartz. the valvular tissue where lymphatics are absent, and they may be multifocal or diffusely extend along the epicardial surface. Signs of malignant cardiac involvement in cancer patients include pericardial effusion or tamponade, tachyarrhythmias, and heart failure symptoms. Workup is simi-lar to other cardiac tumors. Treatment is generally with com-bined chemotherapy and radiation and is rarely effective.REFERENCESEntries highlighted in bright blue are key references. 1. Task Force for the Diagnosis and Management of Syncope; European Society of Cardiology (ESC); European Heart Rhythm Association (EHRA); et al. Guidelines for the diag-nosis and management of syncope (version 2009). Eur Heart J. 2009;30(21):2631-2671. 2. Braunwald E, Bonow RO. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 9th ed. Philadel-phia: Saunders; 2012. 3. New York Heart Association. Diseases of the Heart and Blood Vessels: Nomenclature and Criteria for Diagnosis, 6th ed. Boston: Little, |
Surgery_Schwartz_5650 | Surgery_Schwartz | Medicine, 9th ed. Philadel-phia: Saunders; 2012. 3. New York Heart Association. Diseases of the Heart and Blood Vessels: Nomenclature and Criteria for Diagnosis, 6th ed. Boston: Little, Brown; 1964. 4. Lee DH, Buth KJ, Martin BJ, Yip AM, Hirsch GM. Frail patients are at increased risk for mortality and pro-longed institutional care after cardiac surgery. Circulation. 2010;121(8):973-978. 5. Smilowitz NR, Gupta N, Ramakrishna H, Guo Y, Berger JS, Bangalore S. Perioperative major adverse cardiovascular and cerebrovascular events associated with noncardiac surgery. JAMA Cardiol. 2017;2(2):181-187. 6. Nishimura RA, Otto CM, Bonow RO, et al. 2017 AHA/ACC focused update of the 2014 AHA/ACC guideline for the man-agement of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on clinical practice guidelines. J Am Coll Cardiol. 2017;70(2):252-289. 7. Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on | Surgery_Schwartz. Medicine, 9th ed. Philadel-phia: Saunders; 2012. 3. New York Heart Association. Diseases of the Heart and Blood Vessels: Nomenclature and Criteria for Diagnosis, 6th ed. Boston: Little, Brown; 1964. 4. Lee DH, Buth KJ, Martin BJ, Yip AM, Hirsch GM. Frail patients are at increased risk for mortality and pro-longed institutional care after cardiac surgery. Circulation. 2010;121(8):973-978. 5. Smilowitz NR, Gupta N, Ramakrishna H, Guo Y, Berger JS, Bangalore S. Perioperative major adverse cardiovascular and cerebrovascular events associated with noncardiac surgery. JAMA Cardiol. 2017;2(2):181-187. 6. Nishimura RA, Otto CM, Bonow RO, et al. 2017 AHA/ACC focused update of the 2014 AHA/ACC guideline for the man-agement of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on clinical practice guidelines. J Am Coll Cardiol. 2017;70(2):252-289. 7. Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on |
Surgery_Schwartz_5651 | Surgery_Schwartz | Cardiology/American Heart Association Task Force on clinical practice guidelines. J Am Coll Cardiol. 2017;70(2):252-289. 7. Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on perioperative cardiovascular eval-uation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on practice guide-lines. J Am Coll Cardiol. 2014;64(22):e77-e137. 8. Klocke FJ, Baird MG, Lorell BH, et al. ACC/AHA/ASNC guide-lines for the clinical use of cardiac radionuclide imaging— executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASNC Committee to Revise the 1995 Guidelines for the Clinical Use of Cardiac Radionuclide Imaging). Circulation. 2003;108(11):1404-1418. 9. Badheka AO, Hendel RC. Radionuclide cardiac stress testing. Curr Opin Cardiol. 2011;26(5):370-378. 10. Bax JJ, Boogers MM, Schuijf JD. Nuclear imaging in | Surgery_Schwartz. Cardiology/American Heart Association Task Force on clinical practice guidelines. J Am Coll Cardiol. 2017;70(2):252-289. 7. Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA guideline on perioperative cardiovascular eval-uation and management of patients undergoing noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on practice guide-lines. J Am Coll Cardiol. 2014;64(22):e77-e137. 8. Klocke FJ, Baird MG, Lorell BH, et al. ACC/AHA/ASNC guide-lines for the clinical use of cardiac radionuclide imaging— executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/ASNC Committee to Revise the 1995 Guidelines for the Clinical Use of Cardiac Radionuclide Imaging). Circulation. 2003;108(11):1404-1418. 9. Badheka AO, Hendel RC. Radionuclide cardiac stress testing. Curr Opin Cardiol. 2011;26(5):370-378. 10. Bax JJ, Boogers MM, Schuijf JD. Nuclear imaging in |
Surgery_Schwartz_5652 | Surgery_Schwartz | Circulation. 2003;108(11):1404-1418. 9. Badheka AO, Hendel RC. Radionuclide cardiac stress testing. Curr Opin Cardiol. 2011;26(5):370-378. 10. Bax JJ, Boogers MM, Schuijf JD. Nuclear imaging in heart failure. Cardiology clinics. 2009;27(2):265-276. 11. Proudfit WL, Shirey EK, Sones FM, Jr. Selective cine coro-nary arteriography. Correlation with clinical findings in 1,000 patients. Circulation. 1966;33(6):901-910. 12. Shuttleworth K, Smith K, Watt J, Smith JAL, Leslie SJ. Hybrid instantaneous wave-free ratio-fractional flow reserve versus fractional flow reserve in the real world. Front Cardiovasc Med. 2017:435. 13. Gotberg M, Cook CM, Sen S, Nijjer S, Escaned J, Davies JE. The evolving future of instantaneous wave-free ratio and frac-tional flow reserve. J Am Coll Cardiol. 2017;70(11):1379-1402. 14. Forssmann W. Die sondierung des rechten herzens. Klinische Wochenschrift. 1929;8(45):3. 15. Scanlon PJ, Faxon DP, Audet AM, et al. ACC/AHA guide-lines for coronary angiography. A report | Surgery_Schwartz. Circulation. 2003;108(11):1404-1418. 9. Badheka AO, Hendel RC. Radionuclide cardiac stress testing. Curr Opin Cardiol. 2011;26(5):370-378. 10. Bax JJ, Boogers MM, Schuijf JD. Nuclear imaging in heart failure. Cardiology clinics. 2009;27(2):265-276. 11. Proudfit WL, Shirey EK, Sones FM, Jr. Selective cine coro-nary arteriography. Correlation with clinical findings in 1,000 patients. Circulation. 1966;33(6):901-910. 12. Shuttleworth K, Smith K, Watt J, Smith JAL, Leslie SJ. Hybrid instantaneous wave-free ratio-fractional flow reserve versus fractional flow reserve in the real world. Front Cardiovasc Med. 2017:435. 13. Gotberg M, Cook CM, Sen S, Nijjer S, Escaned J, Davies JE. The evolving future of instantaneous wave-free ratio and frac-tional flow reserve. J Am Coll Cardiol. 2017;70(11):1379-1402. 14. Forssmann W. Die sondierung des rechten herzens. Klinische Wochenschrift. 1929;8(45):3. 15. Scanlon PJ, Faxon DP, Audet AM, et al. ACC/AHA guide-lines for coronary angiography. A report |
Surgery_Schwartz_5653 | Surgery_Schwartz | W. Die sondierung des rechten herzens. Klinische Wochenschrift. 1929;8(45):3. 15. Scanlon PJ, Faxon DP, Audet AM, et al. ACC/AHA guide-lines for coronary angiography. A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (Committee on Coronary Angiography). Developed in collaboration with the Society for Cardiac Angiography and Interventions. J Am Coll Cardiol. 1999;33(6):1756-824. 16. Berman DS, Hachamovitch R, Shaw LJ, et al. Roles of nuclear cardiology, cardiac computed tomography, and cardiac mag-netic resonance: assessment of patients with suspected coro-nary artery disease. J Nucl Med. 2006;47(1):74-82. 17. Chow BJ, Small G, Yam Y, et al. Incremental prognostic value of cardiac computed tomography in coronary artery disease using CONFIRM: COroNary computed tomography angiogra-phy evaluation for clinical outcomes: an InteRnational Multi-center registry. Circ Cardiovasc Imaging. 2011;4(5):463-472. 18. Edmunds LH, Jr. The | Surgery_Schwartz. W. Die sondierung des rechten herzens. Klinische Wochenschrift. 1929;8(45):3. 15. Scanlon PJ, Faxon DP, Audet AM, et al. ACC/AHA guide-lines for coronary angiography. A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (Committee on Coronary Angiography). Developed in collaboration with the Society for Cardiac Angiography and Interventions. J Am Coll Cardiol. 1999;33(6):1756-824. 16. Berman DS, Hachamovitch R, Shaw LJ, et al. Roles of nuclear cardiology, cardiac computed tomography, and cardiac mag-netic resonance: assessment of patients with suspected coro-nary artery disease. J Nucl Med. 2006;47(1):74-82. 17. Chow BJ, Small G, Yam Y, et al. Incremental prognostic value of cardiac computed tomography in coronary artery disease using CONFIRM: COroNary computed tomography angiogra-phy evaluation for clinical outcomes: an InteRnational Multi-center registry. Circ Cardiovasc Imaging. 2011;4(5):463-472. 18. Edmunds LH, Jr. The |
Surgery_Schwartz_5654 | Surgery_Schwartz | using CONFIRM: COroNary computed tomography angiogra-phy evaluation for clinical outcomes: an InteRnational Multi-center registry. Circ Cardiovasc Imaging. 2011;4(5):463-472. 18. Edmunds LH, Jr. The evolution of cardiopulmonary bypass: lessons to be learned. Perfusion. 2002;17(4):243-251. 19. Cohn LH. Cardiac Surgery in the Adult, 4th ed. New York: McGraw-Hill; 2012. 20. Kirklin JK, Westaby S, Blackstone EH, Kirklin JW, Chenoweth DE, Pacifico AD. Complement and the damaging effects of cardiopulmonary bypass. J Thorac Cardiovasc Surg. 1983;86(6):845-857. 21. Asimakopoulos G. Systemic inflammation and cardiac surgery: an update. Perfusion. 2001;16(5):353-360. 22. Salter BS, Weiner MM, Trinh MA, et al. Heparin-induced thrombocytopenia: a comprehensive clinical review. J Am Coll Cardiol. 2016;67(21):2519-2532. 23. Greinacher A. Heparin-induced thrombocytopenia. N Engl J Med. 2015;373(19):1883-1884. 24. Murphy GJ, Angelini GD. Side effects of cardiopulmonary bypass: what is the reality? | Surgery_Schwartz. using CONFIRM: COroNary computed tomography angiogra-phy evaluation for clinical outcomes: an InteRnational Multi-center registry. Circ Cardiovasc Imaging. 2011;4(5):463-472. 18. Edmunds LH, Jr. The evolution of cardiopulmonary bypass: lessons to be learned. Perfusion. 2002;17(4):243-251. 19. Cohn LH. Cardiac Surgery in the Adult, 4th ed. New York: McGraw-Hill; 2012. 20. Kirklin JK, Westaby S, Blackstone EH, Kirklin JW, Chenoweth DE, Pacifico AD. Complement and the damaging effects of cardiopulmonary bypass. J Thorac Cardiovasc Surg. 1983;86(6):845-857. 21. Asimakopoulos G. Systemic inflammation and cardiac surgery: an update. Perfusion. 2001;16(5):353-360. 22. Salter BS, Weiner MM, Trinh MA, et al. Heparin-induced thrombocytopenia: a comprehensive clinical review. J Am Coll Cardiol. 2016;67(21):2519-2532. 23. Greinacher A. Heparin-induced thrombocytopenia. N Engl J Med. 2015;373(19):1883-1884. 24. Murphy GJ, Angelini GD. Side effects of cardiopulmonary bypass: what is the reality? |
Surgery_Schwartz_5655 | Surgery_Schwartz | A. Heparin-induced thrombocytopenia. N Engl J Med. 2015;373(19):1883-1884. 24. Murphy GJ, Angelini GD. Side effects of cardiopulmonary bypass: what is the reality? J Cardiac Surg. 2004;19(6):481-488. 25. Gay WA, Jr, Ebert PA. Functional, metabolic, and morpho-logic effects of potassium-induced cardioplegia. Surgery. 1973;74(2):284-290. 26. Carrel A. VIII. On the experimental surgery of the thoracic aorta and heart. Ann Surg. 1910;52(1):83-95. 27. Vineberg A, Miller G. Internal mammary coronary anastomo-sis in the surgical treatment of coronary artery insufficiency. Can Med Assoc J. 1951;64(3):204-210. 28. Longmire WP, Jr, Cannon JA, Kattus AA. Direct-vision coronary endarterectomy for angina pectoris. N Engl J Med. 1958;259(21):993-999. 29. Senning A. Strip grafting in coronary arteries. Report of a case. J Thorac Cardiovasc Surg. 1961;41:542-549. 30. Sabiston DC, Jr. The William F. Rienhoff, Jr. lecture. The coro-nary circulation. Johns Hopkins Med J. | Surgery_Schwartz. A. Heparin-induced thrombocytopenia. N Engl J Med. 2015;373(19):1883-1884. 24. Murphy GJ, Angelini GD. Side effects of cardiopulmonary bypass: what is the reality? J Cardiac Surg. 2004;19(6):481-488. 25. Gay WA, Jr, Ebert PA. Functional, metabolic, and morpho-logic effects of potassium-induced cardioplegia. Surgery. 1973;74(2):284-290. 26. Carrel A. VIII. On the experimental surgery of the thoracic aorta and heart. Ann Surg. 1910;52(1):83-95. 27. Vineberg A, Miller G. Internal mammary coronary anastomo-sis in the surgical treatment of coronary artery insufficiency. Can Med Assoc J. 1951;64(3):204-210. 28. Longmire WP, Jr, Cannon JA, Kattus AA. Direct-vision coronary endarterectomy for angina pectoris. N Engl J Med. 1958;259(21):993-999. 29. Senning A. Strip grafting in coronary arteries. Report of a case. J Thorac Cardiovasc Surg. 1961;41:542-549. 30. Sabiston DC, Jr. The William F. Rienhoff, Jr. lecture. The coro-nary circulation. Johns Hopkins Med J. |
