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4,800 | Combination therapy with carvedilol and amiodarone in patients with severe heart failure. | Carvedilol and at least in some studies, amiodarone have been shown to improve symptoms and prognosis of patients with heart failure. There are no reports on the outcome of combined treatment with both drugs on top of angiotensin-converting enzyme inhibitors (ACEI), diuretics and digitalis.</AbstractText>In 109 patients with severe heart failure submitted for heart transplantation at one single center between the years 1996 and 1998 [left ventricular ejection fraction (LVEF) 24.6+/-11%, 85% males, 52% idiopathic dilated cardiomyopathy (DCM), mean observation time 1. 9+/-0.4 years] a therapy with low-dose amiodarone (1000 mg/week) plus titrated doses of carvedilol (target 50 mg/day) was instituted. In addition, patients received a prophylactic dual chamber pacemaker (PM) in order to protect from bradycardia and for continuous holter monitoring. The devices were programmed in back-up mode with a basal rate of 40 i.p.m. with a hysteresis of 25%. Significantly, more patients were in sinus rhythm after 1 year than at study entry (85% vs. 63%, P<0.01). In 47 patients, under therapy over at least 1 year, the resting heart rate fell from 90+/-19 to 59+/-5 b.p.m. (P<0.001). Ventricular premature contractions in 24-h holter ECGs were suppressed from 1.0+/-3 to 0.1+/-0.3%/24 h (P167 b.p.m. detected by the pacemaker (1.2+/-2.8 episodes/patient/3 months vs. 0.3+/-0.8 episodes/patient/3 months after 1 year (P<0.01). The LVEF increased from 26+/-10 to 39+/-13% (P<0.001). NYHA class improved from 3. 17+/-0.3 to 1.8+/-0.6 (P<0.001) as well as right heart catheterization data. From the total cohort, seven patients (6%) developed symptomatic documented bradycardic rhythm disturbances requiring reprogramming of their pacemakers to DDD(R)/VVI(R) mode with higher basic rates. Two of these patients developed AV block, four sinu-atrial blocks or sinus bradycardia and one patient had bradycardic atrial fibrillation. During the observation period five patients died (3 sudden, 1 due to heart failure and 1 due to mesenteric infarction). Two patients had undergone heart transplants. The 1-year survival rate (Kaplan-Meier) without transplantation was 89%. Compared to historic control patients with amiodarone only (n=154) or without either agent (n=283) this rate was 64 and 57% (P<0.01).</AbstractText>Heart failure patients benefit from a combined therapy with carvedilol and amiodarone resulting in a markedly improved NYHA stage, an increase in LV ejection fraction, a stabilization of sinus rhythm, a significant reduction in heart rate, a delay of electrical signal conduction and a suppression of ventricular ectopies. Approximately 6% of patients under such a regime became pacemaker-dependent in the first year. Compared to historic controls prognosis was better and the need for heart transplantation was lower. The exact role of either agent in combination or alone should be clarified in larger randomized studies.</AbstractText> |
4,801 | Long-term follow-up of patients requiring intravenous amiodarone to suppress hemodynamically destabilizing ventricular arrhythmias. | Intravenous amiodarone is effective for the acute suppression of recurrent hemodynamically destabilizing ventricular arrhythmias. There are no follow-up data on patients undergoing long-term therapy with intravenous amiodarone. The objective of this investigation was to evaluate long-term outcome.</AbstractText>We reviewed the clinical courses of 245 patients given intravenous amiodarone for sustained ventricular tachyarrhythmias. Of the 107 survivors (84% men; mean age 64 years) released from the hospital taking oral amiodarone, 41 were discharged with an empiric prescription for oral amiodarone. For 64 patients a decision regarding further therapy was based on results of an electrophysiologic study. Two patients were treated empirically with oral amiodarone and an implantable cardioverter defibrillator. Clinical variables and survival curves were the same for the empirically treated group and the group whose treatment was based on electrophysiologic findings (P =.89). Survival at 6, 12, and 18 months was 88%, 81% and 71%, respectively, for empirically treated patients, and 83%, 80% and 73%, respectively, for patients whose therapy was directed with an electrophysiologic study. Of the 64 patients who underwent electrophysiologic studies, 33 received an implantable cardioverter defibrillator. The Kaplan-Meier survival curves for patients with and patients without an implantable cardioverter defibrillator were similar (P =.46).</AbstractText>Patients for whom recurrent ventricular tachycardia and fibrillation are suppressed with intravenous amiodarone and who are discharged receiving oral amiodarone have an 80% 1-year survival rate. Although not randomized, our data suggested that among such patients, electrophysiologic testing, implantation of a cardioverter defibrillator, or both may not be necessary. Ascertaining the best management strategy for these patients will require a prospective randomized trial.</AbstractText> |
