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1,900 | Effects of thyroid hormone on the cardiovascular system. | Increased or reduced action of thyroid hormone on certain molecular pathways in the heart and vasculature causes relevant cardiovascular derangements. It is well established that overt hyperthyroidism induces a hyperdynamic cardiovascular state (high cardiac output with low systemic vascular resistance), which is associated with a faster heart rate, enhanced left ventricular (LV) systolic and diastolic function, and increased prevalence of supraventricular tachyarrhythmias - namely, atrial fibrillation - whereas overt hypothyroidism is characterized by the opposite changes. However, whether changes in cardiac performance associated with overt thyroid dysfunction are due mainly to alterations of myocardial contractility or to loading conditions remains unclear. Extensive evidence indicates that the cardiovascular system responds to the minimal but persistent changes in circulating thyroid hormone levels, which are typical of individuals with subclinical thyroid dysfunction. Subclinical hyperthyroidism is associated with increased heart rate, atrial arrhythmias, increased LV mass, impaired ventricular relaxation, reduced exercise performance, and increased risk of cardiovascular mortality. Subclinical hypothyroidism is associated with impaired LV diastolic function and subtle systolic dysfunction and an enhanced risk for atherosclerosis and myocardial infarction. Because all cardiovascular abnormalities are reversed by restoration of euthyroidism ("subclinical hypothyroidism") or blunted by beta-blockade and L-thyroxine (L-T4) dose tailoring ("subclinical hyperthyroidism"), timely treatment is advisable in an attempt to avoid adverse cardiovascular effects. Interestingly, some data indicate that patients with acute and chronic cardiovascular disorders and those undergoing cardiac surgery may have altered peripheral thyroid hormone metabolism that, in turn, may contribute to altered cardiac function. Preliminary clinical investigations suggest that administration of thyroid hormone or its analogue 3,5-diiodothyropropionic acid greatly benefits these patients, highlighting the potential role of thyroid hormone treatment in patients with acute and chronic cardiovascular disease. |
1,901 | Prevalence of the Brugada electrocardiographic pattern at the Medical Center of Louisiana in New Orleans. | Since 1992 the Brugada syndrome has gained recognition as a cause of ventricular fibrillation. The syndrome was originally described in patients with the diagnostic triad of (1) right bundle branch block, (2) an electrocardiogram (ECG) with persistent ST-segment elevation in leads V1, V2, and V3, and (3) sudden cardiac death. Two different types of ST-segment elevation, coved and saddleback, have been described. All patients originally described had structurally normal hearts. The definition of the Brugada electrocardiogram (originally right bundle branch block and ST-segment elevation in V1, V2, and V3 in characteristic coved or saddleback configuration) has been evolving since the initial description, and not all patients with the Brugada electrocardiogram have the Brugada syndrome. We designed a trial to determine the prevalence in our population at the Medical Center of Louisiana in New Orleans of the Brugada ECG as it was originally defined. ECGs performed in 1997 were examined for changes consistent with the Brugada electrocardiogram. Those ECGs with changes secondary to another identifiable cause were excluded. The amount and type of ST-segment elevation in leads V1, V2, and V3 were recorded for the remaining ECGs. From a total of 55,446 electrocardiograms performed on 27,328 patients, we were able to identify only 18 ECGs with the changes originally described by Brugada, and none of them meet current criteria. Our study suggests that in our patient population the ECG now considered typical of the Brugada syndrome is rare. |
1,902 | Risk of ventricular proarrhythmia with selective opening of the myocardial sarcolemmal versus mitochondrial ATP-gated potassium channel. | Myocardial ATP-gated potassium channels (K-ATPs) are critical in the intracellular signaling cascade resulting in ischemic preconditioning (IP). Mitochondrial K-ATP channels seem to be responsible for IP, whereas the functions of K-ATP channels in the sarcolemmal membrane are less well understood. The proarrhythmic potential of specific versus nonspecific opening of K-ATP channels has not been investigated. In this study, Langendorff-perfused rabbit hearts were exposed to either pinacidil (1.25 microM), a nonselective K-ATP channel agonist, or selective mitochondrial or sarcolemmal K-ATP channel agonists or antagonists. The hearts were then subjected to 12 min of hypoxic perfusion and 40 min of reoxygenation. Hearts were monitored for the induction of ventricular fibrillation (VF). No heart subjected to hypoxia-reoxygenation without drug treatment developed VF (0 of 5). Pinacidil pretreatment induced VF (12 of 14; p = 0.004 versus control). Pinacidil's effect was blocked by HMR-1098 (1-[5-[2-(5-chloro-o-anisamide)ethyl]-2-methoxyphenyl]sulfonyl]-3-methylthiourea) (1 microM), a selective sarcolemmal K-ATP channel antagonist (1 of 7; p = 0.007 versus pinacidil; N.S. versus control). Hearts pretreated with 5-hydroxydecanoate (5-HD) (100 microM), a putatively selective mitochondrial K-ATP channel blocker developed VF in one of eight trials (N.S. versus control). 5-HD did not alter the effects of pinacidil (6 of 8; p < 0.05 versus control; N.S. versus pinacidil alone). Selective mitochondrial K-ATP channel activation with [(3R)-trans-4-((4-chlorophenyl)-N-(1H-imidazol-2-ylmethyl)dimethyl-2H-1-benzopyran-6-carbonitril monohydrochloride] (BMS-191095) (6 microM) resulted in zero of five hearts developing VF (N.S. versus control). Our data suggest that selective opening of the sarcolemmal K-ATP channel during hypoxia-reoxygenation induced VF, whereas opening of the mitochondrial channel was not associated with VF. The findings suggest that caution should be exercised when developing compounds aimed at inducing IP, and nonspecific opening of the K-ATP channel should be avoided. |
1,903 | [Ionic currents and ventricular fibrillation dynamics]. | Ventricular fibrillation is the principal immediate cause of sudden cardiac death. Yet, in contrast to other arrhythmias, ventricular fibrillation is considered to be inaccessible to pharmacologic therapy because of its characteristic and apparently never-ending disarray of electrical waves that seem to propagate chaotically throughout the ventricles. Its prevention has historically been focused on the suppression of ventricular ectopy, with the idea of eliminating potential triggers of fibrillation, which from a clinical standpoint has proven to be detrimental. During the last decade, the application of the theory of wave propagation in non-linear excitable media to the study of cardiac fibrillation has led to a dramatic increase in our understanding of its mechanisms. It is now clear that fibrillation is generated and maintained by rotors that gyrate at exceedingly high frequencies. From such rotors emanate spiral waves of excitation that propagate throughout the myocardium in very complex ways. Among the most important factors that determine rotor dynamics are the electrophysiological properties of the ventricular cells, established by their underlying transmembrane ionic currents. Thus, in recent years, studies have focused on the roles played by specific ionic mechanisms and their modulation by antiarrhythmic drugs in ventricular fibrillation dynamics. This review article summarizes the main findings of such studies, which pave the way for a better understanding of fibrillation, and for the development of new pharmacological approaches that aim to prevent rotor formation and maintenance rather than to suppress the triggering ectopic event. |
1,904 | Treatment of advanced colorectal carcinoma with oxaliplatin and capecitabine: a phase II trial. | The current study was designed to evaluate the antitumor activity and toxicity of capecitabine and oxaliplatin in previously untreated patients with advanced colorectal carcinoma. The primary endpoint of the study was to determine the objective response rate, and a secondary endpoint was to measure the time to disease progression.</AbstractText>A 2-stage trial was planned with an accrual goal of 35 patients. The treatment included oxaliplatin given at a dose of 130 mg/m2 on Day 1 of each 3-week cycle. Initially, capecitabine at a dose of 2000 mg/m2/day in 2 divided doses was given on Days 1-14 of each cycle, but this was reduced to a dose of 1500 mg/m2/day because of toxicity. Patients were followed by computed tomography scans every two cycles to evaluate treatment response, and toxicity was monitored.</AbstractText>The first 13 patients on the trial received the higher dose of capecitabine. Although 5 responses (38.5%) were noted, 5 patients were hospitalized with diarrhea and dehydration. This toxicity led to a decrease in the dose of capecitabine to 1500 mg/m2/day and an additional 35 patients were treated. At the lower dose, the partial response rate was 37.1% (95% confidence interval [95% CI], 21.5-55.1%). The estimated median progression-free survival was 6.9 months (95% CI, 4.4-8.2 months). At the lower dose, four patients were hospitalized with diarrhea/dehydration (with one death reported), one with febrile neutropenia, and one with ventricular fibrillation. Overall, Grade (according to version 2.0 of the National Cancer Institute Common Toxicity Criteria) 3-4 diarrhea was reported to develop in 20% of those patients treated at the capecitabine dose of 1500 mg/m2/day compared with 62% of patients treated at the dose of 2000 mg/m2/day.</AbstractText>The combination of oxaliplatin and capecitabine is an active and convenient regimen for the treatment of patients with advanced colorectal carcinoma and should be compared with other front-line regimens as therapy for disease.</AbstractText>Copyright 2003 American Cancer Society.</CopyrightInformation> |
1,905 | Frequency and outcome of in-hospital resuscitation outside the ICU-setting. | Guidelines on performing cardiopulmonary resuscitation and its research have been published. Only few data concerning in-hospital resuscitation are available from Switzerland. The aim of our study was to evaluate the frequency and outcome of cardiopulmonary arrests in our hospital and to look for ways of improving our resuscitation management.</AbstractText>The prospective study was performed in the Kantonsspital Liestal, a primary care hospital with 360 beds, where about 24'300 in-patients were treated during the 2 year observation period. Only in-hospital resuscitations outside the ICU were included and recorded according to the Utstein criteria.</AbstractText>Within a 24 months period, 61 emergency calls were registered. 25 patients needed cardiopulmonary resuscitation. Initial cardiac rhythms were available for all subjects: 8 patients had asystole, 7 ventricular fibrillation and 10 pulseless electrical activity. 12 of 25 resuscitated patients had a return of spontaneous circulation, 7 lived longer than 24 hours and 6 patients (24%) survived to hospital discharge, 4 of them in a very good or good neurological condition. After 12 months 3 patients (12%) were living independently at home, 2 patients had to be treated in a nursing home and 1 patient had died.</AbstractText>Our data correspond to survival rates in larger studies from abroad but are limited by the number of patients investigated. Improvements are necessary in documentation of resuscitation efforts. Rapid defibrillation must be further stressed. The implementation of a multicentre study is suggested because quality control and further improvement of in-hospital resuscitation are needed in Switzerland.</AbstractText> |
1,906 | 17-year follow-up study of a patient with obstructive hypertrophic cardiomyopathy with a deletion mutation in the cardiac myosin binding protein C gene. | A 60-year-old Japanese man with obstructive hypertrophic cardiomyopathy was found to have a mutation in the cardiac myosin binding protein C gene: a single base deletion of a thymidine residue at nucleotide 11645 (codon 593) in exon 18. He was diagnosed at the age of 43 and has been followed for 17 years. During this follow-up period, echocardiograms and mechanocardiograms revealed progressive hypertrophy until the age of 54, then gradual dilation of the left ventricle associated with a decrease in the obstruction. Paroxysmal atrial fibrillation occurred at the age of 52 and progressed to chronic atrial fibrillation at the age of 53. He had congestive heart failure at the age of 58. |
1,907 | Evaluation of the usefulness of recording the ECG in the 3rd intercostal space and prevalence of Brugada-type ECG in accordance with recently established electrocardiographic criteria. | It has been reported that recording electrocardiograms (ECGs) in the 3rd intercostal space (ICS) is one method that can be used for detecting Brugada syndrome; however, the prevalence of Brugada-type ECGs recorded in the 3rd ICS and the usefulness of recording the ECG in the 3rd ICS in accordance with recently established electrocardiographic criteria is unknown.</AbstractText>ECGs were recorded in both the 4th and 3rd ICS in 17 Brugada-type ECG patients (group A) and in 206 consecutive male subjects (group B). Brugada-type ECGs were divided into 3 types. In group A, the prevalence of type 1 ECG, which is a coved-type ECG with ST-segment elevation of >/=2 mm, increased from 23.5% to 64.7% when ECG was recorded in the 3rd ICS. The conversion to type 1 ECG was found to be related to induction of ventricular arrhythmia. In group B, the prevalence of Brugada-type ECG increased from 1.5% to 5.8% when the ECG was recorded in the 3rd ICS.</AbstractText>Recording the ECG in the 3rd ICS is useful for identifying high-risk patients with Brugada-type ECG and for detecting concealed Brugada-type ECG.</AbstractText> |
1,908 | Arrhythmias late after repair of tetralogy of fallot: a Japanese Multicenter Study. | Arrhythmia is a major late complication in adults with repaired tetralogy of Fallot, although a large-scale study has not been carried out in Japan.</AbstractText>A nationwide multicenter study with 512 operative survivors was performed. Actuarial survival rate at 30 years (maximum follow-up) was 98.4%. Fifty-four patients (10.5%) had clinically important arrhythmias, including 23 patients with bradycardia caused by sick sinus syndrome or atrioventricular block (AVB). A patient with complete AVB (CAVB) without pacemaker implantation (PMI) died later. Two patients had sustained ventricular tachycardia (VT) and syncope was reported in 18 patients with ventricular arrhythmias (VA). Atrial tachyarrhythmias were observed in 13 patients. Older age at operation was a risk factor for atrial fibrillation/flutter, longer postoperative survival duration for VA, and QRS duration >120 ms for VT. Perimembranous ventricular septal defect was related to CAVB. Right ventricular outflow patch was not a risk factor. Importantly, 60% of the subjects had QRS duration <120 ms.</AbstractText>The prevalence of serious arrhythmias is low in Japanese TOF patients as compared with the results from Western countries. CAVB without PMI and VT are the major risk factors for late morbidity and mortality. The excellent result could be related to the narrow QRS after surgery.</AbstractText> |
1,909 | Sildenafil (Viagra) reduces arrhythmia severity during ischaemia 24 h after oral administration in dogs. | Sildenafil (Viagra) prolongs repolarisation in cardiac muscle, an effect that could lead to ventricular fibrillation (VF). Sildenafil (2 mg kg(-1)) was given by mouth to 12 mongrel dogs and, 24 h later, these dogs were anaesthetised, thoracotomised and subjected to a 25 min occlusion of the anterior descending coronary artery. Haemodynamic parameters were similar in this and the control group, but there were fewer and less serious ventricular arrhythmias during occlusion in the sildenafil group (VF 17 vs 60%; ventricular premature beats 140+/-52 vs 437+/-127% and episodes of ventricular tachycardia 4.0+/-3.2 vs 19.3+/-7.7%, all P<0.05). However, reperfusion VF and indices of ischaemia severity (epicardial ST-segment mapping, inhomogeneity) were not modified by the drug. Sildenafil increased the QT interval, especially during ischaemia. Our conclusion is that ischaemia-induced ventricular arrhythmias are reduced by sildenafil, but this protection is less pronounced than that following cardiac pacing or exercise. |
1,910 | Mortality and rate of stroke or embolism in atrial fibrillation during long-term follow-up in the embolism in left atrial thrombi (ELAT) study. | Patients with atrial fibrillation (AF) have a higher mortality and risk of stroke/embolism than patients with sinus rhythm.</AbstractText>The aim of the study was to assess the association of clinical and echocardiographic characteristics with mortality and stroke/embolism and the use of antithrombotic medication in the year 2000 in patients who participated 1990-1995 in the Embolism in Left Atrial Thrombi (ELAT) study.</AbstractText>The study included 409 outpatients with nonrheumatic AF (62 +/- 12 years, 36% women, 39% intermittent AF). Patients with thrombi received anticoagulation, patients without thrombi aspirin until follow-up in 1995; thereafter, anticoagulation according to clinical risk factors was recommended. Primary events were death and secondary events were stroke/embolism. All patients were contacted during the year 2000.</AbstractText>Mean follow-up was 102 months. Mortality was 4%/year; the cause of death was cardiac (n = 84), fatal stroke (n = 26), malignancy (n = 23), sepsis (n = 5), and unknown (n = 24). Multivariate analysis identified age (p < 0.0001), heart failure (p = 0.0013), and reduced left ventricular systolic function (p = 0.0353) as predictors of mortality. Stroke/embolism occurred in 83 patients, with a rate of 3%/year. Multivariate analysis identified age (p = 0.0006) and previous stroke (p = 0.0454) as predictors of stroke/embolism. In the year 2000, 51 (21%) of the 247 surviving patients received no antithrombotic medication, 88 received (36%) oral anticoagulants, 102 (41%) acetylsalicylic acid, and 6 (2%) low-molecular heparin.</AbstractText>Therapy for heart failure and oral anticoagulation in AF should be seriously considered, especially in elderly patients and in those with previous stroke.</AbstractText> |
1,911 | Prognostic significance of the signal averaged electrocardiogram in patients with chronic stable coronary artery disease. Analysis in the time domain and by spectral temporal mapping. | Ventricular late potentials detected by the signal averaged electrocardiogram (SAECG) have been used to predict cardiac death in patients after recent myocardial infarction. The goal of this study was to investigate the prognostic significance of the SAECG in a population of chronic coronary artery disease, with and without previous myocardial infarction.</AbstractText>SAECG was recorded in 698 patients with angiographically proven coronary artery disease and analyzed by time domain analysis (TDA) and by spectral temporal mapping (STM). Cardiac death or ventricular fibrillation (= cardiac event) were used as the primary endpoint for follow-up (25 to 33 months).</AbstractText>A cardiac event occurred in 46 out of 698 patients (6.6%). An abnormal SAECG using TDA was found in 43% of patients with a cardiac event, as compared to 21.7% in those without (p<0.0005). The probability of a cardiac event during follow-up was 4.4% when TDA and STM were both normal, 9.5% and 10.2% when either STM or TDA were abnormal and 28.5% when both were abnormal. A duration of the averaged QRS complex of more than 120 ms and a left ventricular ejection fraction of less than 45% were the only independent predictors of a cardiac event. Logistic regression analysis could predict a cardiac event with a sensitivity of 54% and a specificity of 88%.</AbstractText>In patients with chronic coronary artery disease the duration of the signal averaged QRS complex and left ventricular ejection fraction are independent predictors of cardiac death or ventricular fibrillation.</AbstractText> |
1,912 | Perspectives and new approaches for improving cardiopulmonary resuscitation in adults beyond current guidelines. | Setting clear priorities for the sequence and importance of actions during cardiopulmonary resuscitation (CPR) is of utmost importance for future guidelines. Unless performed under the rare condition of hypoxic arrest, combined compression and ventilation is usually not necessary in one-rescuer resuscitation of adults. After notifying the emergency medical services (EMS), precordial compression at a rate of 100/min is just as effective or may even be preferable in the majority of cases caused by arrhythmic arrest. Considering the pathophysiological and experimental evidence, chest compression has proven to be more important, even in multi-rescuer settings, than resuscitation ventilation with its problems and risks. International recommendations for compression without respiration for rescuers unwilling to perform resuscitation ventilation or for so-called telephone CPR were not included in the guidelines of the European Resuscitation Council (ERC) probably for reasons of brevity and simplification. However, training for basic cardiopulmonary resuscitation of adults with cardiac arrest should also stress the importance of chest compression over ventilation. Moreover, current studies controversially discuss the optimal time point of defibrillation after collapse. These findings point to the enormous demand for research in the field of cardiopulmonary resuscitation. |
1,913 | Dual defibrillator improves quality of life and decreases hospitalizations in patients with drug refractory atrial fibrillation. | to evaluate the impact of dual defibrillator implantation on quality of life and resource utilization in patients with drug refractory atrial fibrillation (AF) without prior ventricular arrhythmias.</AbstractText>Forty patients (28 M, mean age 64 +/- 10) received a dual defibrillator Medtronic 7250. AF was persistent in 60% and paroxysmal in 40%.</AbstractText>The follow-up lasted 15 +/- 4 months (range 12-30). Eighty-five percent of patients had atrial tachyarrhythmia recurrences. Among 1366 treated episodes, overall success rate was 60.1% for antitachy pacing and 88.2% for atrial shock. Within one year after implant, arrhythmia related hospitalization number decreased from 1.5 +/- 2.0 to 0.4 +/- 0.8 ( p < 0.01) and 77% of patients were free from hospitalization. As regard to quality of life, Symptom Checklist/Frequency and Severity Scale improved after implant for all items and SF-36 questionnaire showed significant improvements in physical activities because of health problems and social activities. The patients assigned to early delivery of atrial shock after AF onset, when compared with the patients who did not accept atrial shock, showed a significant reduction of AF burden, a higher reduction of hospitalization number and a greater improvement of quality of life.</AbstractText>Dual defibrillator improved quality of life and decreased resource utilization in patients with drug refractory AF. Early delivering of atrial shock seems to be the most effective option.</AbstractText> |