Surgery_Schwartz_5656 | Surgery_Schwartz | grafting in coronary arteries. Report of a case. J Thorac Cardiovasc Surg. 1961;41:542-549. 30. Sabiston DC, Jr. The William F. Rienhoff, Jr. lecture. The coro-nary circulation. Johns Hopkins Med J. 1974;134(6):314-329. 31. Favaloro RG, Effler DB, Groves LK, Sones FM, Jr, Fergusson DJ. Myocardial revascularization by internal mammary artery implant procedures. Clinical experience. J Thorac Cardiovasc Surg. 1967;54(3):359-370. 32. Greason KL, Schaff HV. Myocardial revascularization by coronary arterial bypass graft: past, present, and future. Curr Prob Cardiol. 2011;36(9):325-368. 33. Crea F, Liuzzo G. Pathogenesis of acute coronary syndromes. J Am Coll Cardiol. 2012;8;61(1):1-11. 34. Fuster V, Badimon L, Badimon JJ, Chesebro JH. The patho-genesis of coronary artery disease and the acute coronary syn-dromes (1). N Engl J Med. 1992;326(4):242-250. 35. Libby P. Mechanisms of acute coronary syndromes and their implications for therapy. N Engl J Med. 2013;368(21): | Surgery_Schwartz. grafting in coronary arteries. Report of a case. J Thorac Cardiovasc Surg. 1961;41:542-549. 30. Sabiston DC, Jr. The William F. Rienhoff, Jr. lecture. The coro-nary circulation. Johns Hopkins Med J. 1974;134(6):314-329. 31. Favaloro RG, Effler DB, Groves LK, Sones FM, Jr, Fergusson DJ. Myocardial revascularization by internal mammary artery implant procedures. Clinical experience. J Thorac Cardiovasc Surg. 1967;54(3):359-370. 32. Greason KL, Schaff HV. Myocardial revascularization by coronary arterial bypass graft: past, present, and future. Curr Prob Cardiol. 2011;36(9):325-368. 33. Crea F, Liuzzo G. Pathogenesis of acute coronary syndromes. J Am Coll Cardiol. 2012;8;61(1):1-11. 34. Fuster V, Badimon L, Badimon JJ, Chesebro JH. The patho-genesis of coronary artery disease and the acute coronary syn-dromes (1). N Engl J Med. 1992;326(4):242-250. 35. Libby P. Mechanisms of acute coronary syndromes and their implications for therapy. N Engl J Med. 2013;368(21): |
Surgery_Schwartz_5657 | Surgery_Schwartz | disease and the acute coronary syn-dromes (1). N Engl J Med. 1992;326(4):242-250. 35. Libby P. Mechanisms of acute coronary syndromes and their implications for therapy. N Engl J Med. 2013;368(21): 2004-2013.Brunicardi_Ch21_p0801-p0852.indd 84401/03/19 5:32 PM 845ACQUIRED HEART DISEASECHAPTER 21 36. National Heart, Lung, and Blood Institute, National Institutes of Health. Morbidity and mortality: 2012 chart book on car-diovascular, lung, and blood diseases. 2012. 37. Smith SC, Jr, Benjamin EJ, Bonow Row, et al. AHA/ACCF secondary prevention and risk reduction therapy for patients with coronary and other atherosclerotic vascular disease: 2011 update: a guideline from the American Heart Association and American College of Cardiology Foundation. Circulation. 2011;124(22):2458-2473. 38. Gibbons RJ, Balady GJ, Bricker Jt, et al. ACC/AHA 2002 guideline update for exercise testing: summary article: a report of the American College of Cardiology/American Heart Association Task Force on | Surgery_Schwartz. disease and the acute coronary syn-dromes (1). N Engl J Med. 1992;326(4):242-250. 35. Libby P. Mechanisms of acute coronary syndromes and their implications for therapy. N Engl J Med. 2013;368(21): 2004-2013.Brunicardi_Ch21_p0801-p0852.indd 84401/03/19 5:32 PM 845ACQUIRED HEART DISEASECHAPTER 21 36. National Heart, Lung, and Blood Institute, National Institutes of Health. Morbidity and mortality: 2012 chart book on car-diovascular, lung, and blood diseases. 2012. 37. Smith SC, Jr, Benjamin EJ, Bonow Row, et al. AHA/ACCF secondary prevention and risk reduction therapy for patients with coronary and other atherosclerotic vascular disease: 2011 update: a guideline from the American Heart Association and American College of Cardiology Foundation. Circulation. 2011;124(22):2458-2473. 38. Gibbons RJ, Balady GJ, Bricker Jt, et al. ACC/AHA 2002 guideline update for exercise testing: summary article: a report of the American College of Cardiology/American Heart Association Task Force on |
Surgery_Schwartz_5658 | Surgery_Schwartz | RJ, Balady GJ, Bricker Jt, et al. ACC/AHA 2002 guideline update for exercise testing: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1997 Exercise Testing Guidelines). Circulation. 2002;106(14):1883-1892. 39. Fihn SD, Gardin JM, Abrams J, et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines, and the American College of Physicians, American Associa-tion for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. 2012;126(25):e354-e471. 40. Fihn SD, Blankenship JC, Alexander KP, et al. 2014 ACC/AHA/AATS/PCNA/SCAI/STS focused update of the guide-line for the diagnosis and | Surgery_Schwartz. RJ, Balady GJ, Bricker Jt, et al. ACC/AHA 2002 guideline update for exercise testing: summary article: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1997 Exercise Testing Guidelines). Circulation. 2002;106(14):1883-1892. 39. Fihn SD, Gardin JM, Abrams J, et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines, and the American College of Physicians, American Associa-tion for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. 2012;126(25):e354-e471. 40. Fihn SD, Blankenship JC, Alexander KP, et al. 2014 ACC/AHA/AATS/PCNA/SCAI/STS focused update of the guide-line for the diagnosis and |
Surgery_Schwartz_5659 | Surgery_Schwartz | of Thoracic Surgeons. Circulation. 2012;126(25):e354-e471. 40. Fihn SD, Blankenship JC, Alexander KP, et al. 2014 ACC/AHA/AATS/PCNA/SCAI/STS focused update of the guide-line for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines, and the American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. 2014;130(19):1749-1767. 41. Hillis LD, Smith PK, Anderson JL, et al. 2011 ACCF/AHA guideline for coronary artery bypass graft surgery: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circula-tion. 2011;124(23):e652-e735. 42. Hannan EL, Racz MJ, Walford G, et al. Long-term outcomes of coronary-artery bypass grafting versus stent implantation. N Engl J Med. | Surgery_Schwartz. of Thoracic Surgeons. Circulation. 2012;126(25):e354-e471. 40. Fihn SD, Blankenship JC, Alexander KP, et al. 2014 ACC/AHA/AATS/PCNA/SCAI/STS focused update of the guide-line for the diagnosis and management of patients with stable ischemic heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines, and the American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. 2014;130(19):1749-1767. 41. Hillis LD, Smith PK, Anderson JL, et al. 2011 ACCF/AHA guideline for coronary artery bypass graft surgery: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circula-tion. 2011;124(23):e652-e735. 42. Hannan EL, Racz MJ, Walford G, et al. Long-term outcomes of coronary-artery bypass grafting versus stent implantation. N Engl J Med. |
Surgery_Schwartz_5660 | Surgery_Schwartz | on Practice Guidelines. Circula-tion. 2011;124(23):e652-e735. 42. Hannan EL, Racz MJ, Walford G, et al. Long-term outcomes of coronary-artery bypass grafting versus stent implantation. N Engl J Med. 2005;352(21):2174-2183. 43. Booth J, Clayton T, Pepper J, et al. Randomized, controlled trial of coronary artery bypass surgery versus percutaneous coronary intervention in patients with multivessel coronary artery disease: six-year follow-up from the Stent or Surgery Trial (SoS). Circulation. 2008;118(4):381-388. 44. Serruys PW, Morice MC, Kappetein AP, et al. Percutane-ous coronary intervention versus coronary-artery bypass grafting for severe coronary artery disease. N Engl J Med. 2009;360(10):961-972. 45. Mohr FW, Morice MC, Kappetein AP, et al. Coronary artery bypass graft surgery versus percutaneous coronary interven-tion in patients with three-vessel disease and left main cor-onary disease: 5-year follow-up of the randomised, clinical SYNTAX trial. Lancet. | Surgery_Schwartz. on Practice Guidelines. Circula-tion. 2011;124(23):e652-e735. 42. Hannan EL, Racz MJ, Walford G, et al. Long-term outcomes of coronary-artery bypass grafting versus stent implantation. N Engl J Med. 2005;352(21):2174-2183. 43. Booth J, Clayton T, Pepper J, et al. Randomized, controlled trial of coronary artery bypass surgery versus percutaneous coronary intervention in patients with multivessel coronary artery disease: six-year follow-up from the Stent or Surgery Trial (SoS). Circulation. 2008;118(4):381-388. 44. Serruys PW, Morice MC, Kappetein AP, et al. Percutane-ous coronary intervention versus coronary-artery bypass grafting for severe coronary artery disease. N Engl J Med. 2009;360(10):961-972. 45. Mohr FW, Morice MC, Kappetein AP, et al. Coronary artery bypass graft surgery versus percutaneous coronary interven-tion in patients with three-vessel disease and left main cor-onary disease: 5-year follow-up of the randomised, clinical SYNTAX trial. Lancet. |
Surgery_Schwartz_5661 | Surgery_Schwartz | graft surgery versus percutaneous coronary interven-tion in patients with three-vessel disease and left main cor-onary disease: 5-year follow-up of the randomised, clinical SYNTAX trial. Lancet. 2013;381(9867):629-638. 46. Weintraub WS, Grau-Sepulveda MV, Weiss JM, et al. Com-parative effectiveness of revascularization strategies. N Engl J Med. 2012;366(16):1467-1476. 47. Zhang Z, Kolm P, Grau-Sepulveda MV, et al. Cost-effective-ness of revascularization strategies: the ASCERT study. J Am Coll Cardiol. 2015;65(1):1-11. 48. Stone GW, Sabik JF, Serruys PW, et al. Everolimus-eluting stents or bypass surgery for left main coronary artery disease. N Engl J Med. 2016;375(23):2223-2235. 49. Tatoulis J, Buxton BF, Fuller JA. Patencies of 2127 arterial to coronary conduits over 15 years. Ann Thorac Surg. 2004;77(1): 93-101. 50. Goldman S, Zadina K, Moritz T, et al. Long-term patency of saphenous vein and left internal mammary artery grafts after coronary artery bypass surgery: results from a | Surgery_Schwartz. graft surgery versus percutaneous coronary interven-tion in patients with three-vessel disease and left main cor-onary disease: 5-year follow-up of the randomised, clinical SYNTAX trial. Lancet. 2013;381(9867):629-638. 46. Weintraub WS, Grau-Sepulveda MV, Weiss JM, et al. Com-parative effectiveness of revascularization strategies. N Engl J Med. 2012;366(16):1467-1476. 47. Zhang Z, Kolm P, Grau-Sepulveda MV, et al. Cost-effective-ness of revascularization strategies: the ASCERT study. J Am Coll Cardiol. 2015;65(1):1-11. 48. Stone GW, Sabik JF, Serruys PW, et al. Everolimus-eluting stents or bypass surgery for left main coronary artery disease. N Engl J Med. 2016;375(23):2223-2235. 49. Tatoulis J, Buxton BF, Fuller JA. Patencies of 2127 arterial to coronary conduits over 15 years. Ann Thorac Surg. 2004;77(1): 93-101. 50. Goldman S, Zadina K, Moritz T, et al. Long-term patency of saphenous vein and left internal mammary artery grafts after coronary artery bypass surgery: results from a |
Surgery_Schwartz_5662 | Surgery_Schwartz | Surg. 2004;77(1): 93-101. 50. Goldman S, Zadina K, Moritz T, et al. Long-term patency of saphenous vein and left internal mammary artery grafts after coronary artery bypass surgery: results from a Department of Veterans Affairs Cooperative Study. J Am Coll Cardiol. 2004;44(11):2149-2156. 51. Dorman MJ, Kurlansky PA, Traad EA, Galbut DL, Zucker M, Ebra G. Bilateral internal mammary artery grafting enhances survival in diabetic patients: a 30-year follow-up of pro-pensity score-matched cohorts. Circulation. 2012;126(25): 2935-2942. 52. Kelly R, Buth KJ, Legare JF. Bilateral internal thoracic artery grafting is superior to other forms of multiple arterial grafting in providing survival benefit after coronary bypass surgery. J Thorac Cardiovasc Surg. 2012;144(6):1408-1415. 53. Athanasiou T, Saso S, Rao C, et al. Radial artery versus saphe-nous vein conduits for coronary artery bypass surgery: forty years of competition—which conduit offers better patency? A systematic review and | Surgery_Schwartz. Surg. 2004;77(1): 93-101. 50. Goldman S, Zadina K, Moritz T, et al. Long-term patency of saphenous vein and left internal mammary artery grafts after coronary artery bypass surgery: results from a Department of Veterans Affairs Cooperative Study. J Am Coll Cardiol. 2004;44(11):2149-2156. 51. Dorman MJ, Kurlansky PA, Traad EA, Galbut DL, Zucker M, Ebra G. Bilateral internal mammary artery grafting enhances survival in diabetic patients: a 30-year follow-up of pro-pensity score-matched cohorts. Circulation. 2012;126(25): 2935-2942. 52. Kelly R, Buth KJ, Legare JF. Bilateral internal thoracic artery grafting is superior to other forms of multiple arterial grafting in providing survival benefit after coronary bypass surgery. J Thorac Cardiovasc Surg. 2012;144(6):1408-1415. 53. Athanasiou T, Saso S, Rao C, et al. Radial artery versus saphe-nous vein conduits for coronary artery bypass surgery: forty years of competition—which conduit offers better patency? A systematic review and |