4,802 | Structural changes of atrial myocardium during chronic atrial fibrillation. | Of all known arrhythmia's, atrial fibrillation (AF) is the most often met in the clinical setting and it is associated with an increase in mortality risk. Several risk factors for AF have been described and several mechanisms of induction and maintenance have been proposed. Studies in patients with AF have shown that structural changes occur in the atria, but the relationship between the structural remodelling and the chronicity of the arrhythmia are not well understood. The changes mainly concern adaptive (dedifferentiation of cardiomyocytes) and maladaptive (degeneration of cells with replacement fibrosis) features. In order to characterise the time course of the structural remodelling the need for animal models which adequately mimic chronic atrial fibrillation in humans is felt essential. In this review, the structural changes that are observed during prolonged sustained AF in patients and animal models, are described. Furthermore, the time course and potential mechanisms of structural remodelling are discussed and methods for elucidation of the underlying molecular mechanisms are presented. |
4,803 | Medical history of hypercholesterolaemia adversely affects the outcome of out-of-hospital cardiopulmonary resuscitation; the 'Shahal' experience in Israel. | To evaluate the impact selected risk factors for cardiac death may have on the success rate in a large cohort of subscribers to 'SHAHAL' who were resuscitated from out-of-hospital cardiac arrest.</AbstractText>In this medical facility currently serving 50 000 subscribers, data were prospectively gathered from between 1987-1998. The information retrieved from the patients' medical records included a medical history of hypertension, diabetes, hypercholesterolaemia (>220.mg. dl(-1)) smoking, angina, previous myocardial infarction, and congestive heart failure. A total of 998 patients aged 74+/-12 years (mean+/-1 SD) were included. Death was announced at the scene for 659 (66%) victims, while 339 (34%) patients were taken to hospital. Of these 140 (14% of the total cohort) survived and were discharged from the hospital. A comparison of various selected parameters between survivors and non-survivors of resuscitation revealed that survivors were younger, had a higher rate of pulseless ventricular tachycardia/ventricular fibrillation, more were among the arrests witnessed by the 'SHAHAL' team, and that more had a shorter time lag to initiation of cardiopulmonary resuscitation than non-survivors. None of the studied risk factors predicted the outcome of cardiopulmonary resuscitation, with the exception of hypercholesterolaemia, which carried a significantly worse prognosis for cardiopulmonary resuscitation (P=0.009).</AbstractText>A medical history of hypercholesterolaemia appears to be an important risk factor which adversely affects the outcome of cardiopulmonary resuscitation.</AbstractText>Copyright 2000 The European Society of Cardiology.</CopyrightInformation> |
4,804 | Out-of-hospital cardiac arrest. | Out-of-hospital cardiac arrest (OHCA), with its high fatality rate, is a significant public health issue. The aetiology of OHCA is reviewed, and management strategies are discussed, including the "chain of survival", the Utstein method of data collection, and recent developments in advanced cardiac life support emphasising defibrillation. |
4,805 | Biphasic waveforms for automatic external defibrillation in human: a review. | Ventricular fibrillation is the principal cause of sudden cardiac arrest and the electrical defibrillation is often the only effective therapy. A very interesting question is represented by the electric parameters of defibrillation shock. Today, monophasic waveform is widely used in Europe and in the United States, but, recently, the Food and Drug Administration grants approval for an automatic external defibrillator (AED) producing a biphasic pulse. In this review we discuss about the effectiveness and the safety of biphasic waveform, by examining a series of human studies between 1982 and 1999. We have found that available data are often incomplete, unclear, dishomogeneous and, consequently, difficult to compare. Furthermore, among the authors there is no concordance about the meaning of "safety", "effectiveness", "success", "equivalence" and "superiority" of biphasic versus monophasic shock: however, biphasic shock, that uses a lower energy level, seems to reduce post-defibrillation heart damage. Due to the lack of homogeneous studies it is not possible to state which kind of signal is more reliable, even if some clinical reports and experimental data seem to tribute to the biphasic waveform a better therapeutic effectiveness and safety. By examining the current scientific literature, we conclude that further studies have to be performed to definitively validate the use of biphasic shock. |