1,914 | The circadian variation of atrial defibrillation thresholds. | A circadian variation exists for ventricular defibrillation thresholds (DFTs) with a morning peak and a corresponding decrease in therapy success rates from implantable cardioverter defibrillators. Such a variation in atrial DFTs may have implications for the timing of internal cardioversion of atrial arrhythmias. The aim of this study was therefore to determine the circadian variation of atrial DFTs in patents with recurrent atrial fibrillation (AF).</AbstractText>Data were collected as part of the worldwide Jewel AF-only study. Patients had recurrent persistent AF and no history of ventricular arrhythmias. The atrial DFT was assessed at device implantation using a step-up protocol and was recorded for 100 patients (age 63.0 +/- 11.7, 74% male, ejection fraction 49.6 +/- 17.8%, left atrial diameter 46 +/- 9 mm). The mean atrial DFT was 6.3 +/- 4.3 J. For the most commonly tested lead configuration (right atrium to coronary sinus in 56 patients), the atrial DFT for patients implanted in the morning (3.3 +/- 1.5 J) was significantly lower than for both the DFT measured in the afternoon (5.8 +/- 3.4 J, p < 0.01) and the DFT measured in the evening (7.4 +/- 5.9 J, p < 0.01).</AbstractText>There may be a significant variation in measured atrial DFT for the right atrium to coronary sinus configuration, with a nadir in the morning. This is the converse to measurements of ventricular DFTs suggesting different regulatory electrophysiological mechanisms. Further investigation of this possible variation is warranted.</AbstractText> |
1,915 | Trials of pacing to control ventricular rate during atrial fibrillation. | Pharmacologic therapy to achieve rate control in patients with atrial fibrillation is often difficult and inadequate. For this reason, ventricular pacing strategies have been developed as an alternative to drug therapy to alleviate symptoms due to rapid and irregular ventricular rates. Ventricular pacing in combination with AV junctional ablation provides palliative improvement in a wide range of clinical outcomes. Because of the irreversible complete AV block associated with this procedure, strategies to control the ventricular response to atrial fibrillation by ventricular pacing alone have been investigated. These strategies are primarily directed at regularizing the ventricular response by pacing at or near the mean intrinsically conducted ventricular rate. These specialized ventricular pacing algorithms provide striking ventricular regularity at rest but may be less effective during activity. No study has yet demonstrated clinically significant improvements in clinical outcomes with these algorithms. The clinical benefits of rate regularization alone without the strict rate control provided by AV junctional ablation are likely to be very limited. Other device based approaches to control ventricular rate in atrial fibrillation include transvenous vagal stimulation. This strategy is in early stages of development but may be promising. |
1,916 | Facilitating electrical cardioversion of persistant atrial fibrillation by antiarrhythmic drugs: update on clinical trial results. | Results from clinical trials suggest that antiarrhythmic drugs (AD) can facilitate electrical cardioversion (EC) for persistent atrial fibrillation (AF) (duration >48 hours, no spontaneous termination) by suppression of immediate reinitiation of AF following the procedure. Class IC agents may increase the atrial defibrillation threshold (DFT) by significantly reducing the availability of Na+-channel for depolarization. In contrast, class III agents may decrease the atrial DFT by markedly prolonging atrial refractoriness. Among all AD, ibutilide and amoidarone have been shown to be most effective in enhancing the acute outcome of EC. In patients who are over 65 years of age at high risks of stroke (e.g., atherosclerotic cardiovascular disease, diabetes, hypertension, previous thromboembolism, etc.), the rhythm control strategy offers no survival advantage over the rate control strategy and frequently subjects patients to serious adverse effects of AD therapy. It can not be overemphasized that adequate anticoagulation (INR 2.0-3.0) with warfarin is needed regardless of whichever strategy is chosen unless there are contraindications. On the other hand, in patients who are under 65 years of age without structural heart disease or other risk factors of stroke, rhythm control can be the treatment of choice. Specifically, if a patient has failed EC alone or if the patient has characteristics (e.g., duration of AF >6 months, left atrium >50 mm, etc.) that EC could fail, AD may be given before the procedure to facilitate EC. In the subgroup of patients who are symptomatic with hypertrophic cardiomyopathy and severe diastolic dysfunction requiring maintenance of sinus rhythm to have sufficient ventricular function for optimization of cardiac output, an aggressive approach for rhythm control with amiodarone along with adequate anticoagulation with warfarin should be encouraged. |
1,917 | Biphasic versus monophasic shock waveform for conversion of atrial fibrillation. | Cardioversion of atrial fibrillation (AF) using traditional monophasic shock waveform is unsuccessful in up to 20% of cases, and often requires several shocks of up to 360 J. Based on the success with biphasic shock waveform in converting ventricular fibrillation, it was postulated that biphasic shocks would allow cardioversion with lower energy. In a international multicenter, double-blind, randomized trial of 203 patients, damped sine wave monophasic shocks were compared with impedance-compensated truncated exponential biphasic waveform shocks. Patients received up to five shocks: 100 J, 150 J, 200 J, a fourth shock at maximum output for the initial waveform (200 J biphasic, 360 J monophasic) and a final cross-over shock at maximum output of the alternate waveform. For each energy level, the biphasic waveform compared favorably to the monophasic waveform in successful cardioversion (100 J: 60% versus 22%, P < 0.0001; 150 J: 77% versus 44%, p < 0.0001; 200 J: 90% versus 53%, p < 0.0001). Success with 200 J biphasic was equivalent to 360 J monophasic shock (91% versus 85%, p = 0.29). Patients randomized to biphasic waveform required fewer shocks and lower total energy delivered; in addition, this waveform was associated with less dermal injury and no blistering. Biphasic shocks converted AF present for less than 48 hours with 80% efficacy, but conversion of AF present for more than 48 hours and more than 1 year the success rate was only 63 and 20%, respectively. The results of this study is similar to other investigations comparing biphasic and monophasic shock waveforms for conversion of atrial fibrillation. We recommend starting with biphasic energy of 100 J for atrial fibrillation of less than 48 hours duration, but using higher energies (150 J, 200 J or greater) when AF has been present for longer periods. |
1,918 | Quality of life variables in the selection of rate versus rhythm control in patients with atrial fibrillation: observations from the Canadian Trial of Atrial Fibrillation. | Many patients with atrial fibrillation develop symptoms attributable to the cardiac arrhythmia itself. These symptoms may be improved either by restoring sinus rhythm or by controlling the rapid and irregular ventricular response that often accompanies this arrhythmia. One of the principal goals of therapy of atrial fibrillation management is improvement of patient symptoms; it is important to quantify these symptoms by some form of quality of life analysis. The Canadian Trial of Atrial Fibrillation (CTAF) was a multi-centre randomized clinical trial of amiodarone compared with either propafenone or sotalol in patients with recent atrial fibrillation. The quality of life (QOL) substudy of CTAF was a prospective, comprehensive assessment of quality of life of patients enrolled in CTAF. Summary measures of physical and mental health on the generic QOL scale (SF-36) improved significantly with treatment from baseline to 3 months (41.9 +/- 9.6 to 43.7 +/- 9.2, p = 0.001 for the physical component and 47.5 +/- 10.4 to 49.0 +/- 9.8, p = 0.023 for the mental component). On an arrhythmia specific scale (SCL), a significant and larger improvement was noted from baseline to 3 months in both arrhythmia symptom frequency and severity (symptom frequency from 20.4 +/- 9.4 to 16.2 +/- 9.5, symptom severity from 16.7 +/- 8.2 to 12.9 +/- 7.6, both p < 0.001). The quality of life improvements were similar in the amiodarone group compared to the sotalol or propafenone groups, both for the SF-36 and the disease-specific symptom checklist (SCL) measures. In contrast, an atrial fibrillation severity scale (AFSS) did show differences between the assigned drug therapies, which were associated with different rates of arrhythmia recurrence in the parent study. By 3 months global well-being was significantly worse for patients who had recurrent atrial fibrillation compared to those who did not (6.9 +/- 1.8 versus 7.4 +/- 1.8, p = 0.04). Similarly, symptom severity at 3 months was 11.8 +/- 7.4 for patients without recurrence, compared to 14.8 +/- 7.4 for those with recurrence ( p = 0.001). Interestingly, none of the usual clinical variables that might be perceived to be associated with quality of life, e.g., male versus female sex, age, NYHA class, beta blocker use, and ejection fraction, had much impact on subjective quality of life measures. Quality of life improves with treatment atrial fibrillation and at least some of these improvements are related to the restoration and maintenance of sinus rhythm. |
1,919 | Role of beta-blocker therapy in heart failure and atrial fibrillation. | Heart failure is a serious disorder associated with substantial morbidity and mortality. Approximately 15-30% patients with systolic heart failure are in atrial fibrillation and the proportion increases with severity of heart failure. Patients with heart failure and atrial fibrillation have worse outcome than those in sinus rhythm. Beta-blockers, together with angiotensin-converting enzymes inhibitors, are the standard therapy in patients with chronic heart failure. Retrospective studies have suggested that despite the improvement in left ventricular systolic function after treatment with beta-blockers, the exercise capacity and symptoms in those heart failure patients with atrial fibrillation was not improved as much as those in sinus rhythm. Moreover, the use of bisoprolol in the Cardiac Insufficiency Bisoprolol Study II, unlike those in sinus rhythm, failed to produce any survival benefit in patients with poor systolic function and atrial fibrillation. It seems that those patients with heart failure and atrial fibrillation may have different response to beta-blocker therapy. Prospective trials to clarify the impact of beta-blocker therapy and the optimal therapeutic strategy in this high-risk group of patients are warranted. |
1,920 | Beta blockers improve outcome in patients with heart failure and atrial fibrillation: U.S. carvedilol study. | Atrial fibrillation (AF) is present in a significant number of patients with heart failure (HF) caused by left ventricular systolic dysfunction and is associated with increased morbidity and mortality. The deleterious interaction of AF and HF is mediated through a number of mechanisms including hemodynamic alterations and activation of the sympathetic nervous system. Beta-blockers have been shown to improve symptoms and survival in patients with HF. In addition, beta-blockers have been used in patients with AF, primarily for rate control. A retrospective analysis of the U.S. Carvedilol Heart Failure Trial demonstrated that carvedilol improves outcomes in the high-risk subgroup of patients with HF and concomitant AF. |
1,921 | Role of dofetilide in patients with atrial fibrillation. Insights from the Symptomatic Atrial Fibrillation Investigative Research on Dofetilide (SAFIRE-D) study. | Dofetilide is a class III antiarrhythmic drug (potassium channel blocker) that has been approved by the regulatory agencies in the United States and throughout the world to convert atrial fibrillation and maintain sinus rhythm. Therapy is initiated in-hospital during heart rhythm monitoring. Doses are selected according to the QT interval and estimated creatinine clearance. In patients with heart failure and prior myocardial infarction, dofetilide was very effective in converting atrial fibrillation and maintaining normal sinus rhythm. In patients with persistent atrial fibrillation, dofetilide compared to placebo was significantly better in converting atrial fibrillation and maintaining sinus rhythm. This was especially true for the highest dose of 500 microg twice-a-day. Caution must be used when initiating dofetilide therapy to avoid torsade de pointes ventricular tachycardia, especially in patients with heart failure, hypertrophy, bradycardia and female gender. |
1,922 | Does conversion and prevention of atrial fibrillation enhance survival in patients with left ventricular dysfunction? Evidence from the Danish Investigations of Arrhythmia and Mortality ON Dofetilide/(DIAMOND) study. | Atrial fibrillation is a common arrhythmia in patients with left ventricular dysfunction associated with increased morbidity and mortality. The present study investigated the potential of dofetilide to restore and maintain sinus rhythm in patients with left ventricular dysfunction, which might reduce mortality and hospitalizations.</AbstractText>In the Danish Investigations of Arrhythmia and Mortality ON Dofetilide (DIAMOND) studies, 506 patients were in atrial fibrillation (AF) or atrial flutter (AFl) at baseline. Over the course of study, cardioversion occurred in 148 (59%) dofetilide- and 86 (34%) placebo-treated patients. In these patients, the probability of maintaining sinus rhythm for 1 year was 79% with dofetilide versus 42% with placebo ( P < 0.001). Dofetilide had no effect on all-cause mortality, but restoration and maintenance of sinusrhythm (independent of study treatment) was associated with a significant reduction in mortality (risk ratio [RR], 0.44; 95% CI, 0.30 to 0.64; P < 0.0001). In addition, dofetilide therapy was associated with a significantly lower risk ratio versus placebo for either all-cause (RR, 0.70; 95% CI, 0.56 to 0.89; P < or = 0.005) or congestive heart failure (RR, 0.69; 95% CI, 0.51 to 0.93; P < or = 0.02) rehospitalization.</AbstractText>Dofetilide is safe and increases the probability of obtaining and maintaining sinus rhythm in patients with structural heart disease. The present study suggests that restoration of sinus rhythm--on placebo or dofetilide--is associated with improved survival.</AbstractText> |
1,923 | Rationale for the Atrial Fibrillation and Congestive Heart Failure (AF-CHF) trial. | Congestive heart failure and atrial fibrillation (AF) are two important and growing problems in medicine and cardiology. Both conditions often coexist and complicate each other's management. Two therapeutic strategies are available for patients with AF and congestive heart failure: the first aims at restoring and maintaining sinus rhythm, whereas the second focuses exclusively on optimizing ventricular rate. Prior studies of AF and congestive heart failure were not randomized and most were retrospective. Although some studies suggested that AF had no effect on survival, in most recent large congestive heart failure trials, AF was reported to be an independent risk factor for mortality or major morbidity. The primary objective of the Atrial Fibrillation in Congestive Heart Failure (AF-CHF) trial is to compare the two widely used treatment strategies with respect to cardiovascular mortality. AF-CHF is a prospective, multicenter trial that will randomize 1450 CHF patients with left ventricular ejection fraction (LVEF) < or =35% and a documented recent episode of atrial fibrillation to either a rhythm control or a rate control strategy. From recent trial data, we anticipate an 18.75% 2-year cardiovascular mortality in the rate control arm and a 25% event reduction in the rhythm control group. As of December 2003, 960 patients have been randomized. Enrollment is expected to be completed in September 2004 with a minimum follow-up of 2 years. |
1,924 | Significance of atrial fibrillation during acute myocardial infarction, and its current management: insights from the GUSTO-3 trial. | The Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO)-3 atrial fibrillation (AF) substudy assessed the prognostic significance of AF during acute myocardial infarction (AMI), the use of antiarrhythmic therapies, and whether different antiarrhythmic therapies were associated with different outcomes. The timing of the onset of AF relative to other post-AMI complications was recorded in the study. Of the 13,858 patients who were in sinus rhythm at the time of enrolment into GUSTO-3, 906 (6.5%) developed AF and 12,952 did not. Worsening heart failure, hypotension, third-degree heart block, and ventricular fibrillation were independent predictors of new-onset AF. The risks of 30-day and 1-year mortality were increased among patients with AF versus patients without AF before (odds ratio [OR] 2.74, 95% confidence interval [CI] 2.56-3.34; and OR 2.93, 95% CI 2.48-3.46, respectively) and after adjustment for baseline factors and pre-AF complications (OR 1.49, 95% CI 1.17-1.89; and OR 1.64, 95% CI 1.35-2.01, respectively). A total of 1,138 patients had data available on the management of their AF, including 117 with a history of paroxysmal AF and 138 with chronic AF prior to AMI. Of these 1,138 patients, 317 (28%) received antiarrhythmic therapies: class I antiarrhythmic drugs in 12%, sotalol in 5% and amiodarone in 15%. Electrical cardioversion was attempted in 116 patients (10%). Sinus rhythm was restored in 72% of patients given class I drugs, 67% of those given sotalol, 79% of those given amiodarone, and 64% of those who underwent electrical cardioversion. After adjustment for baseline characteristics and pre-AF complications, none of the specific antiarrhythmic therapies was associated with a higher chance of having sinus rhythm at discharge or before deterioration to in-hospital death. However, the use of class I antiarrhythmic drugs or sotalol was associated with lower unadjusted 30-day and 1-year mortality rates. After adjustment for baseline factors and pre-AF complications, the ORs for 30-day and 1-year mortality were 0.42 (95% CI 0.19-0.89) and 0.58 (95% CI 0.33-1.04), respectively, with class I agents, and 0.31 (95% CI 0.07-1.32) and 0.31 (95% CI 0.09-1.02), respectively, with sotalol. In contrast, there was no association between the use of amiodarone or electrical cardioversion and 30-day or 1-year mortality. New AF is often secondary to other post-AMI complications, but is in itself an independent predictor of a worse outcome. Clinical management of AF is variable, but in GUSTO-3 there was a strong trend towards lower mortality associated with the use of class I antiarrhythmic agents or sotalol. Randomized trials are needed to investigate this observation further. |
1,925 | Mechanisms by which SCN5A mutation N1325S causes cardiac arrhythmias and sudden death in vivo. | Mutations in the cardiac sodium channel gene SCN5A are responsible for type-3 long QT disease (LQT3). The genesis of cardiac arrhythmias in LQT3 is multifaceted, and the aim of this study was to further explore mechanisms by which SCN5A mutations lead to arrhythmogenesis in vivo.</AbstractText>We engineered selective cardiac expression of a long QT syndrome (LQTS) mutation (N1325S) in human SCN5A and generated a transgenic mouse model, TGM(NS31).</AbstractText>Conscious and unrestrained TGM(NS31)L12 mice demonstrated a significant prolongation of the QT-interval and a high incidence of spontaneous polymorphic ventricular tachycardia (VT) and fibrillation (VF), often resulting in sudden cardiac death (n=52:156). Arrhythmias were suppressed by mexiletine, a sodium channel blocker for the late persistent sodium current. Action potentials (APs) from TGM(NS31)L12 ventricular myocytes exhibited early afterdepolarizations and longer 90% AP durations (APD90=69 +/- 5.9 ms) than control (APD90=46.7 +/- 4.8 ms). Voltage-clamp experiments in transgenic myocytes revealed a peak inward sodium current (INa) followed by a slow recovery from inactivation. After mexiletine application, transgenic ventricular APDs were shortened, and recovery from inactivation of INa was enhanced. These suggest that the N1325S transgene is responsible for the abnormal signals present in transgenic cells as well as the genesis of lethal arrhythmias in mice. Interestingly, transgenic but not wild-type myocytes displayed longer APDs with a shortening of CLs.</AbstractText>Our findings show that a new model for LQTS has been established, and we report on an arrhythmogenic mechanism that, unlike other SCN5A mutations, results in poor restitution of APD with increasing rate as a possible substrate for arrhythmogenesis.</AbstractText> |