Surgery_Schwartz_5663 | Surgery_Schwartz | T, Saso S, Rao C, et al. Radial artery versus saphe-nous vein conduits for coronary artery bypass surgery: forty years of competition—which conduit offers better patency? A systematic review and meta-analysis. Eur J Cardiothorac Surg. 2011;40(1):208-220. 54. Collins P, Webb CM, Chong CF, et al. Radial artery versus saphenous vein patency randomized trial: five-year angio-graphic follow-up. Circulation. 2008;117(22):2859-2864. 55. Zacharias A, Schwann TA, Riordan CJ, Durham SJ, Shah AS, Habib RH. Late results of conventional versus all-arterial revascularization based on internal thoracic and radial artery grafting. Ann Thorac Surg. 2009;87(1):19-26e2. 56. Zacharias A, Habib RH, Schwann TA, Riordan CJ, Durham SJ, Shah A. Improved survival with radial artery versus vein con-duits in coronary bypass surgery with left internal thoracic artery to left anterior descending artery grafting. Circulation. 2004;109(12):1489-1496. 57. Tatoulis J, Wynne R, Skillington PD, Buxton BF. Total | Surgery_Schwartz. T, Saso S, Rao C, et al. Radial artery versus saphe-nous vein conduits for coronary artery bypass surgery: forty years of competition—which conduit offers better patency? A systematic review and meta-analysis. Eur J Cardiothorac Surg. 2011;40(1):208-220. 54. Collins P, Webb CM, Chong CF, et al. Radial artery versus saphenous vein patency randomized trial: five-year angio-graphic follow-up. Circulation. 2008;117(22):2859-2864. 55. Zacharias A, Schwann TA, Riordan CJ, Durham SJ, Shah AS, Habib RH. Late results of conventional versus all-arterial revascularization based on internal thoracic and radial artery grafting. Ann Thorac Surg. 2009;87(1):19-26e2. 56. Zacharias A, Habib RH, Schwann TA, Riordan CJ, Durham SJ, Shah A. Improved survival with radial artery versus vein con-duits in coronary bypass surgery with left internal thoracic artery to left anterior descending artery grafting. Circulation. 2004;109(12):1489-1496. 57. Tatoulis J, Wynne R, Skillington PD, Buxton BF. Total |
Surgery_Schwartz_5664 | Surgery_Schwartz | coronary bypass surgery with left internal thoracic artery to left anterior descending artery grafting. Circulation. 2004;109(12):1489-1496. 57. Tatoulis J, Wynne R, Skillington PD, Buxton BF. Total arte-rial revascularization: a superior strategy for diabetic patients who require coronary surgery. Ann Thorac Surg. 2016;102(6): 1948-1955. 58. Caracciolo EA, Davis KB, Sopko G, et al. Comparison of sur-gical and medical group survival in patients with left main equivalent coronary artery disease. Long-term CASS experi-ence. Circulation. 1995;91(9):2335-2344. 59. Grover FL, Hammermeister KE, Burchfiel C. Initial report of the Veterans Administration Preoperative Risk Assessment Study for Cardiac Surgery. Ann Thorac Surg. 1990;50(1): 12-26; discussion 27-28. 60. Yusuf S, Zucker D, Peduzzi P, et al. Effect of coronary artery bypass graft surgery on survival: overview of 10-year results from randomised trials by the Coronary Artery Bypass Graft Surgery Trialists Collaboration. Lancet. | Surgery_Schwartz. coronary bypass surgery with left internal thoracic artery to left anterior descending artery grafting. Circulation. 2004;109(12):1489-1496. 57. Tatoulis J, Wynne R, Skillington PD, Buxton BF. Total arte-rial revascularization: a superior strategy for diabetic patients who require coronary surgery. Ann Thorac Surg. 2016;102(6): 1948-1955. 58. Caracciolo EA, Davis KB, Sopko G, et al. Comparison of sur-gical and medical group survival in patients with left main equivalent coronary artery disease. Long-term CASS experi-ence. Circulation. 1995;91(9):2335-2344. 59. Grover FL, Hammermeister KE, Burchfiel C. Initial report of the Veterans Administration Preoperative Risk Assessment Study for Cardiac Surgery. Ann Thorac Surg. 1990;50(1): 12-26; discussion 27-28. 60. Yusuf S, Zucker D, Peduzzi P, et al. Effect of coronary artery bypass graft surgery on survival: overview of 10-year results from randomised trials by the Coronary Artery Bypass Graft Surgery Trialists Collaboration. Lancet. |
Surgery_Schwartz_5665 | Surgery_Schwartz | P, et al. Effect of coronary artery bypass graft surgery on survival: overview of 10-year results from randomised trials by the Coronary Artery Bypass Graft Surgery Trialists Collaboration. Lancet. 1994;344(8922): 563-570. 61. De Lorenzo A, Tura B, Bassan F, Pittella F, Rocha AS. Out-comes of patients with left main coronary artery disease under-going medical or surgical treatment: a propensity-matched analysis. Cor Artery Dis. 2011;22(8):585-589. 62. Influence of diabetes on 5-year mortality and morbidity in a randomized trial comparing CABG and PTCA in patients with multivessel disease: the Bypass Angioplasty Revascularization Investigation (BARI). Circulation. 1997;96(6):1761-1769. 63. Jones RH, Kesler K, Phillips HR 3rd, et al. Long-term survival benefits of coronary artery bypass grafting and percutaneous transluminal angioplasty in patients with coronary artery dis-ease. J Thorac Cardiovasc Surg. 1996;111(5):1013-1025. 64. ElBardissi AW, Aranki SF, Sheng S, O’Brien SM, | Surgery_Schwartz. P, et al. Effect of coronary artery bypass graft surgery on survival: overview of 10-year results from randomised trials by the Coronary Artery Bypass Graft Surgery Trialists Collaboration. Lancet. 1994;344(8922): 563-570. 61. De Lorenzo A, Tura B, Bassan F, Pittella F, Rocha AS. Out-comes of patients with left main coronary artery disease under-going medical or surgical treatment: a propensity-matched analysis. Cor Artery Dis. 2011;22(8):585-589. 62. Influence of diabetes on 5-year mortality and morbidity in a randomized trial comparing CABG and PTCA in patients with multivessel disease: the Bypass Angioplasty Revascularization Investigation (BARI). Circulation. 1997;96(6):1761-1769. 63. Jones RH, Kesler K, Phillips HR 3rd, et al. Long-term survival benefits of coronary artery bypass grafting and percutaneous transluminal angioplasty in patients with coronary artery dis-ease. J Thorac Cardiovasc Surg. 1996;111(5):1013-1025. 64. ElBardissi AW, Aranki SF, Sheng S, O’Brien SM, |
Surgery_Schwartz_5666 | Surgery_Schwartz | grafting and percutaneous transluminal angioplasty in patients with coronary artery dis-ease. J Thorac Cardiovasc Surg. 1996;111(5):1013-1025. 64. ElBardissi AW, Aranki SF, Sheng S, O’Brien SM, Greenberg CC, Gammie JS. Trends in isolated coronary artery bypass grafting: an analysis of the Society of Thoracic Surgeons adult cardiac surgery database. J Thorac Cardiovasc Surg. 2012;143(2):273-281. 65. Angelini GD, Taylor FC, Reeves BC, Ascione R. Early and midterm outcome after off-pump and on-pump surgery in Beating Heart Against Cardioplegic Arrest Studies (BHACAS Brunicardi_Ch21_p0801-p0852.indd 84501/03/19 5:32 PM 846SPECIFIC CONSIDERATIONSPART II1 and 2): a pooled analysis of two randomised controlled trials. Lancet. 2002;359(9313):1194-1199. 66. Lemma MG, Coscioni E, Tritto FP, et al. On-pump versus off-pump coronary artery bypass surgery in high-risk patients: operative results of a prospective randomized trial (on-off study). J Thorac Cardiovasc Surg. | Surgery_Schwartz. grafting and percutaneous transluminal angioplasty in patients with coronary artery dis-ease. J Thorac Cardiovasc Surg. 1996;111(5):1013-1025. 64. ElBardissi AW, Aranki SF, Sheng S, O’Brien SM, Greenberg CC, Gammie JS. Trends in isolated coronary artery bypass grafting: an analysis of the Society of Thoracic Surgeons adult cardiac surgery database. J Thorac Cardiovasc Surg. 2012;143(2):273-281. 65. Angelini GD, Taylor FC, Reeves BC, Ascione R. Early and midterm outcome after off-pump and on-pump surgery in Beating Heart Against Cardioplegic Arrest Studies (BHACAS Brunicardi_Ch21_p0801-p0852.indd 84501/03/19 5:32 PM 846SPECIFIC CONSIDERATIONSPART II1 and 2): a pooled analysis of two randomised controlled trials. Lancet. 2002;359(9313):1194-1199. 66. Lemma MG, Coscioni E, Tritto FP, et al. On-pump versus off-pump coronary artery bypass surgery in high-risk patients: operative results of a prospective randomized trial (on-off study). J Thorac Cardiovasc Surg. |
Surgery_Schwartz_5667 | Surgery_Schwartz | E, Tritto FP, et al. On-pump versus off-pump coronary artery bypass surgery in high-risk patients: operative results of a prospective randomized trial (on-off study). J Thorac Cardiovasc Surg. 2012;143(3):625-631. 67. Mack MJ, Brown P, Houser F, et al. On-pump versus off-pump coronary artery bypass surgery in a matched sample of women: a comparison of outcomes. Circulation. 2004; 110(11 suppl 1):II1-II6. 68. Hu S, Zeng Z, Yuan X, et al. Increasing long-term major vas-cular events and resource consumption in patients receiving off-pump coronary artery bypass: a single-center prospective observational study. Circulation. 2010;121(16):1800-1808. 69. Lamy A, Devereaux PJ, Prabhakaran D, et al. Off-pump or on-pump coronary-artery bypass grafting at 30 days. N Engl J Med. 2012;366(16):1489-1497. 70. Diegeler A, Börgermann J, Kappert U, et al. Off-pump versus on-pump coronary-artery bypass grafting in elderly patients. N Engl J Med. 2013;368(13):1189-1198. 71. Hattler B, Messenger JC, | Surgery_Schwartz. E, Tritto FP, et al. On-pump versus off-pump coronary artery bypass surgery in high-risk patients: operative results of a prospective randomized trial (on-off study). J Thorac Cardiovasc Surg. 2012;143(3):625-631. 67. Mack MJ, Brown P, Houser F, et al. On-pump versus off-pump coronary artery bypass surgery in a matched sample of women: a comparison of outcomes. Circulation. 2004; 110(11 suppl 1):II1-II6. 68. Hu S, Zeng Z, Yuan X, et al. Increasing long-term major vas-cular events and resource consumption in patients receiving off-pump coronary artery bypass: a single-center prospective observational study. Circulation. 2010;121(16):1800-1808. 69. Lamy A, Devereaux PJ, Prabhakaran D, et al. Off-pump or on-pump coronary-artery bypass grafting at 30 days. N Engl J Med. 2012;366(16):1489-1497. 70. Diegeler A, Börgermann J, Kappert U, et al. Off-pump versus on-pump coronary-artery bypass grafting in elderly patients. N Engl J Med. 2013;368(13):1189-1198. 71. Hattler B, Messenger JC, |
Surgery_Schwartz_5668 | Surgery_Schwartz | A, Börgermann J, Kappert U, et al. Off-pump versus on-pump coronary-artery bypass grafting in elderly patients. N Engl J Med. 2013;368(13):1189-1198. 71. Hattler B, Messenger JC, Shroyer Al, et al. Off-Pump coronary artery bypass surgery is associated with worse arterial and saphenous vein graft patency and less effec-tive revascularization: results from the Veterans Affairs Randomized On/Off Bypass (ROOBY) trial. Circulation. 2012;125(23):2827-2835. 72. Hannan EL, Wu C, Smith CR, et al. Off-pump versus on-pump coronary artery bypass graft surgery: differences in short-term outcomes and in long-term mortality and need for subsequent revascularization. Circulation. 2007;116(10):1145-1152. 73. Hueb W, Lopes NH, Pereira AC, et al. Five-year follow-up of a randomized comparison between off-pump and on-pump stable multivessel coronary artery bypass grafting. The MASS III Trial. Circulation. 2010;122(11 suppl):S48-S52. 74. Moller CH, Penninga L, Wetterslev J, Steinbrüchel DA, Gluud C. | Surgery_Schwartz. A, Börgermann J, Kappert U, et al. Off-pump versus on-pump coronary-artery bypass grafting in elderly patients. N Engl J Med. 2013;368(13):1189-1198. 71. Hattler B, Messenger JC, Shroyer Al, et al. Off-Pump coronary artery bypass surgery is associated with worse arterial and saphenous vein graft patency and less effec-tive revascularization: results from the Veterans Affairs Randomized On/Off Bypass (ROOBY) trial. Circulation. 2012;125(23):2827-2835. 72. Hannan EL, Wu C, Smith CR, et al. Off-pump versus on-pump coronary artery bypass graft surgery: differences in short-term outcomes and in long-term mortality and need for subsequent revascularization. Circulation. 2007;116(10):1145-1152. 73. Hueb W, Lopes NH, Pereira AC, et al. Five-year follow-up of a randomized comparison between off-pump and on-pump stable multivessel coronary artery bypass grafting. The MASS III Trial. Circulation. 2010;122(11 suppl):S48-S52. 74. Moller CH, Penninga L, Wetterslev J, Steinbrüchel DA, Gluud C. |
Surgery_Schwartz_5669 | Surgery_Schwartz | and on-pump stable multivessel coronary artery bypass grafting. The MASS III Trial. Circulation. 2010;122(11 suppl):S48-S52. 74. Moller CH, Penninga L, Wetterslev J, Steinbrüchel DA, Gluud C. Off-pump versus on-pump coronary artery bypass grafting for ischaemic heart disease. Cochrane Database Syst Rev. 2012(3):CD007224. 75. Widimsky P, Straka Z, Stros P, et al. One-year coronary bypass graft patency: a randomized comparison between off-pump and on-pump surgery angiographic results of the PRAGUE-4 trial. Circulation. 2004;110(22):3418-3423. 76. Puskas JD, Williams WH, O’Donnell R, et al. Off-pump and on-pump coronary artery bypass grafting are associated with similar graft patency, myocardial ischemia, and freedom from reintervention: long-term follow-up of a randomized trial. Ann Thorac Surg. 2011;91(6):1836-1842; discussion 1842-1843. 77. Sellke FW, Di Maio JM, Caplan LR, et al. Comparing on-pump and off-pump coronary artery bypass grafting: numer-ous studies but few conclusions: a | Surgery_Schwartz. and on-pump stable multivessel coronary artery bypass grafting. The MASS III Trial. Circulation. 2010;122(11 suppl):S48-S52. 74. Moller CH, Penninga L, Wetterslev J, Steinbrüchel DA, Gluud C. Off-pump versus on-pump coronary artery bypass grafting for ischaemic heart disease. Cochrane Database Syst Rev. 2012(3):CD007224. 75. Widimsky P, Straka Z, Stros P, et al. One-year coronary bypass graft patency: a randomized comparison between off-pump and on-pump surgery angiographic results of the PRAGUE-4 trial. Circulation. 2004;110(22):3418-3423. 76. Puskas JD, Williams WH, O’Donnell R, et al. Off-pump and on-pump coronary artery bypass grafting are associated with similar graft patency, myocardial ischemia, and freedom from reintervention: long-term follow-up of a randomized trial. Ann Thorac Surg. 2011;91(6):1836-1842; discussion 1842-1843. 77. Sellke FW, Di Maio JM, Caplan LR, et al. Comparing on-pump and off-pump coronary artery bypass grafting: numer-ous studies but few conclusions: a |
Surgery_Schwartz_5670 | Surgery_Schwartz | Surg. 2011;91(6):1836-1842; discussion 1842-1843. 77. Sellke FW, Di Maio JM, Caplan LR, et al. Comparing on-pump and off-pump coronary artery bypass grafting: numer-ous studies but few conclusions: a scientific statement from the American Heart Association council on cardiovascular surgery and anesthesia in collaboration with the interdisciplin-ary working group on quality of care and outcomes research. Circulation. 2005;111(21):2858-2864. 78. Lichtenberg A, Kilma U, Paeschke H, et al. Impact of multi-vessel coronary artery disease on outcome after isolated mini-mally invasive bypass grafting of the left anterior descending artery. Ann Thorac Surg. 2004;78(2):487-491. 79. Deppe AC, Liakopoulos OJ, Kuhn EW, et al. Minimally inva-sive direct coronary bypass grafting versus percutaneous coro-nary intervention for single-vessel disease: a meta-analysis of 2885 patients. Eur J Cardiothorac Surg. 2015;47(3):397-406; discussion 406. 80. Lee CW, Ahn JM, Cavalcante R, et al. Coronary artery | Surgery_Schwartz. Surg. 2011;91(6):1836-1842; discussion 1842-1843. 77. Sellke FW, Di Maio JM, Caplan LR, et al. Comparing on-pump and off-pump coronary artery bypass grafting: numer-ous studies but few conclusions: a scientific statement from the American Heart Association council on cardiovascular surgery and anesthesia in collaboration with the interdisciplin-ary working group on quality of care and outcomes research. Circulation. 2005;111(21):2858-2864. 78. Lichtenberg A, Kilma U, Paeschke H, et al. Impact of multi-vessel coronary artery disease on outcome after isolated mini-mally invasive bypass grafting of the left anterior descending artery. Ann Thorac Surg. 2004;78(2):487-491. 79. Deppe AC, Liakopoulos OJ, Kuhn EW, et al. Minimally inva-sive direct coronary bypass grafting versus percutaneous coro-nary intervention for single-vessel disease: a meta-analysis of 2885 patients. Eur J Cardiothorac Surg. 2015;47(3):397-406; discussion 406. 80. Lee CW, Ahn JM, Cavalcante R, et al. Coronary artery |
Surgery_Schwartz_5671 | Surgery_Schwartz | intervention for single-vessel disease: a meta-analysis of 2885 patients. Eur J Cardiothorac Surg. 2015;47(3):397-406; discussion 406. 80. Lee CW, Ahn JM, Cavalcante R, et al. Coronary artery bypass surgery versus drug-eluting stent implantation for left main or multivessel coronary artery disease: a meta-analysis of individual patient data. JACC Cardiovasc Interv. 2016;9(24): 2481-2489. 81. Acharya MN, Ashrafian H, Athanasiou T, Casula R. Is totally endoscopic coronary artery bypass safe, feasible and effective? Int Cardiovasc Thoracic Surg. 2012;15(6):1040-1046. 82. Bonatti J, Schachner T, Bonaros N, et al. Effectiveness and safety of total endoscopic left internal mammary artery bypass graft to the left anterior descending artery. Am J Cardiol. 2009;104(12):1684-1688. 83. Srivastava S, Gadasalli S, Agusala M, et al. Beating heart totally endoscopic coronary artery bypass. Ann Thorac Surg. 2010;89(6):1873-1879; discussion 1879-1880. 84. Whellan DJ, McCarey MM, Taylor BS, et al. | Surgery_Schwartz. intervention for single-vessel disease: a meta-analysis of 2885 patients. Eur J Cardiothorac Surg. 2015;47(3):397-406; discussion 406. 80. Lee CW, Ahn JM, Cavalcante R, et al. Coronary artery bypass surgery versus drug-eluting stent implantation for left main or multivessel coronary artery disease: a meta-analysis of individual patient data. JACC Cardiovasc Interv. 2016;9(24): 2481-2489. 81. Acharya MN, Ashrafian H, Athanasiou T, Casula R. Is totally endoscopic coronary artery bypass safe, feasible and effective? Int Cardiovasc Thoracic Surg. 2012;15(6):1040-1046. 82. Bonatti J, Schachner T, Bonaros N, et al. Effectiveness and safety of total endoscopic left internal mammary artery bypass graft to the left anterior descending artery. Am J Cardiol. 2009;104(12):1684-1688. 83. Srivastava S, Gadasalli S, Agusala M, et al. Beating heart totally endoscopic coronary artery bypass. Ann Thorac Surg. 2010;89(6):1873-1879; discussion 1879-1880. 84. Whellan DJ, McCarey MM, Taylor BS, et al. |
Surgery_Schwartz_5672 | Surgery_Schwartz | S, Gadasalli S, Agusala M, et al. Beating heart totally endoscopic coronary artery bypass. Ann Thorac Surg. 2010;89(6):1873-1879; discussion 1879-1880. 84. Whellan DJ, McCarey MM, Taylor BS, et al. Trends in robotic-assisted coronary artery bypass grafts: a study of the Society of Thoracic Surgeons Adult Cardiac Surgery Database, 2006 to 2012. Ann Thorac Surg. 2016;102(1):140-146. 85. Reicher B, Poston RS, Mehra MR, et al. Simultaneous “hybrid” percutaneous coronary intervention and minimally invasive surgical bypass grafting: feasibility, safety, and clini-cal outcomes. Am Heart J. 2008;155(4):661-667. 86. Holzhey DM, Jacobs S, Mochalski M, et al. Minimally inva-sive hybrid coronary artery revascularization. Ann Thorac Surg. 2008;86(6):1856-1860. 87. Katz MR, Van Praet F, de Canniere D, et al. Integrated coro-nary revascularization: percutaneous coronary intervention plus robotic totally endoscopic coronary artery bypass. Circu-lation. 2006;114(1 suppl):I473-I476. 88. Puskas JD, | Surgery_Schwartz. S, Gadasalli S, Agusala M, et al. Beating heart totally endoscopic coronary artery bypass. Ann Thorac Surg. 2010;89(6):1873-1879; discussion 1879-1880. 84. Whellan DJ, McCarey MM, Taylor BS, et al. Trends in robotic-assisted coronary artery bypass grafts: a study of the Society of Thoracic Surgeons Adult Cardiac Surgery Database, 2006 to 2012. Ann Thorac Surg. 2016;102(1):140-146. 85. Reicher B, Poston RS, Mehra MR, et al. Simultaneous “hybrid” percutaneous coronary intervention and minimally invasive surgical bypass grafting: feasibility, safety, and clini-cal outcomes. Am Heart J. 2008;155(4):661-667. 86. Holzhey DM, Jacobs S, Mochalski M, et al. Minimally inva-sive hybrid coronary artery revascularization. Ann Thorac Surg. 2008;86(6):1856-1860. 87. Katz MR, Van Praet F, de Canniere D, et al. Integrated coro-nary revascularization: percutaneous coronary intervention plus robotic totally endoscopic coronary artery bypass. Circu-lation. 2006;114(1 suppl):I473-I476. 88. Puskas JD, |
Surgery_Schwartz_5673 | Surgery_Schwartz | D, et al. Integrated coro-nary revascularization: percutaneous coronary intervention plus robotic totally endoscopic coronary artery bypass. Circu-lation. 2006;114(1 suppl):I473-I476. 88. Puskas JD, Halkos ME, DeRose JJ, et al. Hybrid coronary revascularization for the treatment of multivessel coronary artery disease: a multicenter observational study. J Am Coll Cardiol. 2016;68(4):356-365. 89. Briones E, Lacalle JR, Marin I. Transmyocardial laser revas-cularization versus medical therapy for refractory angina. Cochrane Database Syst Rev. 2009(1):CD003712. 90. Allen KB, Dowling RD, Schuch DR, et al. Adjunctive trans-myocardial revascularization: five-year follow-up of a prospec-tive, randomized trial. Ann Thorac Surg. 2004;78(2):458-465; discussion 458-465. 91. Bridges CR, Horvath KA, Nugent WC, et al. The Society of Thoracic Surgeons practice guideline series: transmyocar-dial laser revascularization. Ann Thorac Surg. 2004;77(4): 1494-14502. 92. Henry TD, Annex BH, McKendall GR, et | Surgery_Schwartz. D, et al. Integrated coro-nary revascularization: percutaneous coronary intervention plus robotic totally endoscopic coronary artery bypass. Circu-lation. 2006;114(1 suppl):I473-I476. 88. Puskas JD, Halkos ME, DeRose JJ, et al. Hybrid coronary revascularization for the treatment of multivessel coronary artery disease: a multicenter observational study. J Am Coll Cardiol. 2016;68(4):356-365. 89. Briones E, Lacalle JR, Marin I. Transmyocardial laser revas-cularization versus medical therapy for refractory angina. Cochrane Database Syst Rev. 2009(1):CD003712. 90. Allen KB, Dowling RD, Schuch DR, et al. Adjunctive trans-myocardial revascularization: five-year follow-up of a prospec-tive, randomized trial. Ann Thorac Surg. 2004;78(2):458-465; discussion 458-465. 91. Bridges CR, Horvath KA, Nugent WC, et al. The Society of Thoracic Surgeons practice guideline series: transmyocar-dial laser revascularization. Ann Thorac Surg. 2004;77(4): 1494-14502. 92. Henry TD, Annex BH, McKendall GR, et |
Surgery_Schwartz_5674 | Surgery_Schwartz | WC, et al. The Society of Thoracic Surgeons practice guideline series: transmyocar-dial laser revascularization. Ann Thorac Surg. 2004;77(4): 1494-14502. 92. Henry TD, Annex BH, McKendall GR, et al. The VIVA trial: Vascular endothelial growth factor in Ischemia for Vascular Angiogenesis. Circulation. 2003;107(10):1359-1365. 93. Simons M, Annex BH, Laham RJ, et al. Pharmacological treat-ment of coronary artery disease with recombinant fibroblast growth factor-2: double-blind, randomized, controlled clinical trial. Circulation. 2002;105(7):788-793. 94. Kumar VA, Brewster LP, Caves JM, Chaikof EL. Tis-sue engineering of blood vessels: functional requirements, progress, and future challenges. Cardiovasc Eng Technol. 2011;2(3):137-148. 95. D’Agostino RS, Jacobs JP, Badwar V, et al. The Society of Tho-racic Surgeons adult cardiac surgery database: 2017 update on outcomes and quality. Ann Thorac Surg. 2017;103(1):18-24. 96. Bonow RO, Carabello BA, Chatterjee K, et al. 2008 focused update | Surgery_Schwartz. WC, et al. The Society of Thoracic Surgeons practice guideline series: transmyocar-dial laser revascularization. Ann Thorac Surg. 2004;77(4): 1494-14502. 92. Henry TD, Annex BH, McKendall GR, et al. The VIVA trial: Vascular endothelial growth factor in Ischemia for Vascular Angiogenesis. Circulation. 2003;107(10):1359-1365. 93. Simons M, Annex BH, Laham RJ, et al. Pharmacological treat-ment of coronary artery disease with recombinant fibroblast growth factor-2: double-blind, randomized, controlled clinical trial. Circulation. 2002;105(7):788-793. 94. Kumar VA, Brewster LP, Caves JM, Chaikof EL. Tis-sue engineering of blood vessels: functional requirements, progress, and future challenges. Cardiovasc Eng Technol. 2011;2(3):137-148. 95. D’Agostino RS, Jacobs JP, Badwar V, et al. The Society of Tho-racic Surgeons adult cardiac surgery database: 2017 update on outcomes and quality. Ann Thorac Surg. 2017;103(1):18-24. 96. Bonow RO, Carabello BA, Chatterjee K, et al. 2008 focused update |
Surgery_Schwartz_5675 | Surgery_Schwartz | of Tho-racic Surgeons adult cardiac surgery database: 2017 update on outcomes and quality. Ann Thorac Surg. 2017;103(1):18-24. 96. Bonow RO, Carabello BA, Chatterjee K, et al. 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Com-mittee to revise the 1998 guidelines for the management of patients with valvular heart disease). Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascu-lar Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2008;52(13):e1-142. 97. Rosendaal FR. The Scylla and Charybdis of oral anticoagulant treatment. N Engl J Med. 1996;335(8):587-589. 98. Nishimura RA, et al. 2014 AHA/ACC guideline for the man-agement of patients with valvular heart disease: a report Brunicardi_Ch21_p0801-p0852.indd 84601/03/19 5:32 PM | Surgery_Schwartz. of Tho-racic Surgeons adult cardiac surgery database: 2017 update on outcomes and quality. Ann Thorac Surg. 2017;103(1):18-24. 96. Bonow RO, Carabello BA, Chatterjee K, et al. 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Com-mittee to revise the 1998 guidelines for the management of patients with valvular heart disease). Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascu-lar Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2008;52(13):e1-142. 97. Rosendaal FR. The Scylla and Charybdis of oral anticoagulant treatment. N Engl J Med. 1996;335(8):587-589. 98. Nishimura RA, et al. 2014 AHA/ACC guideline for the man-agement of patients with valvular heart disease: a report Brunicardi_Ch21_p0801-p0852.indd 84601/03/19 5:32 PM |