1,926 | Electrophysiological changes in heart failure and their relationship to arrhythmogenesis. | This review focuses mainly on studies in non-ischemic animal models of heart failure. These animals develop ventricular arrhythmias, mostly non-sustained ventricular tachycardia, and often die suddenly. Clinical studies suggest that sudden death is due to ventricular tachycardia or fibrillation in about 50% of cases, the other half to bradyarrhythmias or electromechanical dissociation. Electrophysiologic changes in heart failure are not confined to the ventricles: the intrinsic sinus rate is reduced due to a downregulation of If and sensitivity to acetylcholine is enhanced by upregulation of the muscarinic receptor. Reduction of heart rate may be a protective mechanism since at rapid rates contractility is reduced and the likelihood for triggered activity due to delayed afterdepolarizations is enhanced. The beneficial effect of beta-adrenergic blockade in patients may be partly due to the reduction in sinus rate. Although the results of different studies often vary, the most consistent electrophysiological changes in the ventricles are prolongation of the action potential, especially at slow rates, a reduction in the transient outward current Ito, the rapid and slow components of the delayed rectifier Ikr and Iks, and the inward rectifier Ik1. Abnormalities in intracellular calcium handling play a major role in the genesis of delayed afterdepolarizations. Triggered activity based on delayed afterdepolarizations has been demonstrated in failing myocardium and are caused by spontaneous release of calcium from the sarcoplasmic reticulum (SR), especially in the presence of noradrenaline. Three factors combine to the enhanced propensity for the occurrence of delayed afterdepolarizations: (1) increased activity of the Na/Ca exchanger, (2) a reduced inward rectifier, (3) residual beta-adrenergic responsiveness required to raise the reduced sarcoplasmic calcium content to a level where spontaneous calcium release occurs. Early afterdepolarizations have also been demonstrated, especially in human myocytes from failing hearts in the presence of noradrenaline. Mapping experiments have shown that the ventricular arrhythmias are mainly due to non-reentrant mechanisms, most likely triggered activity based on delayed afterdepolarizations. |
1,927 | Acute comparative effect of right and left ventricular pacing in patients with permanent atrial fibrillation. | We tested the hypothesis that left ventricular (LV) pacing is superior to right ventricular (RV) apical pacing in patients undergoing atrioventricular (AV) junction ablation and pacing for permanent atrial fibrillation. The potential benefit of LV over RV pacing needs to be evaluated without the confounding effect of other variables that can influence cardiac performance. An acute intrapatient comparison of the QRS width and echocardiographic parameters between RV versus LV pacing was performed within 24 h after ablation in 44 patients. Both modes of pacing were also compared with pre-implantation values. Compared with RV pacing, LV pacing caused a 5.7% increase in the ejection fraction (EF) and a 16.7% decrease in the mitral regurgitation (MR) score; the QRS width was 4.8% shorter with LV pacing. Similar results were observed in patients with or without systolic dysfunction and/or native left bundle branch block, except for a greater improvement in MR in the latter group. Compared with pre-ablation measures, the EF increased by 11.2% and 17.6% with RV and LV pacing, respectively; the MR score decreased by 0% and 16.7%; and the diastolic filling time increased by 12.7% and 15.6%.Rhythm regularization achieved with AV junction ablation improved EF with both RV and LV pacing; LV pacing provided an additional modest but favorable hemodynamic effect, as reflected by a further increase of EF and reduction of MR. The effect seems to be equal in patients with both depressed and preserved systolic functions and in those with and without native left bundle branch block. |
1,928 | Is early hospital discharge feasible following normothermic coronary artery surgery on the fibrillating heart? | Protocols for the earlier discharge of cardiac surgical patients are gaining popularity. We present our experience with an early hospital discharge policy following coronary artery bypass grafting (CABG) on the fibrillating heart.</AbstractText>Three-hundred and ninety-two consecutive patients who underwent elective CABG by a single surgeon were retrospectively reviewed. CABG was performed initially (1998-1999) in 191 patients with cardiopulmonary bypass (CPB) normothermia, intermittent aortic cross-clamping (AXC) and ventricular fibrillation and later (2001-2003) in 201 patients without CPB. Emphasis was given on short AXC and CPB times, early extubation, early mobilization and atrial fibrillation prophylaxis. Discharge criteria were as follows: walking on stairs unassisted, sinus rhythm for 24 hours, normal bowel function, apyrexia, family support at home. A 6-week follow-up clinic visit was arranged. Hospital re-admissions were carefully monitored.</AbstractText>The mean (+/-SD) age of the patients was 62+/-9.6 years and the mean Parsonnet score was 6.7. The mean hospital stay was 6.1+/-2.5 days. Sixty-three (16%) and 171 (44%) patients were discharged by postoperative day 4 and 5, respectively. The following factors were independently associated with longer hospital stay: number of grafts performed (>3), requirement for postoperative inotropic support and social circumstances inadequate for early discharge. Twenty-three patients (5.8%) were re-admitted in the 6-week postoperative period. Shorter hospital stay was not associated with increased risk of re-admission.</AbstractText>Early discharge after CABG with ventricular fibrillation is achievable, comparable to "fast-track techniques" without the use of CPB and is not associated with higher re-admission rates. We recommend the routine use of this protocol in all patients undergoing primary elective CABG.</AbstractText> |
1,929 | Inducibility of life-threatening ventricular arrhythmias is related to maximum left ventricular thickness and clinical markers of sudden cardiac death in patients with hypertrophic cardiomyopathy attributable to the Asp175Asn mutation in the alpha-tropomyosin gene. | We investigated inducibility of life-threatening arrhythmias with programmed ventricular stimulation (PVS) in relation to clinical markers of sudden cardiac death (SCD) in subjects with hypertrophic cardiomyopathy (HCM) attributable to the Asp175Asn mutation in the alpha-tropomyosin gene (TPM1-Asp175Asn). PVS was performed with up to three extrastimuli and distribution of markers of SCD was evaluated in 21 adult subjects with the TPM1-Asp175Asn. Sustained polymorphic ventricular tachycardia (VT) or ventricular fibrillation (VF) was induced in seven of 21 subjects (33%). Inducible subjects had more severe left ventricular hypertrophy (LVH) and an increased number of markers of SCD (family history of SCD, syncope or presyncope, fall in systolic blood pressure (BP) during exercise, documented non-sustained VT (NSVT), and marked LVH) compared to non-inducible subjects (IVS 2.4 +/- 0.3 cm vs. 1.6 +/- 0.5 cm, P < 0.001; and two to three vs. one to two markers of SCD, P = 0.007, respectively). In conclusion, in HCM attributable to the Asp175Asn mutation in the alpha-tropomyosin gene, life-threatening arrhythmias were induced in one third of the patients. Inducibility was associated with the maximum left ventricular (LV) thickness and the number of markers of SCD, suggesting that in HCM patients with an identical causative mutation, susceptibility to ventricular arrhythmias is related to the cardiomyopathic phenotype. |
1,930 | Automated external defibrillator use among the general population. | Automated External Defibrillators (AED) are becoming more prominent in public locations within the mainstream of our society. They are marketed as providing the ability for a broader range of people, beyond clinicians and community emergency medical services personal, to successfully defibrillate a person in cardiac arrest. The objectives of this study were to determine whether or not a member of the general population, without previous exposure to an AED, could successfully operate an AED, thus delivering the necessary shock in ventricular fibrillation arrest. In addition, we analyzed the relationship between health care training and the time required to defibrillate a patient using an AED and investigated the overall success of operating an AED with respect to health care training. Utilizing an AED trainer, we conducted a timed trial study of five subject categories (general population; first-year dental students; third-year dental students; dentists, hygienists, and nurses; and anesthesiologists and surgeons) as each operator attempted to defibrillate a mannequin (n=50). Their times, success in defibrillation, and comments were recorded. The general population group experienced an 80 percent failure rate, while the other groups showed an inverse relationship between failure rates and the amount of health care training. Overall, only 58 percent of the subjects successfully performed the defibrillation with the AED. Operator speed in relation to the amount of health care training showed another inverse relationship as times decreased from group one (general population) to group five (anesthesiologists and surgeons). The findings suggest that prior exposure to an AED leads to a greater number of successful defibrillations. It remains unclear at this time as to whether a member of the general population can successfully operate an AED. |
1,931 | Chronic kidney disease and sudden death: strategies for prevention. | The association between chronic kidney disease and cardiovascular death is accounted for, in part, by higher rates of serious arrhythmias. Research shows an independent relationship between worsened renal function and atrial fibrillation, heart block, ventricular tachycardia, ventricular fibrillation, and asystole. These higher rates also associate with underlying structural heart disease including left ventricular hypertrophy, cardiac fibrosis, valvular disease, and left ventricular systolic and diastolic dysfunction. In addition, chronic intermittent ischemia is implicated in the arrhythmias observed during hemodialysis. The superimposed conditions of acidosis and fluxes in both potassium and magnesium also contribute to higher rates of arrhythmias. Baseline estimated glomerular filtration rate is linked to worsened outcomes and increased defibrillation thresholds in patients receiving implantable cardioverter defibrillators. Preventive strategies include meticulous management of electrolytes, baseline treatment for cardiovascular disease, and when indicated, implantable cardioverter defibrillators. Future research into the mechanisms and prevention of sudden cardiac death in patients with chronic kidney disease is warranted. |
1,932 | Atrioventricular nodal fast pathway modification: mechanism for lack of ventricular rate slowing in atrial fibrillation. | Atrioventricular node (AVN) modification is one of the alternatives for ventricular rate control in patients with drug refractory atrial fibrillation (AF). However, the underlying mechanisms, and in particular the role of the dual pathway electrophysiology is not clear. By using a novel index, His electrogram (HE) alternans, we have previously demonstrated in rabbits that both the slow (SP) and the fast pathways (FP) are involved in AVN conduction during AF. This electrophysiological-morphological study was designed to address the role of selective FP ablation on AVN conduction during AF.</AbstractText>In 12 rabbit AVN preparations dual pathway conduction was confirmed by HE alternans during A1A2 pacing protocol, as well as during AF. On average 48% of the conducted beats during AF utilized the FP. Selective FP ablation (n=12) guided by HE alternans resulted in only-SP conduction, with longer AVN conduction time at basic beats, but without change of AVN effective refractory period (ERP). Interestingly, despite elimination of all FP-conducted beats during AF, the selective FP ablation allowed previously concealed SP beats to be conducted, resulting in little net effect on the ventricular rate (average His-His interval 199+/-10 ms before versus 201+/-13 ms after FP ablation, p>0.05). Morphological evidence indicated that FP ablation created lesions within the transitional cells of the superior approaches at the junction between the central fibrous body and the AVN. However, extension of FP ablation lesion into the compact AVN domain resulted in non-selective AVN modification and slowing of ventricular rate during AF.</AbstractText>Despite its longer ERP, FP is responsible for a substantial number of ventricular beats during AF. However, selective FP ablation has a minor effect on ventricular rate. The most likely mechanism for this phenomenon is that FP ablation allows previously concealed SP beats to be conducted. On the other hand, ventricular rate slowdown could be achieved if FP ablations caused collateral damage in the compact node. This study highlights the usefulness of HE alternans as a novel tool to monitor dual pathway conduction during AF and to guide AVN modification.</AbstractText> |
1,933 | Effects of shock strengths on ventricular defibrillation failure. | The mechanism of defibrillation is controversial. Reentry appearing immediately after the shock has been shown to be responsible for defibrillation failure in some studies while other studies have demonstrated that a rapid train of focal activations with the first focus appearing >50 ms after the shock is responsible for failed defibrillation. We tested the hypothesis that both patterns can occur, but at different shock strengths.</AbstractText>Biphasic 6/4 ms shocks of 100-900 V in 100-V increments were given after 10 s of ventricular fibrillation from electrodes in right ventricular apex and right atrium in five isolated pig hearts. Transmembrane activity was optically mapped from the anterior and posterior epicardium using two CCD cameras. The defibrillation threshold (DFT) was 786+/-199 V. The interval from the shock to the earliest post-shock activation was zero for shocks <400 V but increased with increasing shock voltage to 62+/-6 ms at 800 V. The number of post-shock phase singularities, which is related to reentry incidence, decreased continuously from pre-shock values for 100-V shocks to zero as the shock strength increased to 600 V. Focal activations were observed after shocks >600 V with no epicardial reentry present.</AbstractText>Reentry is responsible for defibrillation failure for low-strength shocks. As the shock strength approaches the DFT, a focal epicardial activation pattern becomes responsible for failed defibrillation. Thus, the mechanism of defibrillation failure depends on shock strength, with focal activation as the mechanism for the clinically important near-DFT strength shocks.</AbstractText> |
1,934 | Correlation between dispersion of repolarization (QT dispersion) and ventricular ectopic beat frequency in patients with acute myocardial infarction: a marker for risk of arrhythmogenesis? | QT dispersion (QTd) has evoked a lot of interest in recent years as regards the basic concept of dispersion of repolarization, which it is supposed to reflect on a surface ECG, as being a marker or substrate for arrhythmogenesis. QTd has been shown to be high in patients with ventricular fibrillation and tachycardia. But there is still some debate about its possible role as a marker or substrate for arrhythmogenesis. We studied whether it has any correlation with simple benign ventricular ectopic beats (VEB) after acute myocardial infarction.</AbstractText>We studied four different dispersion parameters (QTd, QTcd, JTcd, AQTd) on 2 different days after AMI and also obtained a 24-h ambulatory ECG on the 2nd day after admission in 64 out of a total of 90 patients. Patients were divided into five groups based on VEB frequency/h on a 24-h ambulatory ECG.</AbstractText>We found a gradual increase in dispersion parameters across the five groups with increasing frequency of VEB. A significant difference was noticed between group 1 (VEB 0.0-0.9/h) and group V (>30/h) on the day of admission: QTd 88.8+/-28.5 versus 123.3+/-23.4, P<0.02; QTcd 100.5+/-27.6 versus 160.3+/-30.7, P<0.01; JTcd 95.5+/-31.0 versus 160.4+/-30.9, P<0.01; AQTd 29.6+/-8.2 versus 48.6+/-13.7, P<0.01. We also noticed a significant positive correlation between VEB frequency and dispersion parameters on both days.</AbstractText>We hypothesize that with increasing dispersion of repolarization the chances or the frequency of ventricular arrhythmias increase. Our findings also point to a definite role of QTd as an arrhythmogenic marker or substrate.</AbstractText> |
1,935 | Treatment of cardiac arrest with automatic external defibrillators: impact on outcome. | Sudden cardiac death is the leading cause of death in the US and most developed nations. Ventricular fibrillation (VF) is the most common initial rhythm in survivors of cardiac arrest. The most important factor in determining survival from VF is the time from collapse to administration of the first defibrillation shock. Automatic external defibrillators (AEDs) have been developed and widely deployed in an attempt to reduce the time to defibrillation. Data on early defibrillation using AEDs has led to a number of public access defibrillator placements in the US and ongoing studies of public access AED use. The safety of lay person AED use is clear. Clearly some concentrated captive populations (e.g. airports, airplanes) may benefit from public access AEDs. Therefore, widespread AED education as a means of increasing public acceptance of lay person AED use must be a priority. As technology evolves costs will decline, however, the current economic reality requires careful consideration of the cost effectiveness of specific AED placement. |
1,936 | Current management of symptomatic atrial fibrillation. | Atrial fibrillation (AF) is the most commonly encountered sustained arrhythmia. Heart rate control, reduction of symptoms, and prevention of embolism are major goals of treatment. Whether the strategy of cardioversion with subsequent maintenance of sinus rhythm has an advantage over heart rate control is under active investigation. Digoxin, non-dihydropyridine calcium channel antagonists, beta-adrenoceptor antagonists (beta-blockers), and amiodarone are the pharmacologic agents most commonly used to achieve rate control. In patients with drug-resistant AF, atrioventricular nodal ablation (or modification) with implantation of a permanent pacemaker is an alternative therapy. Conversion to sinus rhythm can best be achieved by electrical cardioversion. In selected patients, pharmacologic cardioversion can also be attempted. The use of antiarrhythmic drugs for the maintenance of sinus rhythm depends on several factors: (i) the nature of the arrhythmia (first attack, paroxysmal AF with frequent attacks, paroxysmal AF with infrequent attacks, or persistent AF); (ii) the associated symptoms; (iii) and the risk of severe adverse effects associated with the chosen drug. If the administration of an antiarrhythmic drug is appropriate, the choice of the drug must be tailored to the specific characteristics of the given patient. In lone AF, class Ic antiarrhythmic drugs are the best tolerated. These agents should be combined with a calcium channel antagonist or a beta-blocker to prevent rapid ventricular response in the case of conversion of AF to atrial flutter. In this situation, catheter ablation of atrial flutter at the isthmus (hybrid therapy) should be performed. All class I antiarrhythmic agents should be avoided in patients with structural heart disease. Alternative approaches that may be used if sinus rhythm cannot be maintained with drug therapy include: (i) the ablation of arrhythmogenic pulmonary veins; (ii) the implantation of an atrial defibrillator; (iii) the use of specific pacing sites; (iv) or pacing modes. Whether these approaches will reach clinical relevance merits further investigation. Intraoperative catheter ablation or surgical ablation (maze procedure) seems a promising approach for curing AF in patients undergoing cardiac surgery. Among all of the available treatment options, the most consistent proof of efficacy in reducing mortality and morbidity from AF exists for antithrombotic treatment. |
1,937 | Electrotherapeutic management of patients with heart failure. | Heart failure is associated with poor long term survival due to progressive refractory heart dysfunction and sudden cardiac death. Cardiac resynchronization through atrio-biventricular pacing has been introduced to treat patients affected by drug-refractory heart failure with desynchronized ventricular activation, as for complete left bundle branch block. The technique is aimed to overcome interventricular and intraventricular conduction delays leading to ventricular dysynchrony, paradoxical septal wall motion, presystolic mitral regurgitation and reduced diastolic filling times. Short term studies demonstrated that biventricular pacing (and perhaps left ventricular pacing alone) may improve both systolic and diastolic function. Initial studies in patients receiving long term pacing consistently showed significant QRS shortening associated with improvement in symptoms, left ventricular ejection fraction, exercise tolerance, quality of life and New York Heart Association functional class. As far as sudden cardiac death prevention in heart failure is concerned, implantable cardioverter defibrillator (ICD) implantation has been demonstrated to be the most effective therapy in patients with prior cardiac arrest due to ventricular fibrillation or poorly tolerated ventricular tachycardia. Low left ventricular ejection fraction, unsustained ventricular tachycardia and inducibility at electrophysiological study also may identify high risk patients requiring ICD implantation. Further studies are needed to evaluate the effect of cardiac resynchronization on hard end-points, such as survival and long term clinical outcome, and to upgrade risk stratification criteria to be used in selection of candidates for ICD implantation. |
1,938 | Use of beta-blockers in atrial fibrillation. | Atrial fibrillation is the most common arrhythmia in the general population and is frequently associated with organic heart disease. beta-adrenoceptor antagonists (b-blockers) are very effective in preventing atrial fibrillation after coronary artery bypass surgery. It has been shown recently that the beta-blocker metoprolol controlled release/extended release (CR/XL) is also effective in maintaining sinus rhythm after conversion of atrial fibrillation. There is concern that class I antiarrhythmic drugs, such as quinidine, disopyramide, and flecainide in particular, may increase mortality. The risk of proarrhythmia associated with beta-blocker treatment is very low. Therefore b-blockers, such as metoprolol CR/XL, may be the first line of treatment to maintain sinus rhythm, especially after myocardial infarction and in patients with chronic heart failure and in those with arterial hypertension. In patients with persistent atrial fibrillation, AV-nodal conduction-slowing drugs, such as calcium channel antagonists and beta-blockers are used to control the ventricular rate during atrial fibrillation. Several studies clearly show that beta-blockers alone, or in combination with digoxin are very effective in controlling the ventricular rate at rest and during exercise. beta-blockers are effective in maintaining sinus rhythm and controlling the ventricular rate during atrial fibrillation. Given these effects and their favorable effects on mortality, beta-blockers should be considered as first-line agents in the management of patients with atrial fibrillation. |
1,939 | Atrial fibrillation in patients after cardiovascular surgery: incidence, risk factors, preventive and therapeutic strategies. | Atrial fibrillation in patients undergoing cardiovascular surgery is a common problem, occurring in 25-50% of patients. Older patients and those with a prior history of atrial fibrillation are at highest risk, as are those patients in whom preoperative treatment with beta-blockers has been discontinued. The immediate sequelae of this common complication include hemodynamic instability and congestive heart failure with long-term consequences including thromboembolic phenomena and increased cost and length of hospitalization. beta-Blockers, amiodarone, and sotalol have all been shown to decrease the incidence of postoperative atrial fibrillation, but their use may be limited by their adverse effects. Other agents have some promise as prophylactic agents, but need further verification. Biatrial pacing has been shown to be effective, especially when beta-blockers are used simultaneously. The goals for the treatment of atrial fibrillation include maintaining hemodynamic stability, controlling ventricular rate, preventing thromboembolic complications, and restoring sinus rhythm. The most effective strategy for the prevention of atrial fibrillation is to identify the highest-risk patients and target them for prophylaxis with beta-blockers, amiodarone, sotalol or pacing. |
1,940 | [Atrial fibrillation as end point of hypertension. Can antihypertensive therapy prevent it?]. | The most effective and safest option for the prevention of atrial fibrillation and its sequelae--cardiovascular morbidity and mortality, stroke)--is primary prophylaxis. Here, the management of arterial hypertension--the most common cause underlying atrial fibrillation--is of considerable importance. In addition to blood pressure reduction, substances with an action of the autonomic nervous system and the renin-angiotensin-aldosterone system (ACE-inhibitors, AT1 antagonists, beta blockers) have a positive effect on the remodeling, so-called, of the atrial myocytes, and thus on the occurrence of atrial fibrillation with its associated stroke risk. For patients with elevated blood pressure, therefore, the therapeutic strategy should, in the individual case, give consideration to the possibility of exerting a positive effect on atrial fibrillation. |
1,941 | Implications of prolonged pause in patients with chronic atrial fibrillation with mitral valve disease undergoing atrial compartment operation. | Prolonged pause is commonly seen in patients with atrial fibrillation (AF), but the electrophysiologic mechanism and clinical importance of this phenomenon are not clear. This study examined the incidence and clinical importance of prolonged pause in patients with chronic AF and mitral valve disease before and after AF surgery.</AbstractText>Holter recordings were made in 53 mitral valve patients undergoing concomitant valve surgery and atrial compartment operation for chronic AF. There were 38 patients (72%) with successful AF conversion and 15 patients (28%) with failed AF conversion. Cardiac rhythms before and after operation were compared. An R-R interval > or = 2.0 sec was defined as prolonged pause. Serum digoxin and potassium concentration were determined within 24 hours of Holter monitoring.</AbstractText>Before operation, prolonged ventricular pause was common during AF in both groups (76% for the successful AF conversion group and 73% for the failed AF conversion group, p > 0.05). There were 62 +/- 77 episodes of prolonged pause in the successful AF conversion group and 59 +/- 44 in the failed group (p > 0.05). The longest pause lasted 2.47 +/- 0.26 sec in the successful AF conversion group and 2.43 +/- 0.41 sec in the failed AF conversion group (p > 0.05), with most prolonged pauses occurring at night (72% in the successful and 73% in the failed AF conversion group, p > 0.05). After conversion to sinus rhythm, only 1 patient (3%) showed an episode of prolonged pause (p < 0.001). No patient exhibited atrioventricular (AV) block. In patients with successful AF conversion, the maximal heart rate decreased from 150 +/- 28 to 126 +/- 17 beats/min (p < 0.001), the minimal heart rate increased from 43 +/- 6 to 56 +/- 5 beats/min (p < 0.001), and ventricular premature beats (VPB) counts decreased from 599 +/- 935 to 223 +/- 453/24 hours (p < 0.05). In contrast, patients with failed AF conversion showed no significant changes in the incidence of prolonged pause, maximal and minimal heart rates, and VPB counts after operation. None of the patients received pacemaker implantation during a mean follow-up period of 42 +/- 11 months in the successful group and 45 +/- 13 months in the failed AF conversion group.</AbstractText>We conclude that prolonged pause is common in AF with mitral valve disease and does not indicate the presence of sinus or AV nodal dysfunction requiring artificial pacing.</AbstractText> |
1,942 | Quantifying ventricular fibrillation: in silico research and clinical implications. | Cardiovascular disease remains the leading cause of death in otherwise healthy humans. In particular, most cases of sudden cardiac death occur as a result of failure of the mechanical function of the heart which is triggered by a turbulent pattern of electrical excitation of the heart e.g., ventricular fibrillation (VF). Although the exact mechanisms of VF remain unknown, increasing evidence indicates that it is organized by multiple reentrant sources (wavelets). |
1,943 | Combined phase singularity and wavefront analysis for optical maps of ventricular fibrillation. | Much of the research into the mechanisms of ventricular fibrillation (VF) employs high-resolution mapping of electrical activation and recovery patterns. We previously developed a method for analyzing electrically mapped VF patterns that was based on identifying individual VF wavefronts. We now introduce a related method designed to take into account the information on repolarization that is present in optically mapped VF data. The new method first converts raw fluorescence data to an angular variable that tracks the phase of the mapped tissue through the depolarization-repolarization cycle. We define wavefronts in this context as isolines of phase that terminate either at boundaries or at singular points within the phase field. These singularities are the pivots of functional reentry and are important determinants of VF patterns. We parameterize VF by constructing data structures that describe wavefronts and singularities and also maintain wavefront-wavefront, wavefront-singularity, and singularity-singularity relationships. We describe one important application of this parameterization, which is to identify, localize, and characterize the importance of occurrences of propagation block during VF. |
1,944 | Filament behavior in a computational model of ventricular fibrillation in the canine heart.<Pagination><StartPage>28</StartPage><EndPage>34</EndPage><MedlinePgn>28-34</MedlinePgn></Pagination><Abstract><AbstractText>The aim of this paper was to quantify the behavior of filaments in a computational model of re-entrant ventricular fibrillation. We simulated cardiac activation in an anisotropic monodomain with excitation described by the Fenton-Karma model with Beeler-Reuter restitution, and geometry by the Auckland canine ventricle. We initiated re-entry in the left and right ventricular free walls, as well as the septum. The number of filaments increased during the first 1.5 s before reaching a plateau with a mean value of about 36 in each simulation. Most re-entrant filaments were between 10 and 20 mm long. The proportion of filaments touching the epicardial surface was 65%, but most of these were visible for much less than one period of re-entry. This paper shows that useful information about filament dynamics can be gleaned from models of fibrillation in complex geometries, and suggests that the interplay of filament creation and destruction may offer a target for antifibrillatory therapy.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Clayton</LastName><ForeName>Richard H</ForeName><Initials>RH</Initials><AffiliationInfo><Affiliation>Department of Computer Science, University of Sheffield, Regent Court, 211 Portobello Street, Sheffield S1 4DP, UK. [email protected]</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Holden</LastName><ForeName>Arun V</ForeName><Initials>AV</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D023362">Evaluation Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D023361">Validation Study</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>IEEE Trans Biomed Eng</MedlineTA><NlmUniqueID>0012737</NlmUniqueID><ISSNLinking>0018-9294</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000200" MajorTopicYN="Y">Action Potentials</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018780" MajorTopicYN="N">Body Surface Potential Mapping</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003198" MajorTopicYN="N">Computer Simulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004285" MajorTopicYN="N">Dogs</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006329" MajorTopicYN="N">Heart Conduction System</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008955" MajorTopicYN="Y">Models, Cardiovascular</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008959" MajorTopicYN="Y">Models, Neurological</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018485" MajorTopicYN="Y">Muscle Fibers, Skeletal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009200" MajorTopicYN="N">Myocardial Contraction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010496" MajorTopicYN="N">Pericardium</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013611" MajorTopicYN="N">Tachycardia, Atrioventricular Nodal Reentry</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014693" MajorTopicYN="N">Ventricular Fibrillation</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2004</Year><Month>1</Month><Day>16</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2004</Year><Month>3</Month><Day>18</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2004</Year><Month>1</Month><Day>16</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">14723491</ArticleId><ArticleId IdType="doi">10.1109/TBME.2003.820356</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">14723130</PMID><DateCompleted><Year>2004</Year><Month>06</Month><Day>21</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1019-5297</ISSN><JournalIssue CitedMedium="Print"><Issue>7</Issue><PubDate><Year>2003</Year><Season>Oct-Nov</Season></PubDate></JournalIssue><Title>Likars'ka sprava</Title><ISOAbbreviation>Lik Sprava</ISOAbbreviation></Journal>[Clinical and instrumental predictors of survival in patients with chronic heart failure and intact systolic left ventricle function]. | The aim of this paper was to quantify the behavior of filaments in a computational model of re-entrant ventricular fibrillation. We simulated cardiac activation in an anisotropic monodomain with excitation described by the Fenton-Karma model with Beeler-Reuter restitution, and geometry by the Auckland canine ventricle. We initiated re-entry in the left and right ventricular free walls, as well as the septum. The number of filaments increased during the first 1.5 s before reaching a plateau with a mean value of about 36 in each simulation. Most re-entrant filaments were between 10 and 20 mm long. The proportion of filaments touching the epicardial surface was 65%, but most of these were visible for much less than one period of re-entry. This paper shows that useful information about filament dynamics can be gleaned from models of fibrillation in complex geometries, and suggests that the interplay of filament creation and destruction may offer a target for antifibrillatory therapy.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Clayton</LastName><ForeName>Richard H</ForeName><Initials>RH</Initials><AffiliationInfo><Affiliation>Department of Computer Science, University of Sheffield, Regent Court, 211 Portobello Street, Sheffield S1 4DP, UK. [email protected]</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Holden</LastName><ForeName>Arun V</ForeName><Initials>AV</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D023362">Evaluation Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D023361">Validation Study</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>IEEE Trans Biomed Eng</MedlineTA><NlmUniqueID>0012737</NlmUniqueID><ISSNLinking>0018-9294</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000200" MajorTopicYN="Y">Action Potentials</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018780" MajorTopicYN="N">Body Surface Potential Mapping</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003198" MajorTopicYN="N">Computer Simulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004285" MajorTopicYN="N">Dogs</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006329" MajorTopicYN="N">Heart Conduction System</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006352" MajorTopicYN="N">Heart Ventricles</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008955" MajorTopicYN="Y">Models, Cardiovascular</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008959" MajorTopicYN="Y">Models, Neurological</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018485" MajorTopicYN="Y">Muscle Fibers, Skeletal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009200" MajorTopicYN="N">Myocardial Contraction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010496" MajorTopicYN="N">Pericardium</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013611" MajorTopicYN="N">Tachycardia, Atrioventricular Nodal Reentry</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014693" MajorTopicYN="N">Ventricular Fibrillation</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2004</Year><Month>1</Month><Day>16</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2004</Year><Month>3</Month><Day>18</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2004</Year><Month>1</Month><Day>16</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">14723491</ArticleId><ArticleId IdType="doi">10.1109/TBME.2003.820356</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">14723130</PMID><DateCompleted><Year>2004</Year><Month>06</Month><Day>21</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1019-5297</ISSN><JournalIssue CitedMedium="Print"><Issue>7</Issue><PubDate><Year>2003</Year><Season>Oct-Nov</Season></PubDate></JournalIssue><Title>Likars'ka sprava</Title><ISOAbbreviation>Lik Sprava</ISOAbbreviation></Journal><ArticleTitle>[Clinical and instrumental predictors of survival in patients with chronic heart failure and intact systolic left ventricle function].</ArticleTitle><Pagination><StartPage>28</StartPage><EndPage>31</EndPage><MedlinePgn>28-31</MedlinePgn></Pagination><Abstract>165 patients with clinically-manifested chronic heart failure (CHF) and preserved (ejection fraction--EF > 40%) left ventricular (LV) systolic function have been investigated. 135 of them have ischaemic heart disease (IHD) and high blood pressure, 8 patients are without IHD and 22 patients with normal blood pressure. 62 patients have chronic atrial fibrillation. Survival value in patients with CHF and preserved LV systolic function was compared to survival value of those with CHF and impaired ejection fraction (EF < 40%). Patients with preserved LV systolic function have been found to be with better survival value than those with impaired ejection fraction (68 and 33% accordingly). |
1,945 | Effects of a novel cardioselective ATP-sensitive potassium channel antagonist, 1-[[5-[2-(5-chloro-o-anisamido)ethyl]-beta-methoxyethoxyphenyl]sulfonyl]-3-methylthiourea, sodium salt (HMR 1402), on susceptibility to ventricular fibrillation induced by myocardial ischemia: in vitro and in vivo studies. | In the present study, a novel sulfonylthiourea, 1-[[5-[2-(5-chloro-o-anisamido)ethyl]-beta-methoxyethoxyphenyl]sulfonyl]-3-methylthiourea, sodium salt (HMR 1402), was investigated using in vitro and in vivo systems. HMR 1402 inhibited rilmakalim-induced currents in rat and guinea pig myocytes (IC(50) = 60 and 509 nM, respectively). Hypoxia-induced shortening of action potential duration at 90% repolarization was also significantly attenuated by HMR 1402 (68.1 +/- 3.9% of control at 0.3 microM). In contrast, HMR 1402 had a smaller effect on pancreatic beta-cells (rat insuloma cells, RINm5F) hyperpolarized with 100 microM diazoxide (IC(50) = 3.9 microM, compared with glibenclamide IC(50) = 9 nM). In a similar manner, hypoxia induced increases in coronary flow in isolated guinea pig hearts were only slightly reduced by HMR 1402. These data strongly suggest that HMR 1402 has pharmacological selectivity for cardiac myocytes and, therefore, may protect against ischemically induced ventricular fibrillation (VF) without the untoward effects of nonselective compounds. To test this hypothesis, VF was induced in 8 dogs with healed myocardial infarctions by a 2-min coronary occlusion during the last minute of exercise. On a subsequent day, the exercise plus ischemia test was repeated after HMR 1402 (3.0 mg/kg i.v., n = 4, infusion 4 microg/kg/min for 1 h before exercise, n = 4). This drug significantly reduced the incidence of VF protecting seven of eight animals (p = 0.0007) without altering plasma insulin, blood glucose, or the increases in mean coronary blood flow induced by either exercise or 15-s coronary occlusions. Thus, the ATP-sensitive potassium channel antagonist HMR 1402 can prevent ischemically induced VF without altering coronary blood flow or blood glucose. |
1,946 | Intraluminal coronary shunting preserves regional myocardial perfusion and function. | Coronary artery hemostasis during offpump coronary artery bypass (OPCAB) may be achieved with extraluminal coronary occlusion or intraluminal coronary shunting. We sought to determine with a normal porcine beating-heart model whether coronary shunting preserves regional myocardial perfusion and function compared with coronary occlusion.</AbstractText>Six pigs (50-60 kg) underwent sternotomy and instrumentation. Two pairs of ultrasonic crystals were placed in the distribution of t h e left anterior descending (LAD) and left circumflex (LCx) arteries for measurement of fractional change in area (FCA), an index of regional contractility. Regional myocardial blood flow (RMBF) was determined with radiolabeled microspheres. Data were recorded for each animal at baseline and after LAD arteriotomy and vascular control with (1) a 1.5-mm intraluminal shunt, (2) proximal occlusion, and (3) proximal and distal occlusion.</AbstractText>One pig experienced ventricular fibrillation during LAD manipulation and was excluded from the study. Data were summarized for the remaining 5 animals. Coronary shunting maintained RMBF and function (FCA) compared with baseline. Proximal occlusion led to 50% (P =.05) and 47% (P =.04) decreases in RMBF and FCA, respectively, in the LAD region. Proximal and distal occlusion led to 55% (P =.03) and 51% (P = 02) decreases in RMBF and FCA, respectively, in the LAD region. There were no significant changes in RMBF or FCA in the LCx (control) region.</AbstractText>Intraluminal coronary shunting is capable of preserving distal myocardial perfusion and function in a normal porcine heart. Coronary occlusion, in contrast, significantly reduces regional perfusion and function. More frequent use of intracoronary shunting may facilitate OPCAB by minimizing ischemia and hemodynamic compromise.</AbstractText> |
1,947 | Spontaneous ventricular tachycardia and fibrillation in a patient with a positive microvolt T wave alternans test and negative electrophysiological study. | This report describes a patient with a previous myocardial infarction who presented with syncope. The patient had a positive microvolt T wave alternans test, a negative electrophysiological study, and a normal heart rate variability. In hospital, the patient had episodes of ventricular tachycardia and fibrillation. An implantable cardioverter defibrillator was implanted and during the following week it discharged appropriately. |
1,948 | Transcutaneous implantation of an internal cardioverter defibrillator in a small infant with recurrent myocardial ischemia and cardiac arrest simulating sudden infant death syndrome. | This report describes the implantation of a transcutaneous ICD system using a small patch electrode in the subscapular position, and an active-can device in a 5.3-kg infant. The indication for ICD implantation was recurrent cardiac arrest in the presence of normal coronary anatomy. Metabolic evaluation suggested a defect in fatty acid oxidation. |
1,949 | Wolff-Parkinson-White syndrome concomitant with asymptomatic Brugada syndrome. | A 29-year-old man was referred for electrophysiological testing and radiofrequency ablation because of repeated episodes of palpitation over 2 years. A 12-lead electrocardiogram during sinus rhythm showed manifest Wolff-Parkinson-White syndrome and during palpitation showed narrow QRS tachycardia at a rate of 213 beats/min. Following successful radiofrequency ablation of the left anterolateral accessory pathway, sustained atrial fibrillation was induced by atrial extrastimulation. Cibenzoline (2 mg/kg body weight) was injected to terminate atrial fibrillation. ST-T segment elevation in the right precordial leads was observed following cibenzoline administration. Ventricular fibrillation was reproducibly induced by ventricular extrastimuli (S1: 600 ms, S2: 220 ms, S3: 210 ms). |
1,950 | Cardioverter defibrillator implantation in a child with isolated noncompaction of the ventricular myocardium and ventricular fibrillation. | Isolated noncompaction of the ventricular myocardium is a rare unclassified cardiomyopathy and is thought to be due to arrest of myocardial morphogenesis. In fetal life, it is characterized by an excessively prominent trabecular meshwork and deep intratrabecular recesses, and occurs in the left ventricle in the absence of structural heart disease. Echocardiography provides evidence for the diagnosis. The noncompacted ventricular myocardium may be accompanied by depressed ventricular function, systemic embolism, Wolff-Parkinson-White syndrome, left bundle branch block, and ventricular arrhythmia. Although onset of symptoms is frequently delayed until adulthood, symptomatic children have a poor prognosis. In this report, we describe a case of 6-year-old girl who had a history of recurrent syncope. Transthoracic echocardiographic examination showed a localized prominent trabeculation and deep intratrabecular recesses at the inferoapical region of the left ventricle. She had several episodes of ventricular fibrillation which was refractory to pharmacological treatment. An implantable cardioverter defibrillator (ICD) was successfully operated three times during follow-up. |