Surgery_Schwartz_5676 | Surgery_Schwartz | 1996;335(8):587-589. 98. Nishimura RA, et al. 2014 AHA/ACC guideline for the man-agement of patients with valvular heart disease: a report Brunicardi_Ch21_p0801-p0852.indd 84601/03/19 5:32 PM 847ACQUIRED HEART DISEASECHAPTER 21of the American College of Cardiology/American Heart Association Task Force on practice guidelines. Circulation. 2014;129(23):e521-e643. 99. Hammermeister K. Outcomes 15 years after valve replacement with a mechanical versus a bioprosthetic valve: final report of the Veterans Affairs randomized trial. J Am Coll Cardiol. 2000;36(4):1152-1158. 100. Bloomfield P. Choice of heart valve prosthesis. Heart. 2002;87(6):583-589. 101. Butchart EG, et al. Better anticoagulation control improves survival after valve replacement. J Thorac Cardiovasc Surg. 2002;123(4):715-723. 102. Puskas J, Gerdisch M, Nichols D, et al. Reduced anticoagula-tion after mechanical aortic valve replacement: interim results from the prospective randomized on X-valve anticoagulation clinical | Surgery_Schwartz. 1996;335(8):587-589. 98. Nishimura RA, et al. 2014 AHA/ACC guideline for the man-agement of patients with valvular heart disease: a report Brunicardi_Ch21_p0801-p0852.indd 84601/03/19 5:32 PM 847ACQUIRED HEART DISEASECHAPTER 21of the American College of Cardiology/American Heart Association Task Force on practice guidelines. Circulation. 2014;129(23):e521-e643. 99. Hammermeister K. Outcomes 15 years after valve replacement with a mechanical versus a bioprosthetic valve: final report of the Veterans Affairs randomized trial. J Am Coll Cardiol. 2000;36(4):1152-1158. 100. Bloomfield P. Choice of heart valve prosthesis. Heart. 2002;87(6):583-589. 101. Butchart EG, et al. Better anticoagulation control improves survival after valve replacement. J Thorac Cardiovasc Surg. 2002;123(4):715-723. 102. Puskas J, Gerdisch M, Nichols D, et al. Reduced anticoagula-tion after mechanical aortic valve replacement: interim results from the prospective randomized on X-valve anticoagulation clinical |
Surgery_Schwartz_5677 | Surgery_Schwartz | J, Gerdisch M, Nichols D, et al. Reduced anticoagula-tion after mechanical aortic valve replacement: interim results from the prospective randomized on X-valve anticoagulation clinical trial randomized Food and Drug Administration inves-tigational device exemption trial. J Thorac Cardiovasc Surg. 2014;147(4):1202-1210; discussion 1210-1211. 103. Cannegieter SC, Rosendaal FR, Briet E. Thromboembolic and bleeding complications in patients with mechanical heart valve prostheses. Circulation. 1994;89(2):635-641. 104. Hoffmann G, Lutter G, Cremer J. Durability of bioprosthetic cardiac valves. Dtsch Arztebl Int. 2008;105(8):143-148. 105. Pibarot P, Dumesnil JG, Jobin J, Cartier P, Honos G, Durand LG. Hemodynamic and physical performance during maximal exercise in patients with an aortic bioprosthetic valve: com-parison of stentless versus stented bioprostheses. J Am Coll Cardiol. 1999;34(5):1609-1617. 106. Fries R, Wendler O, Schieffer H, Schäfers HJ. Comparative rest and exercise | Surgery_Schwartz. J, Gerdisch M, Nichols D, et al. Reduced anticoagula-tion after mechanical aortic valve replacement: interim results from the prospective randomized on X-valve anticoagulation clinical trial randomized Food and Drug Administration inves-tigational device exemption trial. J Thorac Cardiovasc Surg. 2014;147(4):1202-1210; discussion 1210-1211. 103. Cannegieter SC, Rosendaal FR, Briet E. Thromboembolic and bleeding complications in patients with mechanical heart valve prostheses. Circulation. 1994;89(2):635-641. 104. Hoffmann G, Lutter G, Cremer J. Durability of bioprosthetic cardiac valves. Dtsch Arztebl Int. 2008;105(8):143-148. 105. Pibarot P, Dumesnil JG, Jobin J, Cartier P, Honos G, Durand LG. Hemodynamic and physical performance during maximal exercise in patients with an aortic bioprosthetic valve: com-parison of stentless versus stented bioprostheses. J Am Coll Cardiol. 1999;34(5):1609-1617. 106. Fries R, Wendler O, Schieffer H, Schäfers HJ. Comparative rest and exercise |
Surgery_Schwartz_5678 | Surgery_Schwartz | bioprosthetic valve: com-parison of stentless versus stented bioprostheses. J Am Coll Cardiol. 1999;34(5):1609-1617. 106. Fries R, Wendler O, Schieffer H, Schäfers HJ. Comparative rest and exercise hemodynamics of 23-mm stentless versus 23-mm stented aortic bioprostheses. Ann Thorac Surg. 2000;69(3): 817-22. 107. Pavoni D, Badano LP, Ius F, et al. Limited long-term durabil-ity of the Cryolife O’Brien stentless porcine xenograft valve. Circulation. 2007;116(11 suppl): I307-I313. 108. Powell R, Pelletier MP, Chu MWA, Bouchard D, Melvin KN, Adams C. The perceval sutureless aortic valve: review of outcomes, complications, and future direction. Innovations (Phila). 2017;12(3):155-173. 109. Ross DN. Homograft replacement of the aortic valve. Lancet. 1962;2(7254):487. 110. Anguera I, Miro JM, San Roman JA, et al. Periannular com-plications in infective endocarditis involving prosthetic aortic valves. Am J Cardiol. 2006;98(9):1261-1268. 111. Vogt F, et al. Pulmonary homografts for aortic | Surgery_Schwartz. bioprosthetic valve: com-parison of stentless versus stented bioprostheses. J Am Coll Cardiol. 1999;34(5):1609-1617. 106. Fries R, Wendler O, Schieffer H, Schäfers HJ. Comparative rest and exercise hemodynamics of 23-mm stentless versus 23-mm stented aortic bioprostheses. Ann Thorac Surg. 2000;69(3): 817-22. 107. Pavoni D, Badano LP, Ius F, et al. Limited long-term durabil-ity of the Cryolife O’Brien stentless porcine xenograft valve. Circulation. 2007;116(11 suppl): I307-I313. 108. Powell R, Pelletier MP, Chu MWA, Bouchard D, Melvin KN, Adams C. The perceval sutureless aortic valve: review of outcomes, complications, and future direction. Innovations (Phila). 2017;12(3):155-173. 109. Ross DN. Homograft replacement of the aortic valve. Lancet. 1962;2(7254):487. 110. Anguera I, Miro JM, San Roman JA, et al. Periannular com-plications in infective endocarditis involving prosthetic aortic valves. Am J Cardiol. 2006;98(9):1261-1268. 111. Vogt F, et al. Pulmonary homografts for aortic |
Surgery_Schwartz_5679 | Surgery_Schwartz | San Roman JA, et al. Periannular com-plications in infective endocarditis involving prosthetic aortic valves. Am J Cardiol. 2006;98(9):1261-1268. 111. Vogt F, et al. Pulmonary homografts for aortic valve replace-ment: long-term comparison with aortic grafts. Heart Surg Forum. 2011;14(4):E237-E241. 112. Ross DN. Replacement of aortic and mitral valves with a pul-monary autograft. Lancet. 1967;2(7523):956-958. 113. Gerosa G, McKay R, Davies J, Ross DN. Comparison of the aortic homograft and the pulmonary autograft for aortic valve or root replacement in children. J Thorac Cardiovasc Surg. 1991;102(1):51-60; discussion 60-61. 114. David TE, Uden DE, Strauss HD. The importance of the mitral apparatus in left ventricular function after correction of mitral regurgitation. Circulation. 1983;68(3 pt 2):II76-II82. 115. Enriquez-Sarano M, Schaff HV, Orszulak TA, Tajik AJ, Bailey KR, Frye RL. Valve repair improves the outcome of surgery for mitral regurgitation. A multivariate analysis. | Surgery_Schwartz. San Roman JA, et al. Periannular com-plications in infective endocarditis involving prosthetic aortic valves. Am J Cardiol. 2006;98(9):1261-1268. 111. Vogt F, et al. Pulmonary homografts for aortic valve replace-ment: long-term comparison with aortic grafts. Heart Surg Forum. 2011;14(4):E237-E241. 112. Ross DN. Replacement of aortic and mitral valves with a pul-monary autograft. Lancet. 1967;2(7523):956-958. 113. Gerosa G, McKay R, Davies J, Ross DN. Comparison of the aortic homograft and the pulmonary autograft for aortic valve or root replacement in children. J Thorac Cardiovasc Surg. 1991;102(1):51-60; discussion 60-61. 114. David TE, Uden DE, Strauss HD. The importance of the mitral apparatus in left ventricular function after correction of mitral regurgitation. Circulation. 1983;68(3 pt 2):II76-II82. 115. Enriquez-Sarano M, Schaff HV, Orszulak TA, Tajik AJ, Bailey KR, Frye RL. Valve repair improves the outcome of surgery for mitral regurgitation. A multivariate analysis. |
Surgery_Schwartz_5680 | Surgery_Schwartz | pt 2):II76-II82. 115. Enriquez-Sarano M, Schaff HV, Orszulak TA, Tajik AJ, Bailey KR, Frye RL. Valve repair improves the outcome of surgery for mitral regurgitation. A multivariate analysis. Circulation. 1995;91(4):1022-1028. 116. David TE, Armstrong S, McCrindle BW, Manlhiot C. Late outcomes of mitral valve repair for mitral regurgitation due to degenerative disease. Circulation. 2013;127(14): 1485-1492. 117. Pfannmueller B, Verevkin A, Borger Ma, et al. Role of tricus-pid valve repair for moderate tricuspid regurgitation during minimally invasive mitral valve surgery. Thorac Cardiovasc Surg. 2013;61(5):386-391. 118. Roberts WC, Perloff JK. Mitral valvular disease. A clinico-pathologic survey of the conditions causing the mitral valve to function abnormally. Ann Intern Med. 1972;77(6):939-975. 119. Snopek G, Pogorzelska H, Rywik TM, Browarek A, Janas J, Korewicki J. Usefulness of endothelin-1 concentration in capillary blood in patients with mitral stenosis as a predic-tor of | Surgery_Schwartz. pt 2):II76-II82. 115. Enriquez-Sarano M, Schaff HV, Orszulak TA, Tajik AJ, Bailey KR, Frye RL. Valve repair improves the outcome of surgery for mitral regurgitation. A multivariate analysis. Circulation. 1995;91(4):1022-1028. 116. David TE, Armstrong S, McCrindle BW, Manlhiot C. Late outcomes of mitral valve repair for mitral regurgitation due to degenerative disease. Circulation. 2013;127(14): 1485-1492. 117. Pfannmueller B, Verevkin A, Borger Ma, et al. Role of tricus-pid valve repair for moderate tricuspid regurgitation during minimally invasive mitral valve surgery. Thorac Cardiovasc Surg. 2013;61(5):386-391. 118. Roberts WC, Perloff JK. Mitral valvular disease. A clinico-pathologic survey of the conditions causing the mitral valve to function abnormally. Ann Intern Med. 1972;77(6):939-975. 119. Snopek G, Pogorzelska H, Rywik TM, Browarek A, Janas J, Korewicki J. Usefulness of endothelin-1 concentration in capillary blood in patients with mitral stenosis as a predic-tor of |
Surgery_Schwartz_5681 | Surgery_Schwartz | G, Pogorzelska H, Rywik TM, Browarek A, Janas J, Korewicki J. Usefulness of endothelin-1 concentration in capillary blood in patients with mitral stenosis as a predic-tor of regression of pulmonary hypertension after mitral valve replacement or valvuloplasty. Am J Cardiol. 2002;90(2): 188-189. 120. Gorlin R. The mechanism of the signs and symptoms of mitral valve disease. Br Heart J. 1954;16(4):375-380. 121. Martin RP, Rakowski H, Kleiman JH, Beaver W, London E, Popp RL. Reliability and reproducibility of two dimensional echocardiograph measurement of the stenotic mitral valve ori-fice area. Am J Cardiol. 1979;43(3):560-568. 122. Cheriex EC, Pieters FA, Janssen JH, de Swart H, Palmans-Meulemans A. Value of exercise Doppler-echocardiography in patients with mitral stenosis. Int J Cardiol. 1994;45(3):219-226. 123. Delling FN, Vasan RS. Epidemiology and pathophysiology of mitral valve prolapse: new insights into disease progression, genetics, and molecular basis. Circulation. | Surgery_Schwartz. G, Pogorzelska H, Rywik TM, Browarek A, Janas J, Korewicki J. Usefulness of endothelin-1 concentration in capillary blood in patients with mitral stenosis as a predic-tor of regression of pulmonary hypertension after mitral valve replacement or valvuloplasty. Am J Cardiol. 2002;90(2): 188-189. 120. Gorlin R. The mechanism of the signs and symptoms of mitral valve disease. Br Heart J. 1954;16(4):375-380. 121. Martin RP, Rakowski H, Kleiman JH, Beaver W, London E, Popp RL. Reliability and reproducibility of two dimensional echocardiograph measurement of the stenotic mitral valve ori-fice area. Am J Cardiol. 1979;43(3):560-568. 122. Cheriex EC, Pieters FA, Janssen JH, de Swart H, Palmans-Meulemans A. Value of exercise Doppler-echocardiography in patients with mitral stenosis. Int J Cardiol. 1994;45(3):219-226. 123. Delling FN, Vasan RS. Epidemiology and pathophysiology of mitral valve prolapse: new insights into disease progression, genetics, and molecular basis. Circulation. |
Surgery_Schwartz_5682 | Surgery_Schwartz | J Cardiol. 1994;45(3):219-226. 123. Delling FN, Vasan RS. Epidemiology and pathophysiology of mitral valve prolapse: new insights into disease progression, genetics, and molecular basis. Circulation. 2014;129(21): 2158-2170. 124. Enriquez-Sarano M, Akins CW, Vahanian A. Mitral regurgita-tion. Lancet. 2009;373(9672):1382-1394. 125. Carpentier A. Cardiac valve surgery—the “French correction.” J Thorac Cardiovasc Surg. 1983;86(3):323-337. 126. Zile MR, Gaasch WH, Carroll JD, Levine HJ. Chronic mitral regurgitation: predictive value of preoperative echocardio-graphic indexes of left ventricular function and wall stress. J Am Coll Cardiol. 1984;3(2 pt 1):235-242. 127. Castello R, Fagan L, Jr, Lenzen P, Pearson AC, Labovitz AJ. Comparison of transthoracic and transesophageal echocar-diography for assessment of left-sided valvular regurgitation. Am J Cardiol. 1991;68(17):1677-1680. 128. Enriquez-Sarano M. Quantitative determinants of the out-come of asymptomatic mitral regurgitation. N Engl | Surgery_Schwartz. J Cardiol. 1994;45(3):219-226. 123. Delling FN, Vasan RS. Epidemiology and pathophysiology of mitral valve prolapse: new insights into disease progression, genetics, and molecular basis. Circulation. 2014;129(21): 2158-2170. 124. Enriquez-Sarano M, Akins CW, Vahanian A. Mitral regurgita-tion. Lancet. 2009;373(9672):1382-1394. 125. Carpentier A. Cardiac valve surgery—the “French correction.” J Thorac Cardiovasc Surg. 1983;86(3):323-337. 126. Zile MR, Gaasch WH, Carroll JD, Levine HJ. Chronic mitral regurgitation: predictive value of preoperative echocardio-graphic indexes of left ventricular function and wall stress. J Am Coll Cardiol. 1984;3(2 pt 1):235-242. 127. Castello R, Fagan L, Jr, Lenzen P, Pearson AC, Labovitz AJ. Comparison of transthoracic and transesophageal echocar-diography for assessment of left-sided valvular regurgitation. Am J Cardiol. 1991;68(17):1677-1680. 128. Enriquez-Sarano M. Quantitative determinants of the out-come of asymptomatic mitral regurgitation. N Engl |