1,951 | Shock on T versus direct current voltage for induction of ventricular fibrillation: a randomized prospective comparison. | VF is induced during ICD implantation to determine efficacy of therapy. Establishing the best clinical method of induction of VF would potentially be beneficial in reducing the number of induction attempts and reducing the frequency of inadvertent induction of VT. Commonly used methods to induce VF include shock in the T wave vulnerable period (T shock) and high frequency stimulation. This study compared the efficacy of T shock with a new induction method using a 9-V DC pulse. The study was a randomized, prospective, case crossover trial in patients receiving ICDs. VF was induced by T shock and DC in a randomized sequence during an ICD implant. VF was induced at least four times in each patient (two T shocks and two DC inductions) and with each induction; attempts were continued with modifications until successful. A paired evaluation between the T shock/DC induction was performed in 37 patients (28 men, age 64 +/- 12 years) with a left ventricular ejection fraction of 0.40 +/- 0.20. Arrhythmia indications were VT (n = 23), VF (n = 10), and VT/VF (n = 4). Drug therapy included amiodarone (n = 10), metoprolol (n = 6), digoxin (n = 1), and lidocaine (n = 1). The average T shock voltage was 207.0 +/- 16.1 V. The S1 cycle drive length was consistently 400 ms, and the mean S2 coupling interval was 317.8 +/- 19.6 ms. The length of time DC applied averaged 3.8 +/- 1.4 seconds. A total of 148 episodes of VF were included in the analysis. T shock induced VF with a cycle length of 213.5 +/- 35.1 ms, and DC induced VF with a cycle length of 214.6 +/- 34.5 ms (P = 0.86). Although VF was eventually induced for each randomization, the number of attempts required were dependent on the method of induction. The successful DC first attempt VF induction rate was 96%, with three patients requiring two attempts during one of the DC inductions. T shock had a 68% first attempt success rate with 21 patients requiring multiple T shocks to induce VF. All nine female patients had at least one unsuccessful first attempt T shock, which contributed to an overall unsuccessful first attempt induction rate significantly higher in women then men (36.1% vs 12.5%, P = 0.001). A constant DC voltage induction of VF may be more effective than T shock for induction of VF in a clinical setting because it reduces the number of attempts required to induce VF. By either method, VF appears to be more difficult to induce in women. DC induction has the advantage of simple programming of only duration of stimulation. These findings have implications particularly for ICD implantation with conscious sedation. |
1,952 | Evaluation of cardiovascular status in severe leptospirosis. | To note incidence and profile of cardiac involvement in severe leptospirosis in South Gujarat.</AbstractText>A study was carried out on twenty-five serologically proved leptospirosis patients referred to Government Medical College, New Civil Hospital, Surat between June 2002 to September 2002. In all the patients detailed history, physical examination and specific investigations were done to find out the incidence and profile of cardiac involvement in severe leptospirosis.</AbstractText>Out of twenty-five seropositive patients, 14(56%) had cardiovascular manifestations. Electrocardiography abnormalities were seen in 13(52%) patients. The commonest finding was first-degree AV block seen in II(44%) patients followed by ST-segment depression in four (16%) patients, T-wave inversion in leads II, III and avF in two (8%) patients, corrected QT-interval prolongation in three (12%) patients and ventricular premature beats in two (8%) patients. Atrial fibrillation was seen in only one patient. Left ventricular function as assessed by two-dimensional echocardiography was normal in all patients.</AbstractText>In cardiovascular involvement of leptospirosis, although electrocardiographic abnormalities were commonly seen, there was no left ventricular dysfunction.</AbstractText> |
1,953 | Dissociation between ionic remodeling and ability to sustain atrial fibrillation during recovery from experimental congestive heart failure. | Congestive heart failure (CHF) downregulates atrial transient outward (I(to)), slow delayed rectifier (I(Ks)), and L-type Ca(2+) (I(Ca,L)) currents and upregulates Na(+)-Ca(2+) exchange current (I(NCX)) (ionic remodeling) and causes atrial fibrosis (structural remodeling). The relative importance of ionic versus structural remodeling in CHF-related atrial fibrillation (AF) is controversial.</AbstractText>We measured hemodynamic and echocardiographic parameters, mean duration of burst pacing-induced AF (DAF), and atrial-myocyte ionic currents in dogs with CHF induced by 2-week ventricular tachypacing (240 bpm), CHF dogs allowed to recover without pacing for 4 weeks (REC), and unpaced controls. Left ventricular ejection fraction averaged 58.6+/-1.2% (control), 36.2+/-2.3% (CHF, P<0.01), and 57.9+/-1.6% (REC), indicating full hemodynamic recovery. Similarly, left atrial pressures were 2.2+/-0.3 (control), 13.1+/-1.5 (CHF), and 2.4+/-0.4 (REC) mm Hg. CHF reduced I(to) density by approximately 65% (P<0.01), decreased I(Ca,L) density by approximately 50% (P<0.01), and diminished I(Ks) density by approximately 40% (P<0.01) while increasing I(NCX) density by approximately 110% (P<0.05). In REC, all ionic current densities returned to control values. DAF increased in CHF (1132+/-207 versus 14.3+/-8.8 seconds, control) and remained increased with REC (1014+/-252 seconds). Atrial fibrous tissue content also increased in CHF (2.1+/-0.2% for control versus 10.2+/-0.7% for CHF, P<0.01), with no recovery observed in REC (9.4+/-0.8%, P<0.01 versus control, P=NS versus CHF).</AbstractText>With reversal of CHF, there is complete recovery of ionic remodeling, but the prolonged-AF substrate and structural remodeling remain. This suggests that structural, not ionic, remodeling is the primary contributor to AF maintenance in experimental CHF.</AbstractText> |
1,954 | National trends in antiarrhythmic and antithrombotic medication use in atrial fibrillation. | Atrial fibrillation is the most common cardiac arrhythmia associated with significant medical complications. We examined trends in the medical therapy of atrial fibrillation in the United States from 1991 through 2000.</AbstractText>Data from 1355 visits among patients with atrial fibrillation were obtained from the National Ambulatory Medical Care Survey, a nationally representative assessment of office-based practice. We assessed trends in medication use for ventricular rate control (digoxin, beta-blockers, and calcium channel blockers), sinus rhythm maintenance (class IA, IC, and III antiarrhythmics), and thromboembolism prevention (oral anticoagulants and aspirin).</AbstractText>Overall rate control medication use decreased from 72% of visits in 1991-1992 to 56% in 1999-2000 (P =.01 for trend) due to declining digoxin use (64% to 37%, P<.001 for trend). beta-Blocker and calcium channel blocker use remained unchanged. Although there was no change in overall sinus rhythm medication use over time, amiodarone hydrochloride use increased from 0.2% to 6.4% (P<.001 for trend), while quinidine use decreased from 5.0% to 0.0% (P =.01 for trend). Oral anticoagulant use increased (28% to 41%, P =.01 for trend), with the greatest increase in patients aged 80 years and older (14% to 48%, P<.001 for trend). Despite this, only 46.5% of patients at high risk for stroke were taking anticoagulants in 1999-2000.</AbstractText>Digoxin use in atrial fibrillation decreased over time, without concomitant increases in beta-blocker or calcium channel blocker use. Amiodarone replaced quinidine as the dominant sinus rhythm medication. Although oral anticoagulant use increased over time, particularly in the oldest patients, fewer than half of the patients at high risk for stroke were anticoagulated.</AbstractText> |
1,955 | Detecting instabilities of cardiac rhythm. | Diminished beat-to-beat variations in cardiac cycle lengths (CLs) are associated with poor prognosis after acute myocardial infarction and in patients with heart failure. Short-long-short sequences of cardiac cycles, or ultra-short rhythm instabilities, precede initiation of ventricular tachyarrhythmias in some patients. However, little is known about clinical or prognostic significance of abrupt short-term instabilities in CL (AICL) that occur minutes to hours before the event, in part because appropriate analytical methods are lacking. Although various techniques have been used to analyze CL changes, methods for analysis of AICL are limited. We compared performance of time domain, spectral, nonlinear, and pattern recognition techniques with respect to the detection and quantification of AICL. Because of high intra- and inter-subject variability of CL, pattern recognition techniques compared favorably to other studied methods. In continuous ambulatory ECG recordings, AICL occurred hours before spontaneous initiation of sustained atrial and ventricular arrhythmias in different patient populations. AICL were also found prior to the onset of spontaneous ventricular arrhythmias in a mouse model of congestive heart failure. To quantify AICL, we used the number of unstable orthogonal projection coefficients; this number gradually increased hours before the event. Removal of ectopic beats reduced but did not eliminate AICL. To illustrate potential physiological effects and temporal evolution of AICL, we used a simple, continuous, two-dimensional model of cardiac tissue governed by the Morris-Lecar equations. Computer simulations in this model showed that AICL may lead to gradual accumulation of spatial irregularities of the propagation wavefront giving rise to the initiation of reentry. Time-frequency analysis of the most significant eigenvectors of cardiac rhythm in subjects undergoing head-up tilt showed that AICL could indicate instabilities and unsuccessful adaptation of autonomic nervous system activity to physiological stimuli. |
1,956 | Analysis of complex T-wave oscillations for prediction of ventricular fibrillation. | Increased attention has been focused on oscillatory behavior of the T wave as a manifestation of heightened electrical instability and risk for ventricular fibrillation (VF). This interest has stemmed from an increasing number of experimental and clinical studies indicating that the relatively simple ABAB oscillation of T-wave alternans (TWA) can be quantified to assess risk for arrhythmias. However, an important unanswered question is whether TWA represents the initial phase of a stepwise progression to higher-order oscillations that culminate in sudden arrhythmic death. Signals were analyzed from epicardial and endocardial ECGs from anesthetized dogs subjected to LAD coronary artery occlusion during fixed-rate atrial pacing. Our study was the first to demonstrate a stepwise increase in complexity of T-wave oscillations from TWA to T-wave tripling and quadrupling and to more complex forms just prior to onset of VF (Circ Res 2002;91:727-732). Discordant T-wave episodes, when T waves alternated out-of-phase, were found to be associated with increases in T-wave complexity and VF. None of the animals that failed to fibrillate exhibited discordant TWA. In these observations, complexity of T-wave oscillations points to a fundamental mechanistic link underlying the ability of TWA to predict lethal arrhythmias. |
1,957 | Arrhythmia database for algorithm testing: surface leads plus intracardiac leads for validation. | Ann Arbor Electrogram Libraries (AAEL) is a database of over 500 electrocardiographic recordings made during clinical electrophysiology studies over a period of 15 years. These data are used by university researchers and cardiac device research and development laboratories to develop and test arrhythmia detection algorithms. The AAEL library is in use by all major implantable cardioverter defibrillator manufacturers as well as several Automated External Defibrillator developers. In 1996, the USFDA Center for Devices and Radiological Health licensed a portion of Volumes I for proposed device testing. The data consist of 7 channels of signals: surface leads I, III, V1, an intra-atrial high right atrium (bipolar), an intra-atrial high right atrium (unipolar), an intraventricular right ventricular apex (bipolar), and intraventricular right ventricular apex (unipolar) from the distal catheter electrode. Data were recorded under careful engineering quality control continuously (30 min-1.5 hr) on FM magnetic tape at a tape speed of 3.75 in/s after signal amplification at a filter setting of 1-500 Hz. Amplifier gain and filter settings were held constant during the entire recording procedure and a 1 mV calibration signal was entered as a reference at the time of recording. All patient recordings contain a baseline sinus rhythm, and subsequently induced ventricular tachycardia and/or ventricular fibrillation, or less frequently, supraventricular tachycardia, atrial tachycardia, and/or atrial fibrillation. Data are typically made available in digitized format (1,000 Hz); digital or FM recordings are also available. AAEL recordings are the only widespread intracardiac test files in the industry. |
1,958 | Noninvasive risk stratification in postinfarction patients with severe left ventricular dysfunction and methodology of the MADIT II noninvasive electrocardiology substudy. | Sudden cardiac death occurs as a result of a complex interplay of changes in myocardial substrate, imbalance of autonomic regulation of the heart, and myocardial vulnerability. Noninvasive electrocardiology serves as a comprehensive tool for investigating factors representing mechanistic pathways leading to cardiac events. Heart rate variability, nonlinear dynamics of heart rate, and heart rate turbulence provide insight into autonomic control of the heart. Prognostic value of these parameters in postinfarction patients is well established for predicting cardiac death, but there is less evidence for their association with sudden death or arrhythmic events. Electrical manifestation of changes in myocardial substrate include QRS and QTc prolongation, presence of conduction disturbances, presence of late potentials, abnormalities of repolarization morphology, and presence of nonsinus rhythm, namely atrial fibrillation. Electrocardiogram (ECG) measures reflecting myocardial vulnerability to arrhythmias include frequent ventricular premature beats, T wave alternans, or QT variability. Prognostic significance of these parameters is documented in studies focused mostly on them as individual markers of risk. The noninvasive electrocardiology substudy of the Multicenter Automatic Defibrillator Implantation Trial II (MADIT II) allows for simultaneous analysis of several of the above ECG markers of risk and will provide insight about relative contribution of mechanistic pathways leading to cardiac death in postinfarction patients with severe left ventricular dysfunction. Combination of a standard 12-lead ECG and 10-minute high-resolution Holter recordings serves to evaluate the prognostic significance of noninvasive electrocardiology parameters for mortality in patients randomized to conventional treatment and for arrhythmic events in patients randomized to implantable cardioverter defibrillator therapy. |
1,959 | Increased susceptibility to ventricular arrhythmias in a rodent model of experimental depression. | Depression is an important public health problem and is considered to be an independent risk factor for coronary artery disease. The pathophysiological mechanisms that link depression with adverse cardiovascular events (e.g., myocardial ischemia, myocardial infarction, and sudden death) are not well established. It is possible that an increased susceptibility to life-threatening cardiac arrhythmias in depressed patients influences the risk of morbidity and mortality in coronary artery disease. This idea was tested with the use of an experimental model of depression that was developed to induce anhedonia, the reduced responsiveness to pleasurable stimuli observed in human depressed patients. Rats exposed to 4 wk of chronic mild stress (e.g., paired housing, strobe light, and white noise) displayed anhedonia, which was operationally defined by the reduced intake of a palatable sucrose solution relative to an established baseline and to control animals. Furthermore, compared with control rats, the anhedonic rats showed increased basal heart rate and decreased heart rate variability. In response to an intravenously infused chemical challenge, aconitine, anhedonic rats exhibited an increased vulnerability to ventricular arrhythmias, as indicated by a reduced threshold for premature ventricular complexes, salvos, and ventricular tachycardia. These findings suggest that the presence of depressive symptoms is associated with a lower threshold for ventricular arrhythmias, which may contribute to the increased risk for adverse cardiovascular events in patients with depression. |
1,960 | Azimilide decreases recurrent ventricular tachyarrhythmias in patients with implantable cardioverter defibrillators. | This study evaluated the effects of azimilide dihydrochloride (AZ) on anti-tachycardia pacing (ATP) and shock-terminated events in patients with implantable cardioverter defibrillators (ICDs).</AbstractText>Animal studies have shown the effectiveness of AZ for therapy of supraventricular and ventricular tachycardia (VT). Azimilide dihydrochloride was investigated as adjunctive treatment for reducing the frequency of VT and, thus, the need for ICD therapies, including ATP and cardioversion/defibrillation (ICD shocks) in patients with inducible monomorphic VT.</AbstractText>A total of 172 patients were randomized to daily treatment with placebo, 35 mg, 75 mg, or 125 mg of oral AZ in this dose-ranging pilot study of patients with ICDs. The majority of patients had a history of documented remote myocardial infarction and congestive heart failure New York Heart Association class II or III.</AbstractText>The frequency of appropriate shocks and ATP were significantly decreased among AZ-treated patients compared with placebo patients. The incidence of ICD therapies per patient-year among the placebo group was 36, and it was 10, 12, and 9 among 35 mg, 75 mg, and 125 mg AZ patients, respectively (hazard ratio = 0.31, p = 0.0001). Azimilide dihydrochloride was generally well tolerated and did not affect left ventricular ejection fraction or minimal energy requirements for defibrillation or pacing.</AbstractText>Azimilide dihydrochloride may be a safe and effective drug for reducing the frequency of VT and ventricular fibrillation in patients with implanted ICDs.</AbstractText> |
1,961 | [Precipitating factors associated with diastolic heart failure in the elderly]. | Beside basal myocardial dysfunction, acute heart failure involves associated factors, which increase pulmonary capillary pressure or decrease colloid osmotic pressure. The aim of this study was to evaluate the prevalence of these precipitating factors in a population presenting with acute heart failure with preserved left ventricular systolic function.</AbstractText>Forty-eight patients (25 men, 78 +/- 10 years) presenting pulmonary edema with a left ventricular ejection fraction > 45% were included. All had a Doppler echocardiography at the time of intravenous loop diuretics initiation. Patients with severe valve disease or symptomatic coronary disease were excluded.</AbstractText>A history of heart failure, coronary disease, hypertension and diabetes was present in 62%, 42%, 64% and 33% of patients, respectively. On admission, mean left ventricular ejection fraction was 61 +/- 9% and 79% of patients had critical elevation in Doppler filling pressures. Associated factors were renal failure (creatinine clearance < 30 ml/min) in 33% patients, silent myocardial ischemia (troponin I > 0.5 ng/ml) in 31%, atrial fibrillation in 29%, high systolic blood pressure (> or = 160 mmHg) in 27%, major sepsis in 25%, severe hypoalbuminemia (< or = 2.5 g/dl) in 23%, and severe anemia (< 10 g/dl) in 17%, respectively. Four patients had no aggravating factor, whereas 34 and 10 patients had 1-2 and 3-4 associated factors, respectively.</AbstractText>Besides diastolic dysfunction, factors leading to a critical decrease in the oncotic pressure such as pulmonary capillary pressure gradient are found in most of the elderly patients presenting acute diastolic heart failure and must be checked systematically.</AbstractText> |
1,962 | A comparison of vasopressin and epinephrine for out-of-hospital cardiopulmonary resuscitation. | Vasopressin is an alternative to epinephrine for vasopressor therapy during cardiopulmonary resuscitation, but clinical experience with this treatment has been limited.</AbstractText>We randomly assigned adults who had had an out-of-hospital cardiac arrest to receive two injections of either 40 IU of vasopressin or 1 mg of epinephrine, followed by additional treatment with epinephrine if needed. The primary end point was survival to hospital admission, and the secondary end point was survival to hospital discharge.</AbstractText>A total of 1219 patients underwent randomization; 33 were excluded because of missing study-drug codes. Among the remaining 1186 patients, 589 were assigned to receive vasopressin and 597 to receive epinephrine. The two treatment groups had similar clinical profiles. There were no significant differences in the rates of hospital admission between the vasopressin group and the epinephrine group either among patients with ventricular fibrillation (46.2 percent vs. 43.0 percent, P=0.48) or among those with pulseless electrical activity (33.7 percent vs. 30.5 percent, P=0.65). Among patients with asystole, however, vasopressin use was associated with significantly higher rates of hospital admission (29.0 percent, vs. 20.3 percent in the epinephrine group; P=0.02) and hospital discharge (4.7 percent vs. 1.5 percent, P=0.04). Among 732 patients in whom spontaneous circulation was not restored with the two injections of the study drug, additional treatment with epinephrine resulted in significant improvement in the rates of survival to hospital admission and hospital discharge in the vasopressin group, but not in the epinephrine group (hospital admission rate, 25.7 percent vs. 16.4 percent; P=0.002; hospital discharge rate, 6.2 percent vs. 1.7 percent; P=0.002). Cerebral performance was similar in the two groups.</AbstractText>The effects of vasopressin were similar to those of epinephrine in the management of ventricular fibrillation and pulseless electrical activity, but vasopressin was superior to epinephrine in patients with asystole. Vasopressin followed by epinephrine may be more effective than epinephrine alone in the treatment of refractory cardiac arrest.</AbstractText>Copyright 2004 Massachusetts Medical Society</CopyrightInformation> |