Surgery_Schwartz_5683 | Surgery_Schwartz | assessment of left-sided valvular regurgitation. Am J Cardiol. 1991;68(17):1677-1680. 128. Enriquez-Sarano M. Quantitative determinants of the out-come of asymptomatic mitral regurgitation. N Engl J Med. 2005;352(9):875-883. 129. Picano E, Pibarot P, Lancellotti P, Monin JL, Bonow RO. The emerging role of exercise testing and stress echocardiography in valvular heart disease. J Am Coll Cardiol. 2009;54(24): 2251-2560. 130. Kitamura N, Uemura S, Kunitomo R, Utoh J, Noji S. A new technique for debridement in rheumatic valvular disease: the rasping procedure. Ann Thorac Surg. 2000;69(1):121-125. 131. Reichart DT, Sodian R, Zenker R, Klinner W, Schmitz C, Reichart B. Long-term (</= 50 years) results of patients after mitral valve commissurotomy—a single-center experience. J Thorac Cardiovasc Surg. 2012;143(4 suppl):S96-S98. 132. Choudhary SK, Dhareshwar J, Govil A, Airan B, Kumar AS. Open mitral commissurotomy in the current era: indications, technique, and results. Ann Thorac Surg. | Surgery_Schwartz. assessment of left-sided valvular regurgitation. Am J Cardiol. 1991;68(17):1677-1680. 128. Enriquez-Sarano M. Quantitative determinants of the out-come of asymptomatic mitral regurgitation. N Engl J Med. 2005;352(9):875-883. 129. Picano E, Pibarot P, Lancellotti P, Monin JL, Bonow RO. The emerging role of exercise testing and stress echocardiography in valvular heart disease. J Am Coll Cardiol. 2009;54(24): 2251-2560. 130. Kitamura N, Uemura S, Kunitomo R, Utoh J, Noji S. A new technique for debridement in rheumatic valvular disease: the rasping procedure. Ann Thorac Surg. 2000;69(1):121-125. 131. Reichart DT, Sodian R, Zenker R, Klinner W, Schmitz C, Reichart B. Long-term (</= 50 years) results of patients after mitral valve commissurotomy—a single-center experience. J Thorac Cardiovasc Surg. 2012;143(4 suppl):S96-S98. 132. Choudhary SK, Dhareshwar J, Govil A, Airan B, Kumar AS. Open mitral commissurotomy in the current era: indications, technique, and results. Ann Thorac Surg. |
Surgery_Schwartz_5684 | Surgery_Schwartz | Surg. 2012;143(4 suppl):S96-S98. 132. Choudhary SK, Dhareshwar J, Govil A, Airan B, Kumar AS. Open mitral commissurotomy in the current era: indications, technique, and results. Ann Thorac Surg. 2003;75(1):41-46. 133. Mohty D, Orszulak TA, Schaff HV, et al. Very long-term sur-vival and durability of mitral valve repair for mitral valve prolapse. Circulation. 2001;104(12 suppl 1):I1-I7. 134. Vassileva CM, Mishkel G, McNeely C, et al. Long-term sur-vival of patients undergoing mitral valve repair and replace-ment: a longitudinal analysis of medicare fee-for-service beneficiaries. Circulation. 2013;127(18):1870-1876. 135. Khan SS, Trento A, DeRobertis M, et al. Twenty-year com-parison of tissue and mechanical valve replacement. J Thorac Cardiovasc Surg. 2001;122(2):257-269. 136. Gillinov AM, Cosgrove DM. Mitral valve repair for degenera-tive disease. J Heart Valve Dis. 2002;11(suppl 1):S15-S20. 137. Fucci C. Improved results with mitral valve repair using new surgical techniques. Eur J | Surgery_Schwartz. Surg. 2012;143(4 suppl):S96-S98. 132. Choudhary SK, Dhareshwar J, Govil A, Airan B, Kumar AS. Open mitral commissurotomy in the current era: indications, technique, and results. Ann Thorac Surg. 2003;75(1):41-46. 133. Mohty D, Orszulak TA, Schaff HV, et al. Very long-term sur-vival and durability of mitral valve repair for mitral valve prolapse. Circulation. 2001;104(12 suppl 1):I1-I7. 134. Vassileva CM, Mishkel G, McNeely C, et al. Long-term sur-vival of patients undergoing mitral valve repair and replace-ment: a longitudinal analysis of medicare fee-for-service beneficiaries. Circulation. 2013;127(18):1870-1876. 135. Khan SS, Trento A, DeRobertis M, et al. Twenty-year com-parison of tissue and mechanical valve replacement. J Thorac Cardiovasc Surg. 2001;122(2):257-269. 136. Gillinov AM, Cosgrove DM. Mitral valve repair for degenera-tive disease. J Heart Valve Dis. 2002;11(suppl 1):S15-S20. 137. Fucci C. Improved results with mitral valve repair using new surgical techniques. Eur J |
Surgery_Schwartz_5685 | Surgery_Schwartz | Cosgrove DM. Mitral valve repair for degenera-tive disease. J Heart Valve Dis. 2002;11(suppl 1):S15-S20. 137. Fucci C. Improved results with mitral valve repair using new surgical techniques. Eur J Cardiothorac Surg. 1995;9(11): 621-626. 138. O’Brien SM, Shahian DM, Filardo G, et al. The Society of Thoracic Surgeons 2008 cardiac surgery risk models: part Brunicardi_Ch21_p0801-p0852.indd 84701/03/19 5:32 PM 848SPECIFIC CONSIDERATIONSPART II2—isolated valve surgery. Ann Thorac Surg. 2009;88(1 suppl): S23-S42. 139. Castillo JG, Anyanwu AC, El-Eshmawi A, Adams DH. All anterior and bileaflet mitral valve prolapses are repairable in the modern era of reconstructive surgery. Eur J Cardiothorac Surg. 2014;45(1):139-145. 140. Braunberger E, Deloche A, Berrebi A, et al. Very long-term results (more than 20 years) of valve repair with carpentier’s techniques in nonrheumatic mitral valve insufficiency. Circu-lation. 2001;104(12 suppl 1):I8-I11. 141. Acker MA, Parides MK, Perrault LP, et al. | Surgery_Schwartz. Cosgrove DM. Mitral valve repair for degenera-tive disease. J Heart Valve Dis. 2002;11(suppl 1):S15-S20. 137. Fucci C. Improved results with mitral valve repair using new surgical techniques. Eur J Cardiothorac Surg. 1995;9(11): 621-626. 138. O’Brien SM, Shahian DM, Filardo G, et al. The Society of Thoracic Surgeons 2008 cardiac surgery risk models: part Brunicardi_Ch21_p0801-p0852.indd 84701/03/19 5:32 PM 848SPECIFIC CONSIDERATIONSPART II2—isolated valve surgery. Ann Thorac Surg. 2009;88(1 suppl): S23-S42. 139. Castillo JG, Anyanwu AC, El-Eshmawi A, Adams DH. All anterior and bileaflet mitral valve prolapses are repairable in the modern era of reconstructive surgery. Eur J Cardiothorac Surg. 2014;45(1):139-145. 140. Braunberger E, Deloche A, Berrebi A, et al. Very long-term results (more than 20 years) of valve repair with carpentier’s techniques in nonrheumatic mitral valve insufficiency. Circu-lation. 2001;104(12 suppl 1):I8-I11. 141. Acker MA, Parides MK, Perrault LP, et al. |
Surgery_Schwartz_5686 | Surgery_Schwartz | (more than 20 years) of valve repair with carpentier’s techniques in nonrheumatic mitral valve insufficiency. Circu-lation. 2001;104(12 suppl 1):I8-I11. 141. Acker MA, Parides MK, Perrault LP, et al. Mitral-valve repair versus replacement for severe ischemic mitral regurgitation. N Engl J Med. 2014;370(1):23-32. 142. Goldstein D, Moskowitz AJ, Geljins AC, et al. Two-year out-comes of surgical treatment of severe ischemic mitral regurgi-tation. N Engl J Med. 2016;374(4):344-353. 143. Feldman T, Wasserman HS, Herrmann HC, et al. Percutane-ous mitral valve repair using the edge-to-edge technique: six-month results of the EVEREST Phase I Clinical Trial. J Am Coll Cardiol. 2005;46(11):2134-2140. 144. Feldman T, Foster E, Glower DD, et al. Percutaneous repair or surgery for mitral regurgitation. N Engl J Med. 2011;364(15): 1395-1406. 145. O’Brien KD. Pathogenesis of calcific aortic valve disease: a disease process comes of age (and a good deal more). Arterio-scler Thromb Vasc Biol. | Surgery_Schwartz. (more than 20 years) of valve repair with carpentier’s techniques in nonrheumatic mitral valve insufficiency. Circu-lation. 2001;104(12 suppl 1):I8-I11. 141. Acker MA, Parides MK, Perrault LP, et al. Mitral-valve repair versus replacement for severe ischemic mitral regurgitation. N Engl J Med. 2014;370(1):23-32. 142. Goldstein D, Moskowitz AJ, Geljins AC, et al. Two-year out-comes of surgical treatment of severe ischemic mitral regurgi-tation. N Engl J Med. 2016;374(4):344-353. 143. Feldman T, Wasserman HS, Herrmann HC, et al. Percutane-ous mitral valve repair using the edge-to-edge technique: six-month results of the EVEREST Phase I Clinical Trial. J Am Coll Cardiol. 2005;46(11):2134-2140. 144. Feldman T, Foster E, Glower DD, et al. Percutaneous repair or surgery for mitral regurgitation. N Engl J Med. 2011;364(15): 1395-1406. 145. O’Brien KD. Pathogenesis of calcific aortic valve disease: a disease process comes of age (and a good deal more). Arterio-scler Thromb Vasc Biol. |
Surgery_Schwartz_5687 | Surgery_Schwartz | N Engl J Med. 2011;364(15): 1395-1406. 145. O’Brien KD. Pathogenesis of calcific aortic valve disease: a disease process comes of age (and a good deal more). Arterio-scler Thromb Vasc Biol. 2006;26(8):1721-1728. 146. Murakami T, Hess OM, Gage JE, Grimm J, Krayenbuehl HP. Diastolic filling dynamics in patients with aortic stenosis. Cir-culation. 1986;73(6):1162-1174. 147. Gunther S, Grossman W. Determinants of ventricular func-tion in pressure-overload hypertrophy in man. Circulation. 1979;59(4):679-688. 148. Marcus ML, Doty DB, Hiratzka LF, Wright CB, Eastham CL. Decreased coronary reserve: a mechanism for angina pectoris in patients with aortic stenosis and normal coronary arteries. N Engl J Med. 1982;307(22):1362-1366. 149. Gaasch WH, Zile MR, Hoshino PK, Weinberg EO, Rhodes DR, Apstein CS. Tolerance of the hypertrophic heart to ischemia. Studies in compensated and failing dog hearts with pressure overload hypertrophy. Circulation. 1990;81(5):1644-1653. 150. Orsinelli DA, Aurigemma | Surgery_Schwartz. N Engl J Med. 2011;364(15): 1395-1406. 145. O’Brien KD. Pathogenesis of calcific aortic valve disease: a disease process comes of age (and a good deal more). Arterio-scler Thromb Vasc Biol. 2006;26(8):1721-1728. 146. Murakami T, Hess OM, Gage JE, Grimm J, Krayenbuehl HP. Diastolic filling dynamics in patients with aortic stenosis. Cir-culation. 1986;73(6):1162-1174. 147. Gunther S, Grossman W. Determinants of ventricular func-tion in pressure-overload hypertrophy in man. Circulation. 1979;59(4):679-688. 148. Marcus ML, Doty DB, Hiratzka LF, Wright CB, Eastham CL. Decreased coronary reserve: a mechanism for angina pectoris in patients with aortic stenosis and normal coronary arteries. N Engl J Med. 1982;307(22):1362-1366. 149. Gaasch WH, Zile MR, Hoshino PK, Weinberg EO, Rhodes DR, Apstein CS. Tolerance of the hypertrophic heart to ischemia. Studies in compensated and failing dog hearts with pressure overload hypertrophy. Circulation. 1990;81(5):1644-1653. 150. Orsinelli DA, Aurigemma |
Surgery_Schwartz_5688 | Surgery_Schwartz | CS. Tolerance of the hypertrophic heart to ischemia. Studies in compensated and failing dog hearts with pressure overload hypertrophy. Circulation. 1990;81(5):1644-1653. 150. Orsinelli DA, Aurigemma GP, Battista S, Krendel S, Gaasch WH. Left ventricular hypertrophy and mortality after aortic valve replacement for aortic stenosis. A high risk sub-group identified by preoperative relative wall thickness. J Am Coll Cardiol. 1993;22(6):1679-1683. 151. Lumley M, Williams R, Asrress KN, et al. Coronary physiol-ogy during exercise and vasodilation in the healthy heart and in severe aortic stenosis. J Am Coll Cardiol. 2016;68(7):688-697. 152. Nishimura RA, Otto CM, Bonow RO, et al. 2017 AHA/ACC focused update of the 2014 aha/acc guideline for the man-agement of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Asso-ciation task force on clinical practice guidelines. Circulation. 2017;135(25):e1159-e1195. 153. Roberts WC, JO JM, Moore TR, Jones | Surgery_Schwartz. CS. Tolerance of the hypertrophic heart to ischemia. Studies in compensated and failing dog hearts with pressure overload hypertrophy. Circulation. 1990;81(5):1644-1653. 150. Orsinelli DA, Aurigemma GP, Battista S, Krendel S, Gaasch WH. Left ventricular hypertrophy and mortality after aortic valve replacement for aortic stenosis. A high risk sub-group identified by preoperative relative wall thickness. J Am Coll Cardiol. 1993;22(6):1679-1683. 151. Lumley M, Williams R, Asrress KN, et al. Coronary physiol-ogy during exercise and vasodilation in the healthy heart and in severe aortic stenosis. J Am Coll Cardiol. 2016;68(7):688-697. 152. Nishimura RA, Otto CM, Bonow RO, et al. 2017 AHA/ACC focused update of the 2014 aha/acc guideline for the man-agement of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Asso-ciation task force on clinical practice guidelines. Circulation. 2017;135(25):e1159-e1195. 153. Roberts WC, JO JM, Moore TR, Jones |
Surgery_Schwartz_5689 | Surgery_Schwartz | a report of the American College of Cardiology/American Heart Asso-ciation task force on clinical practice guidelines. Circulation. 2017;135(25):e1159-e1195. 153. Roberts WC, JO JM, Moore TR, Jones WH. Causes of pure aortic regurgitation in patients having isolated aortic valve replacement at a single US tertiary hospital (1993 to 2005). Circulation. 2006;114(5):422-429. 154. Roberts WC, Ko JM. Frequency by decades of unicuspid, bicus-pid, and tricuspid aortic valves in adults having isolated aortic valve replacement for aortic stenosis, with or without associ-ated aortic regurgitation. Circulation. 2005;111(7):920-925. 155. Grossman W, Jones D, McLaurin LP. Wall stress and pat-terns of hypertrophy in the human left ventricle. J Clin Invest. 1975;56(1):56-64. 156. Ross J, Jr, McCullagh WH. Nature of enhanced performance of the dilated left ventricle in the dog during chronic volume overloading. Circ Res. 1972;30(5):549-556. 157. Wisenbaugh T, Spann SF, Carabello BA. Differences in | Surgery_Schwartz. a report of the American College of Cardiology/American Heart Asso-ciation task force on clinical practice guidelines. Circulation. 2017;135(25):e1159-e1195. 153. Roberts WC, JO JM, Moore TR, Jones WH. Causes of pure aortic regurgitation in patients having isolated aortic valve replacement at a single US tertiary hospital (1993 to 2005). Circulation. 2006;114(5):422-429. 154. Roberts WC, Ko JM. Frequency by decades of unicuspid, bicus-pid, and tricuspid aortic valves in adults having isolated aortic valve replacement for aortic stenosis, with or without associ-ated aortic regurgitation. Circulation. 2005;111(7):920-925. 155. Grossman W, Jones D, McLaurin LP. Wall stress and pat-terns of hypertrophy in the human left ventricle. J Clin Invest. 1975;56(1):56-64. 156. Ross J, Jr, McCullagh WH. Nature of enhanced performance of the dilated left ventricle in the dog during chronic volume overloading. Circ Res. 1972;30(5):549-556. 157. Wisenbaugh T, Spann SF, Carabello BA. Differences in |
Surgery_Schwartz_5690 | Surgery_Schwartz | WH. Nature of enhanced performance of the dilated left ventricle in the dog during chronic volume overloading. Circ Res. 1972;30(5):549-556. 157. Wisenbaugh T, Spann SF, Carabello BA. Differences in myo-cardial performance and load between patients with similar amounts of chronic aortic versus chronic mitral regurgitation. J Am Coll Cardiol. 1984;3(4):916-923. 158. Ross J, Jr. Afterload mismatch in aortic and mitral valve dis-ease: implications for surgical therapy. J Am Coll Cardiol. 1985;5(4):811-826. 159. Nienaber CA, von Kodolitsch Y, Nicolas V, et al. The diagnosis of thoracic aortic dissection by noninvasive imaging proce-dures. N Engl J Med. 1993;328(1):1-9. 160. Smith DC, Bansal RC. Transesophageal echocardiography in the diagnosis of traumatic rupture of the aorta. N Engl J Med. 1995;332(6):356-362. 161. Sasaki Hirai H, Hosono M, et al. Adding coronary artery bypass grafting to aortic valve replacement increases opera-tive mortality for elderly (70 years and older) patients | Surgery_Schwartz. WH. Nature of enhanced performance of the dilated left ventricle in the dog during chronic volume overloading. Circ Res. 1972;30(5):549-556. 157. Wisenbaugh T, Spann SF, Carabello BA. Differences in myo-cardial performance and load between patients with similar amounts of chronic aortic versus chronic mitral regurgitation. J Am Coll Cardiol. 1984;3(4):916-923. 158. Ross J, Jr. Afterload mismatch in aortic and mitral valve dis-ease: implications for surgical therapy. J Am Coll Cardiol. 1985;5(4):811-826. 159. Nienaber CA, von Kodolitsch Y, Nicolas V, et al. The diagnosis of thoracic aortic dissection by noninvasive imaging proce-dures. N Engl J Med. 1993;328(1):1-9. 160. Smith DC, Bansal RC. Transesophageal echocardiography in the diagnosis of traumatic rupture of the aorta. N Engl J Med. 1995;332(6):356-362. 161. Sasaki Hirai H, Hosono M, et al. Adding coronary artery bypass grafting to aortic valve replacement increases opera-tive mortality for elderly (70 years and older) patients |
Surgery_Schwartz_5691 | Surgery_Schwartz | 1995;332(6):356-362. 161. Sasaki Hirai H, Hosono M, et al. Adding coronary artery bypass grafting to aortic valve replacement increases opera-tive mortality for elderly (70 years and older) patients with aortic stenosis. Gen Thorac Cardiovasc Surg. 2013;61(11): 626-631. 162. de Kerchove L, Boodhwani M, Glineur D, et al. Valve sparing-root replacement with the reimplantation technique to increase the durability of bicuspid aortic valve repair. J Thorac Cardio-vasc Surg. 2011 Dec;142(6):1430-8. 163. El Khoury G, de Kerchove L. Principles of aortic valve repair. J Thorac Cardiovasc Surg. 2013;145(3 suppl):S26-S29. 164. Mokhles MM, Rizopoulos D, Andrinopoulou ER, et al. Autograft and pulmonary allograft performance in the sec-ond post-operative decade after the Ross procedure: insights from the Rotterdam Prospective Cohort Study. Eur Heart J. 2012;33(17):2213-2224. 165. Chambers JC, Somerville J, Stone S, Ross DN. Pulmonary autograft procedure for aortic valve disease: long-term results | Surgery_Schwartz. 1995;332(6):356-362. 161. Sasaki Hirai H, Hosono M, et al. Adding coronary artery bypass grafting to aortic valve replacement increases opera-tive mortality for elderly (70 years and older) patients with aortic stenosis. Gen Thorac Cardiovasc Surg. 2013;61(11): 626-631. 162. de Kerchove L, Boodhwani M, Glineur D, et al. Valve sparing-root replacement with the reimplantation technique to increase the durability of bicuspid aortic valve repair. J Thorac Cardio-vasc Surg. 2011 Dec;142(6):1430-8. 163. El Khoury G, de Kerchove L. Principles of aortic valve repair. J Thorac Cardiovasc Surg. 2013;145(3 suppl):S26-S29. 164. Mokhles MM, Rizopoulos D, Andrinopoulou ER, et al. Autograft and pulmonary allograft performance in the sec-ond post-operative decade after the Ross procedure: insights from the Rotterdam Prospective Cohort Study. Eur Heart J. 2012;33(17):2213-2224. 165. Chambers JC, Somerville J, Stone S, Ross DN. Pulmonary autograft procedure for aortic valve disease: long-term results |
Surgery_Schwartz_5692 | Surgery_Schwartz | the Rotterdam Prospective Cohort Study. Eur Heart J. 2012;33(17):2213-2224. 165. Chambers JC, Somerville J, Stone S, Ross DN. Pulmonary autograft procedure for aortic valve disease: long-term results of the pioneer series. Circulation. 1997;96(7):2206-2214. 166. Leon MB, Smith CR, Mack M, et al. Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery. N Engl J Med. 2010;363(17):1597-1607. 167. Leon MB, Smith CR, Mack MJ, et al. Transcatheter or surgical aortic-valve replacement in intermediate-risk patients. N Engl J Med. 2016;374(17):1609-1620. 168. Reardon MJ, Van Mieghem NM, Popma JJ, et al. Surgical or transcatheter aortic-valve replacement in intermediate-risk patients. N Engl J Med. 2017;376(14):1321-1331. 169. Shinn SH, Schaff HV. Evidence-based surgical management of acquired tricuspid valve disease. Nature reviews. Cardiology. 2013;10(4):190-203. 170. Galloway AC, Grossi EA, Baumann FG. Multiple valve operation for advanced valvular | Surgery_Schwartz. the Rotterdam Prospective Cohort Study. Eur Heart J. 2012;33(17):2213-2224. 165. Chambers JC, Somerville J, Stone S, Ross DN. Pulmonary autograft procedure for aortic valve disease: long-term results of the pioneer series. Circulation. 1997;96(7):2206-2214. 166. Leon MB, Smith CR, Mack M, et al. Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo surgery. N Engl J Med. 2010;363(17):1597-1607. 167. Leon MB, Smith CR, Mack MJ, et al. Transcatheter or surgical aortic-valve replacement in intermediate-risk patients. N Engl J Med. 2016;374(17):1609-1620. 168. Reardon MJ, Van Mieghem NM, Popma JJ, et al. Surgical or transcatheter aortic-valve replacement in intermediate-risk patients. N Engl J Med. 2017;376(14):1321-1331. 169. Shinn SH, Schaff HV. Evidence-based surgical management of acquired tricuspid valve disease. Nature reviews. Cardiology. 2013;10(4):190-203. 170. Galloway AC, Grossi EA, Baumann FG. Multiple valve operation for advanced valvular |
Surgery_Schwartz_5693 | Surgery_Schwartz | surgical management of acquired tricuspid valve disease. Nature reviews. Cardiology. 2013;10(4):190-203. 170. Galloway AC, Grossi EA, Baumann FG. Multiple valve operation for advanced valvular heart disease: results and risk factors in 513 patients. J Am Coll Cardiol. 1992;19(4): 725-732. 171. Hunt SA, Abraham WT, Chin MH, et al. 2009 focused update incorporated into the ACC/AHA 2005 guidelines for the diag-nosis and management of heart failure in adults: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. Circulation. 2009;119(14):e391-e479. 172. Kilic A, Ailawadi G. Left ventricular assist devices in heart failure. Expert Rev Cardiovasc Ther. 2012;10(5):649-656. 173. Harper AM, Rosendale JD. The UNOS OPTN waiting list and donor registry: 1988-1996. Clin Transpl. 1996:69-90. 174. Go AS, Mozaffarian D, Roger VL, et al. Heart | Surgery_Schwartz. surgical management of acquired tricuspid valve disease. Nature reviews. Cardiology. 2013;10(4):190-203. 170. Galloway AC, Grossi EA, Baumann FG. Multiple valve operation for advanced valvular heart disease: results and risk factors in 513 patients. J Am Coll Cardiol. 1992;19(4): 725-732. 171. Hunt SA, Abraham WT, Chin MH, et al. 2009 focused update incorporated into the ACC/AHA 2005 guidelines for the diag-nosis and management of heart failure in adults: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. Circulation. 2009;119(14):e391-e479. 172. Kilic A, Ailawadi G. Left ventricular assist devices in heart failure. Expert Rev Cardiovasc Ther. 2012;10(5):649-656. 173. Harper AM, Rosendale JD. The UNOS OPTN waiting list and donor registry: 1988-1996. Clin Transpl. 1996:69-90. 174. Go AS, Mozaffarian D, Roger VL, et al. Heart |
Surgery_Schwartz_5694 | Surgery_Schwartz | Ther. 2012;10(5):649-656. 173. Harper AM, Rosendale JD. The UNOS OPTN waiting list and donor registry: 1988-1996. Clin Transpl. 1996:69-90. 174. Go AS, Mozaffarian D, Roger VL, et al. Heart disease and stroke statistics—2013 update a report from the American Heart Association. Circulation. 2013;127(1):143-152. 175. Levy D, Kenchaiah S, Larson MG, et al. Long-term trends in the incidence of and survival with heart failure. N Engl J Med. 2002;347(18):1397-1402. 176. Jones RH, Velazquez EJ, Michler RE, et al. Coronary bypass surgery with or without surgical ventricular reconstruction. N Engl J Med. 2009;360(17):1705-1717.Brunicardi_Ch21_p0801-p0852.indd 84801/03/19 5:32 PM 849ACQUIRED HEART DISEASECHAPTER 21 177. McGee EC, Jr, McCarthy PM. Do patients with heart failure benefit from coronary artery bypass grafting? Curr Opin Cardiol. 2012;27(6):629-633. 178. Allman KC, Shaw LJ, Hachamovitch R, Udelson JE. Myo-cardial viability testing and impact of revascularization on prognosis in | Surgery_Schwartz. Ther. 2012;10(5):649-656. 173. Harper AM, Rosendale JD. The UNOS OPTN waiting list and donor registry: 1988-1996. Clin Transpl. 1996:69-90. 174. Go AS, Mozaffarian D, Roger VL, et al. Heart disease and stroke statistics—2013 update a report from the American Heart Association. Circulation. 2013;127(1):143-152. 175. Levy D, Kenchaiah S, Larson MG, et al. Long-term trends in the incidence of and survival with heart failure. N Engl J Med. 2002;347(18):1397-1402. 176. Jones RH, Velazquez EJ, Michler RE, et al. Coronary bypass surgery with or without surgical ventricular reconstruction. N Engl J Med. 2009;360(17):1705-1717.Brunicardi_Ch21_p0801-p0852.indd 84801/03/19 5:32 PM 849ACQUIRED HEART DISEASECHAPTER 21 177. McGee EC, Jr, McCarthy PM. Do patients with heart failure benefit from coronary artery bypass grafting? Curr Opin Cardiol. 2012;27(6):629-633. 178. Allman KC, Shaw LJ, Hachamovitch R, Udelson JE. Myo-cardial viability testing and impact of revascularization on prognosis in |
Surgery_Schwartz_5695 | Surgery_Schwartz | artery bypass grafting? Curr Opin Cardiol. 2012;27(6):629-633. 178. Allman KC, Shaw LJ, Hachamovitch R, Udelson JE. Myo-cardial viability testing and impact of revascularization on prognosis in patients with coronary artery disease and left ventricular dysfunction: a meta-analysis. J Am Coll Cardiol. 2002;39(7):1151-1158. 179. Chareonthaitawee P, Gersh BJ, Araoz PA, Gibbons RJ. Revas-cularization in severe left ventricular dysfunction: the role of viability testing. J Am Coll Cardiol. 2005;46(4):567-574. 180. Gerber BL, Rousseau MF, Ahn SA, et al. Prognostic value of myocardial viability by delayed-enhanced magnetic resonance in patients with coronary artery disease and low ejection frac-tion: impact of revascularization therapy. J Am Coll Cardiol. 2012;59(9):825-835. 181. Langenburg SE, Buchanan SA, Blackbourne LH, et al. Pre-dicting survival after coronary revascularization for ischemic cardiomyopathy. Ann Thorac Surg. 1995;60(5):1193-1196; discussion 1196-1197. 182. Yamaguchi A, | Surgery_Schwartz. artery bypass grafting? Curr Opin Cardiol. 2012;27(6):629-633. 178. Allman KC, Shaw LJ, Hachamovitch R, Udelson JE. Myo-cardial viability testing and impact of revascularization on prognosis in patients with coronary artery disease and left ventricular dysfunction: a meta-analysis. J Am Coll Cardiol. 2002;39(7):1151-1158. 179. Chareonthaitawee P, Gersh BJ, Araoz PA, Gibbons RJ. Revas-cularization in severe left ventricular dysfunction: the role of viability testing. J Am Coll Cardiol. 2005;46(4):567-574. 180. Gerber BL, Rousseau MF, Ahn SA, et al. Prognostic value of myocardial viability by delayed-enhanced magnetic resonance in patients with coronary artery disease and low ejection frac-tion: impact of revascularization therapy. J Am Coll Cardiol. 2012;59(9):825-835. 181. Langenburg SE, Buchanan SA, Blackbourne LH, et al. Pre-dicting survival after coronary revascularization for ischemic cardiomyopathy. Ann Thorac Surg. 1995;60(5):1193-1196; discussion 1196-1197. 182. Yamaguchi A, |