1,963 | Susceptibility to ischemia and reperfusion arrhythmias in myocardial hypertrophy: due to flow of injury current? | Left ventricle (LV) hypertrophy is associated with an increased risk of sudden death, which may be due in part to a greater vulnerability to severe ventricular arrhythmias. Our objectives were to determine (i) whether pressure overload-induced LV hypertrophy increases susceptibility to ischemia- and/or reperfusion-induced ventricular fibrillation (VF), and (ii) whether any increased susceptibility is mediated by changes intrinsic to the hypertrophied myocardium. LV pressure overload was induced in rats by abdominal aortic constriction (AC), while controls received sham-operations (SH). Three weeks after the operation, LV weight was 44 +/- 3% greater in AC rats than in SH rats although right ventricle (RV) weights were similar. At this time, isolated hearts (n = 12/group) were subjected to dual coronary perfusion. Alter 15 minutes of aerobic perfusion, either the left or right coronary bed (supplying predominantly LV or RV tissue, respectively) was subjected to 7 minutes of zero-flow ischemia and either 5 minutes of reperfusion (reperfusion study) or 40 minutes of sustained ischemia (ischemia study). AC rats exhibited greater susceptibility than SH rats to both ischemia- and reperfusion-induced ventricular fibrillation, but only when the hypertrophied LV was subjected to ischemia. The increased susceptibility to arrhythmias was not entirely due to a larger ischemic zone, indicating that intrinsic changes within hypertrophied myocarium played a role in arrhythmogenesis. |
1,964 | External cardioversion in patients with persistent atrial fibrillation: a reappraisal of the effects of electrode pad position and transthoracic impedance on cardioversion success. | The optimal methods to perform external cardioversion of atrial fibrillation (AF) have yet to be conclusively determined. This study was performed to examine the relative efficacy of different pad positions on cardioversion success and the relationship between the transthoracic impedance (TTI) and energy requirement for AF cardioversion. Seventy patients with persistent AF undergoing elective cardioversion were randomly assigned to an electrode pad position situated either over the ventricular apex-right infraclavicular area (AL group, n = 31 ) or over the right lower sternal border-left infrascapular area close to the spine (AP group, n = 39). Energy was delivered at an initial 100 joules (J) and then increased to 150 J, 200 J, 300 J, and 360 J if needed. Energy and TTI readings were recorded. Mean TTI was significantly lower in the AP group than in the AL group. However, the cumulative success rates at each energy level were similar in the two groups (23% vs 19.4%, 41% vs 45.2%, 66.7% vs 74.2%, 79.5% vs 77.4%, and 84.6% vs 83.9% at 100 J, 150 J, 200 J, 300 J and 360 J, respectively). In the AP group, converters showed slightly lower TTI compared to nonconverters. In the AL group, converters showed significantly lower TTI compared to nonconverters. However, for all patients as a group, TTI was the only predictor for cardioversion success and showed a significant relationship to the energy required for cardioversion, which can be described by a quadratic equation. Rather than pad position. TTI is the single factor that significantly affects cardioversion and correlates with energy requirement. The relationship between energy requirement and TTI further allows estimation of energy requirements to achieve a successfil cardioversion. |
1,965 | [Coronary artery bypass grafting in patients following percutaneous coronary interventions]. | To investigate and analyze the clinical outcomes of coronary artery bypass grafting (CABG) in patients with history of previous percutaneous coronary interventions (PCI).</AbstractText>We studied 76 patients with a history of PCI who underwent CABG surgery in our institute from August of 1999 to April of 2002, which was 14.0 percent of concurrent CABG. There were 39 cases with PTCA alone and 37 combined with stent implantation, of whom 5 had undergone re-do PCI therapy. Then 46 patients encountered re-stenosis and 6 developed new lesion in native coronary arteries. There were 4 cases with unsuccessful PCI, 11 cases with residual lesion in important vessels and 9 cases with acute complications during PCI. There was a higher incidence of myocardial infarction in group PCI than that in group Non-PCI, and a lower incidence of triple vessel disease (P<0.01).</AbstractText>Group PCI had more emergent surgeries (27.6% vs 13.3%) and fewer OPCAB procedures (91.3% vs 97.2%) than group Non-PCI (P<0.01). The mean number of distal anastomosis in group PCI was smaller than that in group Non-PCI (P<0.01). There were 6 people who died in group PCI, of whom 3 died of heart pump failure,1 of ventricular fibrillation, 1 of neurological complication, and 1 of renal failure. The mortality of group PCI was higher than group Non-PCI (7.9% vs 1.9%, P<0.01). In group PCI, there were 4 with peri-operative myocardial infarction, 1 with late death and 1 with recurrent angina pectoris.</AbstractText>CABG is usually the most effective and necessary way to treat PCI failure, unsatisfactory revascularization and its acute complications. It is most important to promptly and appropriately deal with acute complications of PCI in reducing the mortality.</AbstractText> |
1,966 | Cardiac and metabolic effects in patients who present with a multinodular goitre. | Twenty-six consecutive patients who presented with clinically euthyroid multinodular goitre were studied for an overnight fasting serum lipid profile and 24 h Holter monitoring. Mean serum TSH was 0.6 +/- 0.4 vs 2.4 +/- 1.3 mU/l (p < 0.0001) and mean TT3 2.4 +/- 0.4 vs 2.0 +/- 0.5 nmol/l (p = 0.009) in patients vs controls (n = 15) while mean FT4 was not different from controls. Total serum HDL, LDL cholesterol and triglycerides were lower in patients but creatinine, ferritin and SHBG levels did not differ between patients and controls. The 24-hour ambulatory continuous ECG recordings did not demonstrate significant differences in mean, minimal and maximal heart rate between the study and the control group. Nocturnal heart rate, measured between 23.00 and 06.00 hours, also showed no differences between the two groups. Atrial fibrillation was absent in both the study and the control group. Premature atrial and ventricular complexes occurred equally frequently in both groups. Comparison of patients with a serum TSH below 0.4 mU/l (n = 11) and patients with a TSH above 0.4 mU/l revealed no differences. In conclusion, in consecutive patients who present with multinodular goitre, effects were found on the lipid profile, but not on the heart. It is argued that in this type of patients, cardiac effects depend on the degree of subclinical hyperthyroidism. |
1,967 | Lack of utility of telemetry monitoring for identification of cardiac death and life-threatening ventricular dysrhythmias in low-risk patients with chest pain. | Low-risk patients with chest pain are often admitted to monitored beds; however, the use of telemetry beds in this cohort is not evidence based. We tested the hypothesis that monitoring admitted low-risk patients with chest pain for dysrhythmia is low yield (<1% detection of life-threatening dysrhythmias requiring treatment).</AbstractText>We conducted a prospective cohort study of emergency department (ED) patients with chest pain with a Goldman risk score of less than 8%, a normal initial creatine kinase-MB level, and a negative initial troponin I level admitted to non-ICU monitored beds. Investigators followed the hospital course daily. The main outcome was cardiovascular death and life-threatening ventricular dysrhythmia during telemetry.</AbstractText>Of 3,681 patients with chest pain who presented to the ED, 1,750 patients were admitted to non-ICU monitored beds. Of these, 1,029 patients had a Goldman risk score of less than 8%, a troponin I level of less than 0.3 ng/mL, and a creatine kinase-MB level of less than 5 ng/mL (accounting for 59% of all chest pain telemetry admissions). During hospitalization, there were no patients with sustained ventricular tachycardia/ventricular fibrillation requiring treatment on the telemetry service (0%; 95% confidence interval [CI] 0% to 0.3%). There were 2 deaths: neither was cardiovascular in nature or preventable by monitoring (cardiovascular preventable death rate=0%; 95% CI 0.0% to 0.3%).</AbstractText>The routine use of telemetry monitoring for low-risk patients with chest pain is of limited utility. Admission to nonmonitored beds might help alleviate ED crowding without increasing risk of adverse events caused by dysrhythmia in patients with a Goldman risk of less than 8%, an initial troponin I level of less than 0.3 ng/mL, and a creatine kinase-MB level of less than 5 ng/mL.</AbstractText> |
1,968 | Spontaneous gasping generates cardiac output during cardiac arrest. | To measure stroke volumes coincident with spontaneous gasping during untreated ventricular fibrillation and to evaluate the effects of gasping.</AbstractText>Prospective study in laboratory animals.</AbstractText>University-affiliated research institute.</AbstractText>Male Yorkshire-X domestic pigs.</AbstractText>Pigs were anesthetized (ketamine, 20 mg/kg intramuscularly and sodium pentobarbital, 30 mg/kg intravenously), intubated, and mechanically ventilated. Ventricular fibrillation was electrically induced and untreated for 7 mins. The right femoral artery and vein were cannulated. A 5.5/7.5-MHz biplanar transesophageal echocardiography transducer was advanced into the esophagus.</AbstractText>Stroke volumes were measured as the product of the transaortic blood flow velocity and transesophageal echocardiographic measurements of valve area. In addition, left ventricular volumes were echocardiographically estimated at peak inspiration and at peak expiration of each gasp by transesophageal methods. The stroke volume produced by gasping averaged 23 +/- 6 mL, which represented approximately 60% of a precardiac arrest stroke volume (38 +/- 8 mL, p <.001). Increases in end-tidal carbon dioxide tension coincident with each gasp were consistent with comparable increases in pulmonary blood flow and therefore stroke volumes. Both were associated with increases in aortic pressure from 20 +/- 3 to 33 +/- 8 mm Hg (p <.001) and coronary perfusion pressure from 4 +/- 3 to 13 +/- 7 mm Hg (p <.001).</AbstractText>Our studies confirm that preterminal gasping during ventricular fibrillation increases both ventilation and forward blood flow.</AbstractText> |
1,969 | Canadian Trial of Physiological Pacing: Effects of physiological pacing during long-term follow-up. | The Canadian Trial of Physiological Pacing (CTOPP) reported that the risk of stroke or cardiovascular death was similar between patients receiving ventricular versus physiological pacemakers at the end of the original follow-up period of 3 years. However, the occurrence of atrial fibrillation was significantly less frequent with physiological pacemakers. To assess a potential delayed benefit of physiological pacing, follow-up of patients in this study was extended to 6 years.</AbstractText>A total of 1474 patients requiring a pacemaker for symptomatic bradycardia were randomized to receive ventricular and 1094 to physiological pacemakers. The primary outcome was stroke or cardiovascular death. The study was completed in July 1998, and follow-up was extended to July 2001. At a mean follow-up of 6.4 years, there was no difference between treatment groups in the primary outcome of cardiovascular death or stroke. There was no significant difference in total mortality or stroke between groups. There was a significantly lower rate of development of atrial fibrillation in the physiological group, with a relative risk reduction of 20.1% (CI, 5.4 to 32.5; P=0.009).</AbstractText>The CTOPP extended study does not show a difference in cardiovascular death or stroke, or in total mortality, or in stroke between patients implanted with ventricular or physiological pacemakers over a mean follow-up of >6 years. However, there is a persistent significant reduction in the development of atrial fibrillation with physiological pacing.</AbstractText> |
1,970 | Clinical characteristics of and long-term outcome in Chinese patients with hypertrophic cardiomyopathy. | Data on the phenotypical pattern and natural history of hypertrophic cardiomyopathy in Chinese patients are very limited. The purpose of this study was to describe the clinical characteristics of and long-term outcome in Chinese patients with hypertrophic cardiomyopathy.</AbstractText>We evaluated 118 Chinese patients (62 male) who were diagnosed with hypertrophic cardiomyopathy at Queen Mary Hospital from 1973 to 2002. Diagnosis was based on the demonstration of left ventricular hypertrophy (wall thickness > or =15 mm during diastole), either in a specific region or with diffuse distribution, using echocardiography or magnetic resonance imaging. Clinical predictors of major cardiovascular events related to hypertrophic cardiomyopathy (cardiovascular death, potentially fatal cardiac arrhythmia, and refractory heart failure requiring cardiac transplantation or percutaneous alcohol septal ablation) were evaluated with univariate and multivariate Cox proportional hazards regression models.</AbstractText>The mean (+/- SD) age at presentation was 54 +/- 18 years. During a mean follow-up of 5.8 +/- 4.3 years (range, 1 to 29 years) from presentation, major cardiovascular events related to hypertrophic cardiomyopathy occurred in 19 patients (16%), including 9 deaths. Annual cardiovascular mortality was 1.6%. Fifty-five patients (47%) had one or more cardiovascular complications related to hypertrophic cardiomyopathy, of which atrial fibrillation was the most common (35%, n = 41). The most common type of hypertrophic cardiomyopathy was the apical variant (41%, n = 49). In multivariate analysis, female sex was the only independent predictor of major cardiovascular events related to hypertrophic cardiomyopathy (hazard ratio = 5.86; 95% confidence interval: 1.77 to 7.21; P = 0.007).</AbstractText>Hypertrophic cardiomyopathy in Chinese patients is characterized by late onset of presentation, a high incidence of the apical form of the condition, and adverse clinical outcome in female patients, which suggest a different phenotypical pattern than in white patients.</AbstractText> |
1,971 | Enhancement of myocardial vulnerability by atrial fibrillation. | Certain groups are known to have an increased risk for sudden cardiac death. Epidemiologic studies have suggested that patients with atrial fibrillation may be at higher risk. The authors hypothesize that atrial fibrillation may increase myocardial vulnerability. To test this hypothesis, 37 dogs were studied using programmed electrical stimulation techniques to determine myocardial vulnerability as assessed by the ability to provoke ventricular tachycardia. Prior to atrial fibrillation, programmed electrical stimulation did not induce ventricular tachycardia. Aconitine was then topically applied to the right atrial appendage with care taken not to make contact with the ventricle. Application of aconitine caused atrial fibrillation with an increase in ventricular rate, but did not affect arterial blood pressure. Ventricular tachycardia was induced by programmed electrical stimulation studies in 25 of 26 dogs in atrial fibrillation. The enhanced vulnerability was noted following atrial fibrillation, not after aconitine application to the great veins, which did not cause atrial fibrillation. To further exclude the possibility that aconitine application may cause changes in ventricular threshold, atrial fibrillation was induced by pacing techniques in five dogs. Prior to atrial fibrillation induction, programmed electrical stimulation did not induce ventricular tachycardia. Following atrial fibrillation, ventricular tachycardia could be repeatedly induced. Mean heart rate following atrial fibrillation increased, while pacing animals at this increment in rate did not change the noninducibility of dogs in sinus rhythm. Six patients with a history of atrial fibrillation and ventricular tachycardia were studied to determine if AF lowered myocardial threshold to VT induction. Ventricular tachycardia could only be induced by PES techniques in four of five patients when the patients' rhythm was AF (P < 0.05). This study suggests that atrial fibrillation lowers myocardial threshold for ventricular tachycardia induction and thus enhances myocardial vulnerability. The association of AF with a higher incidence of sudden death may be due to an enhanced electrical instability. |
1,972 | Intracellular Ca dynamics in ventricular fibrillation. | In the heart, membrane voltage (Vm) and intracellular Ca (Cai) are bidirectionally coupled, so that ionic membrane currents regulate Cai cycling and Cai affects ionic currents regulating action potential duration (APD). Although Cai reliably and consistently tracks Vm at normal heart rates, it is possible that at very rapid rates, sarcoplasmic reticulum Cai cycling may exhibit intrinsic dynamics. Non-voltage-gated Cai release might cause local alternations in APD and refractoriness that influence wavebreak during ventricular fibrillation (VF). In this study, we tested this hypothesis by examining the extent to which Cai is associated with Vm during VF. Cai transients were mapped optically in isolated arterially perfused swine right ventricles using the fluorescent dye rhod 2 AM while intracellular membrane potential was simultaneously recorded either locally with a microelectrode (5 preparations) or globally with the voltage-sensitive dye RH-237 (5 preparations). Mutual information (MI) is a quantitative statistical measure of the extent to which knowledge of one variable (Vm) predicts the value of a second variable (Cai). MI was high during pacing and ventricular tachycardia (VT; 1.13 +/- 0.21 and 1.69 +/- 0.18, respectively) but fell dramatically during VF (0.28 +/- 0.06, P < 0.001). Cai at sites 4-6 mm apart also showed decreased MI during VF (0.63 +/- 0.13) compared with pacing (1.59 +/- 0.34, P < 0.001) or VT (2.05 +/- 0.67, P < 0.001). Spatially, Cai waves usually bore no relationship to membrane depolarization waves during nonreentrant fractionated waves typical of VF, whereas they tracked each other closely during pacing and VT. The dominant frequencies of Vm and Cai signals analyzed by fast Fourier transform were similar during VT but differed significantly during VF. Cai is closely associated with Vm closely during pacing and VT but not during VF. These findings suggest that during VF, non-voltage-gated Cai release events occur and may influence wavebreak by altering Vm and APD locally. |
1,973 | Predictors of early ventricular fibrillation before reperfusion therapy for acute ST-elevation myocardial infarction. | Early VF accounts for the majority of deaths during the acute phase of acute MI. In patients treated with fibrinolytics, in-hospital VF occurs most frequently with inferior MI. Contrariwise, out-of-hospital VF seems to be associated with anterior wall MI and preinfarction angina (preconditioning) may protect against VF.</AbstractText>To study clinical characteristics of patients with or without VF before or during reperfusion therapy.</AbstractText>From January 1995 until December 2001, we treated 2826 patients for acute MI and reviewed the clinical records of all patients. Patients who developed early VF were classified according to the first episode of VF: either before or during the angioplasty procedure.</AbstractText>VF developed in 219 (8%) patients. Early VF before reperfusion therapy (n=145, 5%) was independently related to anterior MI (RR 2.3 (95% CI 1.53-3.50), p<0.001), absence of preinfarction angina (RR 2.1 (95% CI 1.38-3.24), p=0.001) and Killip class >1 (RR 3.8 (95% CI 2.34-6.10), p<0.001). The majority of patients with VF during angioplasty (n=74, 3%) had inferior MI (61%).</AbstractText>Early VF before reperfusion therapy is independently associated with anterior MI, absence of preinfarction angina and Killip class >1, whereas the majority of patients with VF during angioplasty have inferior MI.</AbstractText> |
1,974 | Affinity and intrinsic efficacy (IE) of 5'-carbamoyl adenosine analogues for the A1 adenosine receptor--efforts towards the discovery of a chronic ventricular rate control agent for the treatment of atrial fibrillation (AF). | The SAR for the affinity to the A(1) adenosine receptor and relative intrinsic efficacy (IE, [(35)S]-GTPgammaS binding) of a series of 5'-carbamate and 5'-thionocarbamate derivatives of tecadenoson is described. Based on this SAR, selected compounds were evaluated in guinea pig isolated hearts to determine whether they were partial or full agonists with respect to their negative dromotropism, an A(1) AdoR mediated effect. Progress towards obtaining a partial A(1) AdoR agonist to potentially control ventricular rate during atrial fibrillation has been made with the discovery of several potent partial A(1) AdoR agonists (compounds 13, 14, and 17). |
1,975 | Value of the implantable loop recorder for the management of patients with unexplained syncope. | Recurrent syncope often remains unexplained despite extensive multidisciplinary screening. The implantable loop recorder (ILR) may be a tool to define the cardiac arrhythmias underlying syncope.</AbstractText>The study population consisted of 43 consecutive patients with unexplained syncope who underwent extensive cardiological screening and were followed with an ILR. During follow-up, 5 patients had only presyncope, 4 had palpitations, and 15 had a true recurrence of syncope. In all patients with palpitations, 3 with presyncope, and 7 with a recurrence of syncope, the ILR excluded arrhythmias. In the patients with a true recurrence, 1 had symptomatic paroxysmal atrial fibrillation (PAF) treated with drugs, 1 had polymorphic ventricular tachycardia (VT) and received an implantable cardioverter defibrillator (ICD), and 7 had asystole and received a pacemaker. Two patients with presyncope received a pacemaker for Mobitz II block and PAF with brady-tachycardia syndrome. One asymptomatic patient received a pacemaker for significant nocturnal asystole recorded by ILR. Abnormalities in the cardiac screening were observed both in patients with and without syncope, but none of these had a predictive value.</AbstractText>The ILR is a valuable and effective tool to establish an arrhythmic cause for unexplained syncope. The results of head-up tilt testing (HUTT) and electrophysiological study (EPS) are neither sufficiently sensitive nor specific enough in this patient group.</AbstractText> |
1,976 | Performance of a dual-chamber implantable defibrillator algorithm for discrimination of ventricular from supraventricular tachycardia. | Inappropriate therapies remain a major problem in patients with implantable cardioverter defibrillators (ICDs). Decreasing the proportion of inappropriate therapies is a major objective. With the addition of atrial detection and advanced algorithms, dual-chamber ICDs are designed to offer better discrimination of ventricular (VT) and supraventricular (SVT) arrhythmias. The present multicentre, open study aimed to evaluate the performance of a dual-chamber detection algorithm, the Atrial View algorithm, incorporated in a dual-chamber ICD, the Ventak AV (Guidant Inc., St. Paul, Minnesota, USA).</AbstractText>Fifty-one patients (45 males, 62+/-11 years, ejection fraction 42+/-15%) with standard indications received a Ventak AV ICD which analyzes, within the VT zone RR stability, tachycardia onset, atrial rate and AV relationship. Predischarge enhanced-detection algorithms were prospectively programmed: stability 24 ms, onset 9%, atrial fibrillation threshold 200 beats/min, and Vrate>Arate. An additional sustained rate duration criterion was programmed at least at 30 s. ICDs were interrogated every 3 months or when patients received shocks. A blinded review of electrograms for arrhythmia diagnosis and appropriateness of therapy was performed by 2 experts. Over the follow-up period (12+/-3.6 months), a total of 400 tachycardia episodes was recorded within the VT zone. After the review of stored electrograms, 237 (59%) true positive, 143 (36%) true negative, 17 (4%) false positive and 3 (1%) false negative episodes were diagnosed. Considering the 3 VTs incorrectly detected by the detection algorithms, therapy was delivered in 2 cases after sustained rate duration and 1 VT reverted spontaneously. Inappropriate therapy occurred in 17 cases. All but 1 were related to SVT with 1:1 atrioventricular relationship. Finally, on a per episode basis, the detection algorithm sensitivity was 99% and specificity was 89%.</AbstractText>Programming of detection criteria based on stability, onset, atrial fibrillation rate threshold and Vrate>Arate allows a 99% sensitivity and an 89% specificity in Guidant ICDs. Discrimination of SVT with 1:1 atrioventricular relationship, however, remains a challenge for which new algorithms have to be designed.</AbstractText> |
1,977 | Evaluation of body weight as a predictive factor for transvenous ventricular defibrillation characteristics. | To investigate the correlation between body weight and defibrillation threshold (DFT) for transvenous lead systems using a porcine model.</AbstractText>Twenty-eight pigs were anaesthetised and DFTs assessed in single and dual coil configurations using a four-reversal binary search method. DFT was correlated with body weight in the RV --> Can and RV --> SVC + Can configurations. A Pearson correlation coefficient and a two-sided p-value were calculated. A positive correlation exists between body weight and DFT in RV --> Can (r=0.66, p<0.000) and RV --> SVC + Can (r=0.44, p=0.018).</AbstractText>There is a significant correlation between body weight and DFT in swine. This tends to be greater in the two-electrode than in the three-electrode configuration. With these and previous human observations, one may predict a higher DFT in heavy individuals and make appropriate procedural adjustments.</AbstractText> |
1,978 | Risks for atrial fibrillation and congestive heart failure in patients >/=65 years of age with abnormal left ventricular diastolic relaxation. | We sought to determine the risk for the first episodes of atrial fibrillation (AF) and congestive heart failure (CHF) in a cohort of patients aged >/=65 years who had abnormal left ventricular (LV) diastolic relaxation. Records were reviewed for all residents of Olmsted County, Minnesota, who had >/=1 transthoracic echocardiogram performed at the Mayo Clinic between 1990 and 1998, and who were in sinus rhythm and did not have a history of AF, CHF, valvular or congenital heart disease, permanent pacemaker, or stroke. Of 994 patients who qualified and had LV diastolic function assessment, abnormal LV relaxation was identified in 569 (57%), 105 of whom (18%) developed a first episode of AF or CHF over a mean follow-up of 4.0 +/- 2.7 years. Age (p <0.0001), history of myocardial infarction (p <0.0001), history of diabetes mellitus (p = 0.041), electrocardiographic LV hypertrophy (p = 0.0223), and indexed left atrial (LA) volume (p = 0.0003) were independent predictors. A stepwise increase in age-adjusted risk was evident when stratified by tertiles of indexed LA volume (<27 ml/m(2); 27 to 37 ml/m(2); >37 ml/m(2)). Compared with patients with normal LV diastolic function (n = 148, 15%), the risks for first episodes of AF or CHF were not different in those with abnormal diastolic relaxation if LA volume was <27 ml/m(2) (p = 0.303). In conclusion, these data suggest the presence of a wide spectrum of risks for AF or CHF in the elderly who have abnormal LV diastolic relaxation, with the highest risks evident in those with the largest left atria. When LA volume was <27 ml/m(2), however, the risks for these events were not different from those with normal LV diastolic function. |
1,979 | The results of electrophysiological study and radio-frequency catheter ablation in pediatric patients with tachyarrhythmia. | A total of 135 consecutive pediatric patients (pts) with tachyarrhythmia ranging from two to 21 years of age (median age 11 years) underwent electrophysiological study (EPS) between January 1994 and July 2001. Tachycardia could not be induced in 38 of 135 pts (28%) and studies in these patients were accepted as the normal EPS. Supraventricular tachyarrhythmia mechanisms were atrioventricular (AV) accessory pathways in 47 patients (manifest accessory pathways in 23 patients, concealed accessory pathways in 17 patients, permanent junctional reciprocating tachycardia in 7 patients), re-entry without accessory pathway in 26 patients (AV nodal reentry tachycardia in 20 patients, atrial flutter in 5 patients, sinus node re-entry tachycardia in 1 patient) and atrial ectopic tachycardia in eight patients. The diagnosis of ventricular tachycardia (VT) was made in 16 patients. Seventy-three of the 97 patients with the diagnosis of tachyarrhythmia as a result of EPS underwent radiofrequency (RF) catheter ablation. The indications, early results, complications, safety and efficacy of RF catheter ablation were reviewed in these patients. Among the 73 patients who underwent RF ablation (85 procedures), the overall final success rate for all the diagnoses was 82% (60 of 73 patients). The median follow-up period for all patients was 16 months (range 2 to 60 months). Total recurrence rate in 73 patients was 4% (3 patients). Re-ablation was performed in only one of them and was successful. Procedure-related complications occurred in eight patients (11%): transient third-degree AV block in one patient, transient second-degree AV block in one patient, atrial flutter in two patients (1 needed direct current cardioversion), and atrial fibrillation in three patients (2 needed defibrillation and transient pacemaker implantation). In one patient with permanent third-degree AV block a transvenous pacemaker implantation was required. These midterm results suggest that RF catheter ablation has a good success rate and a low complication rate in pediatric patients, especially when it is carried out in experienced pediatric cardiology centers. |
1,980 | Anglo-American vs. Franco-German emergency medical services system. | It has been stated that the Franco-German Emergency Medical Services System (FGS) has considerable drawbacks compared to the Anglo-American Emergency Medical Services System (AAS): 1. The key differences between the AAS and the FGS are that in the AAS, the patients is brought to the doctor, while in the FGS, the doctor is brought to the patient. 2. In the FGS, patients with urgent conditions usually are evaluated and treated by general practitioners in their offices or at the patient's home; initially, very few approach an emergency department. 3. Emergency patients with life-threatening trauma or disease are treated by emergency physicians at the scene and during transport. Paramedics often are first to arrive at the scene, and until the emergency physician arrives at the scene, are allowed to defibrillate, to intubate endotracheally, and to administer life-saving drugs (epinephrine endotracheally, glucose intravenously, etc.). 4. Prehospital emergency physicians treat patients at the scene and during transport. 5. Emergency patients are guaranteed to be reached by an appropriate emergency vehicle and a respective crew within 10 minutes in 80% of the responses and within 15 minutes in 95% of cases. 6. The FGS deploys qualified emergency physicians assisted by qualified paramedics as prehospital intensive care providers; extended immediate care is standard. Total Prehospital Times (TPT) and scene times only are minimally longer than in the AAS. 7. Emergency Medicine is recognized as a supra-specialty to the base specialties. Specific training programs exist for emergency physicians, medical directors of emergency medical services systems (EMSS), and chief emergency physicians (CEP). 8. Resuscitation attempts are carried out not only by anesthesiologists, but also by internists, surgeons, pediatricians, etc. Emergency medicine encompasses cardiopulmonary resuscitation (CPR) and shock cases, and patients with an acute myocardial infarction, stroke, poly-trauma, status asthmaticus, etc. Emergency patients are admitted directly to emergency departments of the hospitals, which, depending upon the size of the hospital. 9. The incidence of life-threatening trauma victims has decreased to <10% in the FGS. Of a total of 830,000 deaths/year, fatal trauma cases ranked the lowest at 4%. 10. Survival figures on cardiac arrest (asystole, ventricular fibrillation/ventricular tachycardia (VF/VT), pulseless electrical activity (PEA, etc.) reported in the German EMSS correspond to those in Europe and the United States. 11. Paramedic training is characterized by a two-year program followed by a theoretical and a practical examination. 12. Paramedics and emergency physicians-in-training are supervised at the scene and during transport. Quality assurance (Q/A) constitutes an integral and legally compulsory part of the EMSS. 13. In the majority of cases, the emergency patients are evaluated and treated by the respective specialties without delays caused by patient transfer to other hospitals. 14. The FGS does not require a greater number of ambulances and/or personnel than does the AAS. 15. The German healthcare system creates less expenses/capita than the does the U.S. system at a similar level of quality of care. 16. Emergency procedures are carried out by anesthesiologists, emergency physicians, surgeons, internists, and other specialists. |
1,981 | Torsades de pointes following cardioversion: case history and literature review. | Torsades de pointes (TDP) is a relatively uncommon but potentially fatal cardiac arrhythmia which occurs in patients with long QT syndromes (LQTS). This literature review and case history investigate the causes, symptoms, presentation and treatment of torsades, focusing on drug induced torsades developing after successful cardioversion. In torsades, imbalanced positive ion flows result in early after-depolarisations (EADs) and increased variability in repolarisation rates. These combine to create an unstable re-entrant polymorphic ventricular tachycardia (VT) which can cause patients to suffer symptoms progressing from syncope to ventricular fibrillation (VF) arrest. Typically, torsades has a twisting morphological presentation on rhythm strips due to the irregularity of its re-entry pattern. The arrhythmia is more common in women. Intravenous magnesium is the initial emergency treatment in torsades. The case history illustrates the progressive acquisition of risk factors for drug induced torsades in a patient treated with sotalol following cardioversion. Typical progressive rhythm strip, electrocardiograph (ECG), and QT & corrected QT interval (QTc) interval changes occurring with the arrhythmia are presented. |
1,982 | Rapid loading of sotalol or amiodarone for management of recent onset symptomatic atrial fibrillation: a randomized, digoxin-controlled trial. | Amiodarone and sotalol are commonly used for the maintenance of sinus rhythm, but the efficacy of these agents administered as high-dose infusions for rapid conversion of atrial fibrillation is unknown. Use in this context would facilitate drug initiation in patients in whom ongoing prophylactic therapy is indicated.</AbstractText>We assessed the efficacy and safety of rapid high-dose intravenous infusions of amiodarone and sotalol for heart rate control and rapid reversion to sinus rhythm in patients who came to the emergency department with recent-onset symptomatic atrial fibrillation. Patients (n = 140) were randomized to receive 1.5mg/kg of sotalol infused in 10 minutes, 10mg/kg of amiodarone in 30 minutes, or 500 microg of digoxin in 20 minutes. Electrical cardioversion was attempted for patients not converting to sinus rhythm within 12 hours.</AbstractText>The rapid infusion of sotalol or amiodarone resulted in more rapid rate control than digoxin. Each of the 3 trial strategies resulted in similar rates of pharmacological conversion to sinus rhythm (amiodarone, 51%; sotalol, 44%; digoxin, 50%; P = not significant). The overall rates of cardioversion after trial drug infusion and defibrillation were high for all groups (amiodarone, 94%; sotalol, 95%,; digoxin, 98%; P = not significant), but there was a trend toward a higher incidence of serious adverse reactions in the amiodarone group.</AbstractText>The rapid infusion of sotalol or amiodarone in patients with symptomatic recent-onset atrial fibrillation results in rapid control of ventricular rate. Even with high-dose rapid infusions, all 3 agents are associated with a poor overall reversion rate within 12 hours. Almost all patients were returned to sinus rhythm with a combination of pharmacological therapy and electrical cardioversion.</AbstractText> |
1,983 | Surgical nurse assistants in cardiac surgery: a UK trainee's perspective. | To assess the impact of surgical nurse assistants on surgical training based on a comparative audit of case-mix and outcome of coronary revascularizations assisted by surgical nurse assistants vs. surgical trainees.</AbstractText>Relevant recent articles on Calman reform of specialist training and European working time directive (EWTD) on junior doctor working hours were reviewed for the discussion. For the audit prospectively entered data of elective and expedite first time coronary artery bypass grafting cases from 2000 to 2003 were analysed. Group A (n=233, Consultant+Surgical nurse assistant), group B (n=1067, Consultant+Junior surgical trainee). Chi-square test, t-test and Fisher's test were used as appropriate for statistical analysis.</AbstractText>Comparative preoperative variables were gender (P=0.8), body mass index (P=0.9), smoking (P=0.3), diabetes mellitus (P=0.2), hypertension (P=1), peripheral vascular disease (P=0.5), previous cerebrovascular accident (CVA)/transient ischemic attack (TIA) (P=0.3), renal dysfunction (P=0.4), preoperative rhythm disturbances (P=0.3), previous Q-wave myocardial infarction (MI) (P=0.4), Canadian Cardiovascular Society angina class (P=0.4), New York Heart Association heart failure class (P=0.4) and left ventricular function (P=0.4). Patients in group B were of higher risk due to age (P=0.01), coronary disease severity (P=0.05), left main stem disease (P=0.001), Parsonnet score (P=0.0001) and Euroscore (P=0.005. Regarding the myocardial protection technique, intermittent cross-clamp fibrillation was used more frequently in group A while antegrade-retrograde cold blood cardioplegia and off-pump coronary artery bypass were used more in group B (P=0.0001). The cross-clamp (P=0.0001) and operation time (P=0.0001) were significantly lower in group A despite a comparable mean number of grafts (P=0.2). There was no significant difference in the immediate postoperative outcome ventilation time (P=0.2), intensive care unit stay, postoperative stay (P=0.2), re-exploration for bleeding (P=0.5), inotrope+intra-aortic balloon pump (P=0.2), postoperative MI (P=0.9), postoperative rhythm disturbances (P=0.9), CVA/TIA (P=0.8), renal dysfunction (P=0.6), wound infection (P=0.7), sternal re-wiring (P=0.2), multi-organ failure (P=0.4) or mortality (P=0.1).</AbstractText>Surgical nurse assistants can be used effectively in low-risk cases without compromising postoperative results. However, initiatives to tackle the EWTD should be focused on areas that do not compromise the training needs of junior surgical trainees. An intermediate grade between the present senior house officer and registrar grades could be a way forward.</AbstractText> |
1,984 | Metabolic changes induced by ischemia and cardioplegia: a study employing cardiac microdialysis in pigs. | The present study investigates dynamic changes of myocardial metabolism in response to ischemia, cardioplegia, and extracorporeal circulation (ECC) in order to differentiate between the contributing effects of each of these interventions. Furthermore, warm blood cardioplegia versus empty beating of the heart were compared as methods to resuscitate the ischemic myocardial metabolism.</AbstractText>Swedish Landrace pigs on ECC (ECC) were compared with pigs on ECC with warm ischemic cardiac arrest (ischemia) or on ECC with warm ischemic arrest followed by warm blood cardioplegia (ischemia-cardioplegia), using sham-operated pigs as controls (n=7 in each group). Microdialysis probes were placed on the surface of the left ventricle and in the femoral artery for serial evaluation of metabolites in the intracardiac extracellular fluid and arterial blood. When hearts started in ventricular fibrillation (VF), it was electroconverted after 10 min of normal blood reperfusion. If VF started after 10 min of reperfusion electroconversion was immediately performed.</AbstractText>There were no differences between groups in arterial contents of serine, citrulline, arginine, inosine, hypoxanthine, guanosine, aspartate, glutamate, pyruvate, or asparagine throughout the observation period. Systemic lactate increased in pigs subjected to ischemia (P<0.001) or ischemia and cardioplegia (P=0.002), highest in the ischemia only group (P=0.002). In left ventricular microdialysates, lactate increased in pigs subjected to ischemia alone (P<0.001 vs. ECC) and ischemia and cardioplegia (P=0.004 vs. ECC). Guanosine increased in ischemia versus ECC (P=0.002), while hypoxanthine was increased in microdialysates of both ischemic (P=0.002) and ischemic-cardioplegic (P=0.001) pig hearts. Inosine was increased in pigs subjected to ischemia and cardioplegia (P<0.001 vs. ECC). All ischemic hearts started with VF, but while in the warm ischemia group VF started within 10 min of reperfusion, the ischemia-cardioplegia group had a longer asystolia with VF starting 11-22 min of blood reperfusion.</AbstractText>The heart should be allowed to start empty beating rather than by the use of warm continuous blood cardioplegia. Microdialysis and sampling of interstitial metabolites may be advantageous when an increased sensitivity is needed or when repeated blood sampling is difficult or contraindicated in monitoring of the myocardium.</AbstractText> |
1,985 | [Assessment of anti-arrhythmic efficacy of a domestic drug allapinin in patients with ischemic heart disease and cardiac arrhythmia]. | Antiarrhythmic activity of oral allapinin was studied in 64 patients with ischemic heart disease. 27 of the patients had undergone coronary artery bypass grafting 2 to 12 months before, 19 patients had postinfarction cardiosclerosis, 38--arterial hypertension, 30--circulation insufficiency stage I. Arrhythmia presented as ventricular extrasystole (n = 28), paroxysmal atrial fibrillation (n = 18), paroxysmal atrial tachycardia (n = 11), frequent supraventricular extrasystole (n = 7). Arrhythmia continued from 6 months to 8 years. An effective single dose was defined with acute pharmacological test. The treatment course lasted for 21 days. Allapinin proved to be highly effective: ventricular ectopic activity was suppressed in 71.4% patients, atrial tachycardia paroxysms were prevented in 72.7%, paroxysms of atrial fibrillation--in 77.8%. Allapinin tolerance was good. Extracardiac side effects occurred most frequently, but dose lowering was necessary only in 6.2%. The drug was discontinued because of cardiac side effects in 4.7% cases. ECG monitoring is a highly informative method of the treatment efficacy control. |
1,986 | Catheter Ablation of Ventricular Fibrillation in Structurally Normal Hearts Targeting the RVOT and Purkinje Ectopy. | Catheter ablation for ventricular fibrillation in structurally normal hearts is in its infancy. Recently, catheter ablation of idiopathic ventricular fibrillation as well as ventricular fibrillation associated with the long QT and Brugada syndromes has been described. This review article is a summary of our current understanding of the technique and results of catheter ablation of ventricular fibrillation in structurally normal hearts. |