Surgery_Schwartz_5696 | Surgery_Schwartz | Buchanan SA, Blackbourne LH, et al. Pre-dicting survival after coronary revascularization for ischemic cardiomyopathy. Ann Thorac Surg. 1995;60(5):1193-1196; discussion 1196-1197. 182. Yamaguchi A, Ino T, Adachi H, et al. Left ventricular volume predicts postoperative course in patients with ischemic cardio-myopathy. Ann Thorac Surg. 1998;65(2):434-438. 183. Penicka M, Bartunek J, Lang O, et al. Severe left ventricular dyssynchrony is associated with poor prognosis in patients with moderate systolic heart failure undergoing coronary artery bypass grafting. J Am Coll Cardiol. 2007;50(14):1315-1323. 184. Ciarka A, Van de Veire N. Secondary mitral regurgita-tion: pathophysiology, diagnosis, and treatment. Heart. 2011;97(12):1012-1023. 185. Grigioni F, Enriquez-Sarano M, Zehr KJ, Bailey KR, Tajik AJ. Ischemic mitral regurgitation: long-term outcome and prog-nostic implications with quantitative Doppler assessment. Cir-culation. 2001;103(13):1759-1764. 186. Trichon BH, Felker GM, Shaw LK, | Surgery_Schwartz. Buchanan SA, Blackbourne LH, et al. Pre-dicting survival after coronary revascularization for ischemic cardiomyopathy. Ann Thorac Surg. 1995;60(5):1193-1196; discussion 1196-1197. 182. Yamaguchi A, Ino T, Adachi H, et al. Left ventricular volume predicts postoperative course in patients with ischemic cardio-myopathy. Ann Thorac Surg. 1998;65(2):434-438. 183. Penicka M, Bartunek J, Lang O, et al. Severe left ventricular dyssynchrony is associated with poor prognosis in patients with moderate systolic heart failure undergoing coronary artery bypass grafting. J Am Coll Cardiol. 2007;50(14):1315-1323. 184. Ciarka A, Van de Veire N. Secondary mitral regurgita-tion: pathophysiology, diagnosis, and treatment. Heart. 2011;97(12):1012-1023. 185. Grigioni F, Enriquez-Sarano M, Zehr KJ, Bailey KR, Tajik AJ. Ischemic mitral regurgitation: long-term outcome and prog-nostic implications with quantitative Doppler assessment. Cir-culation. 2001;103(13):1759-1764. 186. Trichon BH, Felker GM, Shaw LK, |
Surgery_Schwartz_5697 | Surgery_Schwartz | AJ. Ischemic mitral regurgitation: long-term outcome and prog-nostic implications with quantitative Doppler assessment. Cir-culation. 2001;103(13):1759-1764. 186. Trichon BH, Felker GM, Shaw LK, Cabell CH, O’Connor CM. Relation of frequency and severity of mitral regurgitation to survival among patients with left ventricular systolic dysfunction and heart failure. Am J Cardiol. 2003;91(5): 538-543. 187. Ellis SG, Whitlow PL, Raymond RE, Schneider JP. Impact of mitral regurgitation on long-term survival after percutaneous coronary intervention. Am J Cardiol. 2002;89(3):315-318. 188. Vahanian A, Alfieri O, Andreotti F, et al. Guidelines on the management of valvular heart disease: the task force on the management of valvular heart disease of the European Society of Cardiology. Eur Heart J. 2007;28(2):230-268. 189. DiDonato M, Sabatier M, Dor V, Buckberg G; RESTORE Group. Ventricular arrhythmias after LV remodelling: surgi-cal ventricular restoration or ICD? Heart Fail Rev. 2004;9(4): | Surgery_Schwartz. AJ. Ischemic mitral regurgitation: long-term outcome and prog-nostic implications with quantitative Doppler assessment. Cir-culation. 2001;103(13):1759-1764. 186. Trichon BH, Felker GM, Shaw LK, Cabell CH, O’Connor CM. Relation of frequency and severity of mitral regurgitation to survival among patients with left ventricular systolic dysfunction and heart failure. Am J Cardiol. 2003;91(5): 538-543. 187. Ellis SG, Whitlow PL, Raymond RE, Schneider JP. Impact of mitral regurgitation on long-term survival after percutaneous coronary intervention. Am J Cardiol. 2002;89(3):315-318. 188. Vahanian A, Alfieri O, Andreotti F, et al. Guidelines on the management of valvular heart disease: the task force on the management of valvular heart disease of the European Society of Cardiology. Eur Heart J. 2007;28(2):230-268. 189. DiDonato M, Sabatier M, Dor V, Buckberg G; RESTORE Group. Ventricular arrhythmias after LV remodelling: surgi-cal ventricular restoration or ICD? Heart Fail Rev. 2004;9(4): |
Surgery_Schwartz_5698 | Surgery_Schwartz | 2007;28(2):230-268. 189. DiDonato M, Sabatier M, Dor V, Buckberg G; RESTORE Group. Ventricular arrhythmias after LV remodelling: surgi-cal ventricular restoration or ICD? Heart Fail Rev. 2004;9(4): 299-306; discussion 347-351. 190. Mihaljevic T, Lam BK, Rajeswaran J, et al. Impact of mitral valve annuloplasty combined with revascularization in patients with functional ischemic mitral regurgitation. J Am Coll Cardiol. 2007;49(22):2191-2201. 191. Wu AH, Aaronson KD, Bolling SF, Pagani FD, Welch K, Koelling TM. Impact of mitral valve annuloplasty on mortality risk in patients with mitral regurgitation and left ventricular systolic dysfunction. J Am Coll Cardiol. 2005;45(3):381-387. 192. Michler RE, Smith PK, Parides MK, et al. Two-year outcomes of surgical treatment of moderate ischemic mitral regurgita-tion. N Engl J Med. 2016;374(20):1932-1941. 193. Acker MA, Bolling S, Shemin R, et al. Mitral valve surgery in heart failure: insights from the Acorn Clinical Trial. J Thorac Cardiovasc | Surgery_Schwartz. 2007;28(2):230-268. 189. DiDonato M, Sabatier M, Dor V, Buckberg G; RESTORE Group. Ventricular arrhythmias after LV remodelling: surgi-cal ventricular restoration or ICD? Heart Fail Rev. 2004;9(4): 299-306; discussion 347-351. 190. Mihaljevic T, Lam BK, Rajeswaran J, et al. Impact of mitral valve annuloplasty combined with revascularization in patients with functional ischemic mitral regurgitation. J Am Coll Cardiol. 2007;49(22):2191-2201. 191. Wu AH, Aaronson KD, Bolling SF, Pagani FD, Welch K, Koelling TM. Impact of mitral valve annuloplasty on mortality risk in patients with mitral regurgitation and left ventricular systolic dysfunction. J Am Coll Cardiol. 2005;45(3):381-387. 192. Michler RE, Smith PK, Parides MK, et al. Two-year outcomes of surgical treatment of moderate ischemic mitral regurgita-tion. N Engl J Med. 2016;374(20):1932-1941. 193. Acker MA, Bolling S, Shemin R, et al. Mitral valve surgery in heart failure: insights from the Acorn Clinical Trial. J Thorac Cardiovasc |
Surgery_Schwartz_5699 | Surgery_Schwartz | regurgita-tion. N Engl J Med. 2016;374(20):1932-1941. 193. Acker MA, Bolling S, Shemin R, et al. Mitral valve surgery in heart failure: insights from the Acorn Clinical Trial. J Thorac Cardiovasc Surg. 2006;132(3):568-577, 577 e1-e4. 194. McGee EC, Gillinov AM, Blackstone EH, et al. Recur-rent mitral regurgitation after annuloplasty for functional ischemic mitral regurgitation. J Thorac Cardiovasc Surg. 2004;128(6):916-924. 195. Bax JJ, Braun J, Somer ST, et al. Restrictive annuloplasty and coronary revascularization in ischemic mitral regurgita-tion results in reverse left ventricular remodeling. Circulation. 2004;110(11 suppl 1):II103-II108. 196. Bogaert J, Maes A, Van de Werf F, et al. Functional recovery of subepicardial myocardial tissue in transmural myocardial infarction after successful reperfusion: an important contribu-tion to the improvement of regional and global left ventricular function. Circulation. 1999;99(1):36-43. 197. Dor V, Sabatier M, Montiglio F, Civaia F, | Surgery_Schwartz. regurgita-tion. N Engl J Med. 2016;374(20):1932-1941. 193. Acker MA, Bolling S, Shemin R, et al. Mitral valve surgery in heart failure: insights from the Acorn Clinical Trial. J Thorac Cardiovasc Surg. 2006;132(3):568-577, 577 e1-e4. 194. McGee EC, Gillinov AM, Blackstone EH, et al. Recur-rent mitral regurgitation after annuloplasty for functional ischemic mitral regurgitation. J Thorac Cardiovasc Surg. 2004;128(6):916-924. 195. Bax JJ, Braun J, Somer ST, et al. Restrictive annuloplasty and coronary revascularization in ischemic mitral regurgita-tion results in reverse left ventricular remodeling. Circulation. 2004;110(11 suppl 1):II103-II108. 196. Bogaert J, Maes A, Van de Werf F, et al. Functional recovery of subepicardial myocardial tissue in transmural myocardial infarction after successful reperfusion: an important contribu-tion to the improvement of regional and global left ventricular function. Circulation. 1999;99(1):36-43. 197. Dor V, Sabatier M, Montiglio F, Civaia F, |
Surgery_Schwartz_5700 | Surgery_Schwartz | successful reperfusion: an important contribu-tion to the improvement of regional and global left ventricular function. Circulation. 1999;99(1):36-43. 197. Dor V, Sabatier M, Montiglio F, Civaia F, DiDonato M. Endoventricular patch reconstruction of ischemic failing ven-tricle. A single center with 20 years experience. Advantages of magnetic resonance imaging assessment. Heart Fail Rev. 2004;9(4):269-286. 198. Costa MA, Mazzaferri EL, Jr, Sievert H, Abraham WT. Per-cutaneous ventricular restoration using the parachute device in patients with ischemic heart failure: three-year outcomes of the PARACHUTE first-in-human study. Circ Heart Fail. 2014;7(5):752-758. 199. Fenoglio JJ, Jr, Pham TD, Harken AH, Horowitz LN, Josephson ME, Wit AL. Recurrent sustained ventricular tachy-cardia: structure and ultrastructure of subendocardial regions in which tachycardia originates. Circulation. 1983;68(3): 518-533. 200. Scherlag BJ, el-Sherif N, Hope R, Lazzara R. Characteriza-tion and localization of | Surgery_Schwartz. successful reperfusion: an important contribu-tion to the improvement of regional and global left ventricular function. Circulation. 1999;99(1):36-43. 197. Dor V, Sabatier M, Montiglio F, Civaia F, DiDonato M. Endoventricular patch reconstruction of ischemic failing ven-tricle. A single center with 20 years experience. Advantages of magnetic resonance imaging assessment. Heart Fail Rev. 2004;9(4):269-286. 198. Costa MA, Mazzaferri EL, Jr, Sievert H, Abraham WT. Per-cutaneous ventricular restoration using the parachute device in patients with ischemic heart failure: three-year outcomes of the PARACHUTE first-in-human study. Circ Heart Fail. 2014;7(5):752-758. 199. Fenoglio JJ, Jr, Pham TD, Harken AH, Horowitz LN, Josephson ME, Wit AL. Recurrent sustained ventricular tachy-cardia: structure and ultrastructure of subendocardial regions in which tachycardia originates. Circulation. 1983;68(3): 518-533. 200. Scherlag BJ, el-Sherif N, Hope R, Lazzara R. Characteriza-tion and localization of |
Surgery_Schwartz_5701 | Surgery_Schwartz | and ultrastructure of subendocardial regions in which tachycardia originates. Circulation. 1983;68(3): 518-533. 200. Scherlag BJ, el-Sherif N, Hope R, Lazzara R. Characteriza-tion and localization of ventricular arrhythmias resulting from myocardial ischemia and infarction. Circulation Res. 1974;35(3):372-383. 201. Koilpillai C, Quiñones MA, Greenberg B, et al. Rela-tion of ventricular size and function to heart failure sta-tus and ventricular dysrhythmia in patients with severe left ventricular dysfunction. Am J Cardiol. 1996;77(8): 606-611. 202. Hassapoyannes CA, Stuck LM, Hornung CA, Berbin MC, Flowers NC. Effect of left ventricular aneurysm on risk of sud-den and nonsudden cardiac death. Am J Cardiol. 1991;67(6): 454-459. 203. Sartipy U, Albage A, Lindblom D. Improved health-related quality of life and functional status after surgical ventricular restoration. Ann Thorac Surg. 2007;83(4):1381-1387. 204. Isomura T. Surgical left ventricular reconstruction. Gen Tho-rac Cardiovasc | Surgery_Schwartz. and ultrastructure of subendocardial regions in which tachycardia originates. Circulation. 1983;68(3): 518-533. 200. Scherlag BJ, el-Sherif N, Hope R, Lazzara R. Characteriza-tion and localization of ventricular arrhythmias resulting from myocardial ischemia and infarction. Circulation Res. 1974;35(3):372-383. 201. Koilpillai C, Quiñones MA, Greenberg B, et al. Rela-tion of ventricular size and function to heart failure sta-tus and ventricular dysrhythmia in patients with severe left ventricular dysfunction. Am J Cardiol. 1996;77(8): 606-611. 202. Hassapoyannes CA, Stuck LM, Hornung CA, Berbin MC, Flowers NC. Effect of left ventricular aneurysm on risk of sud-den and nonsudden cardiac death. Am J Cardiol. 1991;67(6): 454-459. 203. Sartipy U, Albage A, Lindblom D. Improved health-related quality of life and functional status after surgical ventricular restoration. Ann Thorac Surg. 2007;83(4):1381-1387. 204. Isomura T. Surgical left ventricular reconstruction. Gen Tho-rac Cardiovasc |
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