1,987 | Will direct thrombin inhibitors replace warfarin for preventing embolic events in atrial fibrillation? | Atrial fibrillation is the most frequently encountered tachyarrhythmia requiring therapy. Treatment issues include therapy for any reversible cause; the identification and treatment of any underlying structural disorder; control of the ventricular rate, both for symptom reduction and prevention of tachycardic-induced cardiomyopathy; restoration and maintenance of sinus rhythm when symptoms persist despite rhythm control; and anticoagulation in patients with high-risk markers for systemic embolization: age over 65 years, hypertension, diabetes, ventricular failure, rheumatic valvular disease, and prior stroke or other embolic event. In such patients, anticoagulation with warfarin is currently recommended. Warfarin therapy carries significant risks (especially bleeding), inconveniences (the cost of prothrombin time monitoring, the need for rigid dietary stability, the concerns of drug and herbal interactions), and other concerns (the issue of generic formulation substitution).</AbstractText>Under development are oral thrombin inhibitors. The first to reach clinical approval will likely be ximelagatran. In clinical trials to date, ximelagatran has proven to be equal to or superior to warfarin in the prevention and treatment of thrombophlebitis. In atrial fibrillation patients, the Stroke Prevention Using Oral Thrombin Inhibitor in Atrial Fibrillation (SPORTIF) trials completed so far appear to show a similar or better efficacy for ximelagatran versus warfarin as regards both prevention of embolic events and lower risks of major bleeding, with no serious adverse effects except for apparently reversible alterations in liver function tests in approximately 6% of subjects, all occurring early in therapy to date. If the remaining SPORTIF trial (SPORTIF V) is confirmatory (results to be available in late 2003), it is expected that this exciting new product will be submitted this winter to the Food and Drug Administration for approval. Recent findings also include the observations in the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) and Rate Control Versus Electrical Cardioversion (RACE) trials that anticoagulation should not be discontinued despite the restoration and maintenance of sinus rhythm.</AbstractText>Oral direct thrombin inhibitors, such as ximelagatran, appear likely to replace the use of warfarin in most patients in the near future, because of a better risk-benefit profile.</AbstractText> |
1,988 | Oral class III antiarrhythmics: what is new? | This review describes the latest developments in the clinical usage of class III antiarrhythmics. It also discusses some new studies providing insight into the mechanism of action of these drugs.</AbstractText>New data suggest that amiodarone is one of the most effective drugs for management of ventricular as well as supraventricular tachyarrhythmias. As over the years we have learned to deal with the toxic side effects of this drug, the risk of bradyarrhythmias requiring placement of a pacemaker is becoming more significant. Sotalol was approved for treatment of atrial fibrillation and atrial flutter (AF). It was also found to be effective in management of postoperative AF. Dofetilide has been approved for the conversion and maintenance of sinus rhythm in AF; its role in ventricular arrhythmias remains unclear. Data are emerging regarding clinical efficacy of azimilide and dronedarone.</AbstractText>Management of arrhythmias in patients with structural heart disease remains a challenge. Class III antiarrhythmics are the mainstay of treatment in this group of patients.</AbstractText> |
1,989 | Subanalyses of secondary prevention implantable cardioverter-defibrillator trials: antiarrhythmics versus implantable defibrillators (AVID), Canadian Implantable Defibrillator Study (CIDS), and Cardiac Arrest Study Hamburg (CASH). | Controlled trials for secondary prevention of sudden death--Antiarrhythmics Versus Implantable Defibrillators (AVID), Canadian Implantable Defibrillator Study (CIDS), and Cardiac Arrest Study Hamburg (CASH)--have been published and subanalyses of them provide useful clinical information on the outcome during the follow-up of this population.</AbstractText>Results from a meta-analysis showed a significant risk reduction (RR) of 25 to 27% of total mortality (P < 0.001) and 50 to 52% of arrhythmic death (P < 0.001). Compared with amiodarone, patients treated with an implantable cardioverter-defibrillator (ICD) in AVID had a maximal benefit in survival when the ejection fraction (EF) was between 20 and 34%. In CIDS, the group of higher risk (older than 70 years, EF less than 3.5%, and New York Heart Association class III-IV) presented a 50% RR of mortality. It has been demonstrated that the imbalance in beta-blocker use cannot explain the better survival in the ICD patients. After 3 years the recurrence of arrhythmia was 64% in the ICD group of the AVID trial. Patients enrolled after an episode of ventricular tachycardia were more likely to have appropriate therapy during follow-up. Older age, lower blood pressure, history of atrial fibrillation, diabetes, congestive heart failure, and prior pacemaker were parameters used for high-risk stratification. Conversely, inducibility of ventricular tachyarrhythmias on electrophysiology did not predict death.</AbstractText>Patients with ICD after ventricular tachyarrhythmias have a 28% RR in total mortality. Individuals with EF between 20 to 34% received the highest benefit with ICD therapy.</AbstractText> |
1,990 | An update on clinical trials in pacing: is dual chamber pacing better? | As pacemaker technology has increased in complexity and now offers a variety of additional capabilities, there is uncertainty as to which pacing mode offers more benefit-dual-chamber or single-chamber.</AbstractText>Two large-scale randomized trials, the Canadian Trial of Physiologic Pacing and the Mode Selection Trial, demonstrated that dual-chamber pacing does not reduce the incidence of stroke or improve survival when compared with ventricular pacing. However, dual-chamber pacing does reduce the incidence of atrial fibrillation and in patients with sinus node dysfunction, reduces heart failure symptoms when compared with ventricular pacing. The modest results of these trials were unexpected when viewed in the context of the very favorable retrospective studies.</AbstractText>A rethinking of the physiology of cardiac pacing has led to the concept that although atrioventricular synchrony supports an improvement in cardiac output and ventricular pressures, these favorable hemodynamics may be attenuated by ventricular dyssynchrony from right ventricular apical pacing. In patients with a reduced ejection fraction, this dyssynchrony may be especially detrimental. Two trials (DANPACE and SAVE-PACE) are currently underway that will clarify the clinical significance of reducing forced ventricular desynchronization. The results of these trials may direct pacemaker physicians away from the right ventricular apical lead toward a new imperative of atrioventricular and right ventricular-left ventricular synchrony.</AbstractText> |
1,991 | Difficult cases in heart failure. Percutaneous transluminal septal myocardial ablation in the management of hypertrophic obstructive cardiomyopathy. | Hypertrophic cardiomyopathy is a complex genetic condition with a heterogeneous clinical course. Some patients remain asymptomatic throughout life while others develop one or more of the adverse clinical consequences including symptoms of congestive heart failure with exertional dyspnea and functional disability (usually with preserved left ventricular systolic function), atrial fibrillation, or sudden cardiac death. Because of this heterogenicity in the clinical presentations, management of patients with hypertrophic cardiomyopathy includes a wide range of pharmacologic therapies as well as invasive approaches. In recent years, nonsurgical catheter-based treatment of hypertrophic cardiomyopathy has been increasingly used in the management of a subset of these patients. The authors present a case of percutaneous transluminal septal myocardial ablation in a patient with hypertrophic cardiomyopathy who was symptomatic despite maximal medical treatment. |
1,992 | Prevalence, prognostic significance, and treatment of atrial fibrillation in congestive heart failure with particular reference to the DIAMOND-CHF study. | Atrial fibrillation is a growing health problem and the most common cardiac arrhythmia, affecting 5% of persons above the age of 65 years. The number of hospital discharges for atrial fibrillation has more than doubled in the past decade. It occurs very often in patients with congestive heart failure and the prevalence increases with the severity of the disease. These two conditions seem to be linked together, and congestive heart failure may either be the cause or the consequence of atrial fibrillation. The prognosis of atrial fibrillation is controversial, but studies indicate that atrial fibrillation is a risk factor in congestive heart failure patients. In the last 10-15 years, significant advances in the treatment of heart failure have improved survival, whereas effective management of atrial fibrillation in heart failure patients still awaits similar progress. Empirically, two strategies have evolved for treatment of atrial fibrillation: 1) rhythm control, which means conversion to sinus rhythm and maintenance of sinus rhythm; and 2) rate control, which means reduction of heart rate to an acceptable frequency. It is unknown whether one of these strategies is better than the other. In this review the authors discuss the prevalence, impact, and treatment of atrial fibrillation in heart failure patients. |
1,993 | A cardiac sodium channel mutation identified in Brugada syndrome associated with atrial standstill. | Mutations in the cardiac Na+ channel gene SCN5A are responsible for multiple lethal ventricular arrhythmias including Brugada syndrome and congenital long QT syndrome. Here we report a case of Brugada syndrome with ST elevation in the right precordial and inferior leads accompanied by atrial standstill and spontaneous ventricular fibrillation. Atrial standstill and J wave elevation were provoked by procainamide. Genetic analysis revealed a missense mutation (R367H) in SCN5A. The resultant mutant Na+ channel was nonfunctional when expressed heterologously in Xenopus oocytes. Our study suggests that genetic defects in SCN5A may be associated with atrial standstill in combination with ventricular arrhythmias. |
1,994 | Frequency dependence of the cardiac threshold to alternating current between 10 Hz and 160 Hz. | It is still unclear what fundamental criteria influence the ability of alternating current (AC) to induce ventricular fibrillation (VF) in vivo. As the VF threshold has a bowl-shaped relationship with frequency (showing a minimum threshold at some frequency), similar to the nervous system, one proposed model has assumed that the mechanisms underlying AC stimulation of nerves are at work for VF induction. More recent work has suggested a second approach, whereby a simple RC-like model is sufficient to understand the cardiac AC stimulation threshold's frequency dependence, suggesting that some unarticulated mechanism is at work for VF. The paper directly tests these two models. In 12 intact dogs and 20 intact guinea pigs, DC pulses were used to stimulate AC square and AC sine waves at 10, 20, 40, 80 and 160 Hz. All electrodes were endocardial, with the return electrode being on a paw or thorax. It was found that, for square and sine wave stimulation in both dogs and guinea pigs, the stimulation threshold increased monotonically with frequency from 10 Hz up to 160 Hz (p < 0.01 for dogs and guinea pigs). Between 80 and 160 Hz, the AC stimulation threshold doubled, exactly as predicted by an RC model. It was concluded that the AC stimulation threshold is not bowl-shaped and is best understood with an RC model. As the VF threshold does exhibit a bowl-shape with frequency, as opposed to the stimulation threshold which does not, the VF induction frequency dependence must have different origins. |
1,995 | [Myoglobin and troponin I as markers of myocardial damage during cardioversion of atrial fibrillation]. | We performed direct comparison of safety and efficacy of monophasic and biphasic shock cardioversion (CV) of atrial fibrillation (AF). Troponin I (cTnl) and myoglobin (My) were used as markers of potential myocardial and skeletal muscle damage during the procedure.</AbstractText>63 patients (p.t.s.) with persistent, nonvalvular AF (F/M 18/45; mean age 61.6 +/- 11.4 years) were randomized to CV either with monophasic (F/M 10/24, Group I) or biphasic (F/M 8/21, Group II) shock. Plasma levels of cTnl and My were measured before CV, 6 hours and 24 hours after CV.</AbstractText>The efficacy of CV was significantly higher in Group II (93% vs 85%, p < 0.04). Sinus rhythm restoration required lower total energy used during procedure with biphasic shock (379.8 +/- 301.5 vs 192.8 +/- 100.6 J; p 0.001). There was no significant difference in mean values of cTnl before CV in both groups (0.3 +/- 0.2 vs 0.2 +/- 0.1 ng/mL, p > 0.15). In 14 pts (41%) from Group I and 3 pts (10%) from Group II plasma cTnl concentration above discriminatory level (0.9 ng/mL) were noted. There was a significant increase in mean plasma cTnl level (0.3 +/- 0.2 vs 1.9 +/- 0.9 ng/mL, p < 0.04) 24 hours after the procedure in Group I. We did not observed significant differences in cTnl plasma concentration 6 and 24 hours after CV in Group II (0.2 +/- 0.1 vs 0.4 +/- 0.2 ng/mL, p > 0.15). Both study groups did not significantly differ in mean serum My level at baseline (39.1 +/- 14.2 vs 43.1 +/- 20.9 ng/mL). In Group I mean My serum concentration increased during the first 6 hours after CV (43.1 +/- 20.9 vs 247.9 +/- 53.3 ng/mL, p < 0.02) and there was a significant decreasing in My serum level during the further observation (247.9 +/- 53.3 vs 104.5 +/- 46.1 ng/mL, p < 0.03). Mean serum My concentration remained within normal ranges during the 24 hour follow-up after the biphasic shock CV (43.1 +/- 20.9 vs 43.6 +/- 29.1 ng/mL). Increased of cTnl and My in Group I may be due to myocardial and skeletal muscle damage and correlate closely with cumulative energy delivered (Spearmann correlation index (r) = 0.55, p < 0.01 for My and r = 0.66, p < 0.01 for cTnl). In Group I positive correlation between cumulative energy used during CV and increase of studied markers indexed with left ventricular mass (r = 0.6, p < 0.05 for My and r = 0.74, p < 0.04 for cTnl) was observed. There was no significant correlation between delivered energy and increase of heart markers in Group II noted.</AbstractText>We observed the significant increase in mean serum cTnl and My level 24 hours after CV with monophasic shock and its positive correlation with total energy used during the procedure. There is a conclusion that biphasic shock used during CV of AF is more efficient and may cause less myocardial and skeletal muscle damage due to lower energy delivered.</AbstractText> |
1,996 | Gender differences in advanced heart failure: insights from the BEST study. | The goal of this study was to determine the influence of gender on baseline characteristics, response to treatment, and prognosis in patients with heart failure (HF) and impaired left ventricular ejection fraction (LVEF).</AbstractText>Under-representation of women in HF clinical trials has limited our understanding of gender-related differences in patients with HF.</AbstractText>The impact of gender was assessed in the Beta-Blocker Evaluation of Survival Trial (BEST) which randomized 2,708 patients with New York Heart Association class III/IV and LVEF < or =0.35 to bucindolol versus placebo. Women (n = 593) were compared with men (n = 2,115). Mean follow-up period was two years.</AbstractText>Significant differences in baseline clinical and laboratory characteristics were found. Women were younger, more likely to be black, had a higher prevalence of nonischemic etiology, higher right and left ventricular ejection fraction, higher heart rate, greater cardiothoracic ratio, higher prevalence of left bundle branch block, lower prevalence of atrial fibrillation, and lower plasma norepinephrine level. Ischemic etiology and measures of severity of HF were found to be predictors of prognosis in women and men. However, differences in the predictive values of various variables were noted; most notably, coronary artery disease and LVEF appear to be stronger predictors of prognosis in women. In the nonischemic patients, women had a significantly better survival rate compared with men.</AbstractText>In HF patients with impaired LVEF, significant gender differences are present, and the prognostic predictive values of some variables vary in magnitude between women and men. The survival advantage of women is confined to patients with nonischemic etiology.</AbstractText> |
1,997 | Management of atrial fibrillation: review of the evidence for the role of pharmacologic therapy, electrical cardioversion, and echocardiography. | This review summarizes the available evidence regarding the efficacy of medications used for ventricular rate control, stroke prevention, acute conversion, and maintenance of sinus rhythm, as well as the efficacy of electrical cardioversion and the use of echocardiography in patients with atrial fibrillation.</AbstractText>The Cochrane Collaboration's database of controlled clinical trials and MEDLINE.</AbstractText>Primarily randomized, controlled trials of medications.</AbstractText>Paired reviewers obtained data on efficacy and safety. Strength of evidence was assessed.</AbstractText>Recent clinical trial results showed that most patients with atrial fibrillation have similar outcomes with strategies for controlling ventricular rate compared with strategies for restoring sinus rhythm. For efficacy of primary stroke prevention, compared with placebo, evidence was strong for warfarin and suggestive for aspirin. The evidence for an increased risk for major bleeding was suggestive for warfarin and inconclusive for aspirin. For ventricular rate control, verapamil, diltiazem, atenolol, and metoprolol were qualitatively superior to digoxin and placebo, particularly during exercise. For efficacy of acute conversion, compared with placebo, evidence was strong for ibutilide, flecainide, dofetilide, propafenone, amiodarone, and quinidine. For efficacy of maintenance of sinus rhythm after conversion from atrial fibrillation, evidence was strong for amiodarone, propafenone, disopyramide, and sotalol. Echocardiography was found to be useful in estimating risk for thromboembolism and potentially useful in estimating likelihood of successful cardioversion and maintenance.</AbstractText>For several key questions in the pharmacologic management of atrial fibrillation, strong evidence exists to support 1 or more treatment options.</AbstractText> |
1,998 | Optical mapping of transmural activation induced by electrical shocks in isolated left ventricular wall wedge preparations. | It is believed that electrical shocks interrupt fibrillation by directly stimulating the bulk of ventricular myocardium in excitable states, but how shocks activate intramural tissue layers is not known. In this study, Vm responses and transmural activation patterns induced by shocks during diastole were measured in isolated coronary perfused preparations of porcine left ventricle.</AbstractText>Rectangular shocks (duration = 10 ms; field strength, E = 1-44 V/cm) were applied across preparations (thickness = 14.9 +/- 2.5 mm, n = 9) via large mesh electrodes during diastole or action potential (AP) plateau. Vm responses at the transmural surface were measured using optical mapping technique (resolution = 1.2 mm). Depending on shock strength, three types of Vm responses were observed. (1) Weak shocks (E approximately 1-4 V/cm) applied in diastole induced APs with simple monophasic upstrokes. The latency and time of transmural activation (TTA) rapidly decreased with increasing shock strength. Earliest activation occurred predominantly at the cathodal side of preparations in the areas that exhibited maximal DeltaVm during AP plateau. (2) Intermediate shocks (E approximately 4-23 V/cm) induced monophasic and biphasic upstrokes that were paralleled with predominantly negative plateau DeltaVm. Activation was initiated at multiple transmural sites and rapidly spread across the myocardial wall (TTA = 0.6 +/- 0.2 ms). (3) Very strong shocks (E approximately 23-44 V/cm) could cause triphasic upstrokes, likely reflecting occurrence of membrane electroporation, and delayed activation (TTA = 6.7 +/- 3.8 ms) at sites of largest negative plateau DeltaVm.</AbstractText>Shocks applied during diastole cause direct and rapid (within 1 ms) activation of ventricular bulk over a wide range of shock strengths, supporting the excitatory hypothesis of defibrillation. Very strong shocks can cause multiphasic Vm responses and delayed activation.</AbstractText> |
1,999 | Right ventricular outflow versus apical pacing in pacemaker patients with congestive heart failure and atrial fibrillation. | Prior studies suggest that right ventricular apical (RVA) pacing has deleterious effects. Whether the right ventricular outflow tract (RVOT) is a more optimal site for permanent pacing in patients with congestive heart failure (CHF) has not been established.</AbstractText>We conducted a randomized, cross-over trial to determine whether quality of life (QOL) is better after 3 months of RVOT than RVA pacing in 103 pacemaker recipients with CHF, left ventricular (LV) systolic dysfunction (LV ejection fraction < or = 40%), and chronic atrial fibrillation (AF). An additional aim was to compare dual-site (RVOT + RVA, 31-ms delay) with single-site RVA and RVOT pacing. QRS duration was shorter during RVOT (167 +/- 45 ms) and dual-site (149 +/- 19 ms) than RVA pacing (180 +/- 58 ms, P < 0.0001). At 6 months, the RVOT group had higher (P = 0.01) role-emotional QOL subscale scores than the RVA group. At 9 months, there were no significant differences in QOL scores between RVOT and RVA groups. Comparing RVOT to RVA pacing within the same patient, mental health subscale scores were better (P = 0.03) during RVOT pacing. After 9 months of follow-up, LVEF was higher (P = 0.04) in those assigned to RVA rather than RVOT pacing between months 6 and 9. After 3 months of dual-site RV pacing, physical functioning was worse (P = 0.04) than during RVA pacing, mental health was worse (P = 0.02) than during RVOT pacing, and New York Heart Association (NYHA) functional class was slightly better (P = 0.03) than during RVOT pacing. There were no other significant differences between RVA, RVOT and dual-site RV pacing in QOL scores, NYHA class, distance walked in 6 minutes, LV ejection fraction, or mitral regurgitation.</AbstractText>In patients with CHF, LV dysfunction, and chronic AF, RVOT and dual-site RV pacing shorten QRS duration but after 3 months do not consistently improve QOL or other clinical outcomes compared with RVA pacing.</AbstractText> |
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