4,806 | [Sudden death and ventricular fibrillation of possible ischemic origin in a boy with hypertrophic myocardiopathy]. | It has been presented a case of an eleven-year-old patient admitted with a pattern of ventricular fibrillation and diagnosed as hypertrophic cardiomyopathy. Admission analysis and myocardia anatomy evolution suggested ischemic etiology. We checked the risk factors of sudden death, its relation with ischemic disease and the etiology of ischemia in the hypertrophic myocardiopathy. |
4,807 | Arrhythmogenic right ventricular cardiomyopathy with an initial manifestation of severe left ventricular impairment and normal contraction of the right ventricle. | A case of arrhythmogenic right ventricular cardiomyopathy (ARVC) with an initial manifestation of severe impairment of the left ventricle (LV) and normal contraction of the right ventricle (RV) is presented. A 43-year-old man was admitted to hospital because of congestive heart failure following a common cold. The LV function was diffusely and severely hypokinetic. Coronary arteriogram revealed normal vessels. An endomyocardial biopsy specimen obtained from the RV septum revealed mild infiltration of lymphocytes with focal myocytes necrosis and so healing myocarditis was suspected. The specimen did not include any fatty replacement of myocytes. Since then, the patient suffered from recurrent congestive heart failure as well as nonsustained ventricular tachycardia and required frequent hospitalization. Progressive impairment, dilation, and thinning of both ventricles were observed on serial echocardiographic examinations. Although the RV gradually enlarged and became impaired, severe dilatation and impairment of the LV has always been predominant in the patient's clinical course. After medical follow-up for 10 years, he died suddenly of ventricular fibrillation and pump failure. The autopsy revealed extensive fibrofatty replacement of myocytes in both the ventricles, extending from the outer layer to the inner layer of myocardium in the RV and to the middle layer in the LV. These features were compatible with arrhythmogenic right ventricular cardiomyopathy or perimyocarditis, although only the rightsided bundle of the interventricular septum was completely replaced by fatty tissue, which can not be explained as a sequel of perimyocarditis. Moreover, apoptosis was present in the myocyte nuclei of the myocardial layers bordering the area of fatty replacement. Therefore, myocarditis may have triggered or accelerated the process of apoptosis leading to ARVC. |
4,808 | Micropumps to support the heart during CABG. | To show the effect of myocardial support by micropumps during beating heart CABG for triple vessel disease.</AbstractText>In 12 sheep, three coronary arteries (LAD, intermediate branch and circumflex) were consecutively occluded for 10 min. The animals were divided in two groups: group 1 without support (n=6) and group 2 with biventricular support of intravascular micropumps. The pumps (diameter 6.4 mm) were placed through peripheral access (femoral artery and jugular vein) and advanced under fluoroscopic guidance. The hemodynamic evolution was analyzed during the procedure and 2 h of reperfusion. Myocardial flow was assessed by colored microspheres. Differences between groups were analyzed by ANOVA for repeated measurements and post-hoc testing in case of significance.</AbstractText>All of the pump-supported animals survived the procedure, 1 of the control animals died of resistant ventricular fibrillation. At the end of the reperfusion period, the hemodynamic performance and myocardial contractility was significantly better in the pump-supported group (cardiac output: 2.4+/-0.9 vs. 3.3+/-0.9 l/min, P=0.0192; mean arterial blood pressure: 51+/-23 vs. 73+/-9 mmHg, P=0. 036; first derivative of the left ventricular pressure: 561+/-271 vs. 947+/-316 mmHg/s, P=0.0074). After the procedure, subendocardial blood flow was significantly better in all areas of the left ventricle in group 2 (0.935+/-0.427 ml/min per g vs. 0.409+/-0.183 ml/min per g in group 1; P=0.0366).</AbstractText>The supported heart is more resistant to repetitive local ischemia. Support by microaxial pumps can make beating heart surgery safer and applicable for more complex cases.</AbstractText> |
4,809 | Mechano-electric feedback in right atrium after left ventricular infarction in rats. | Left ventricular myocardial infarction (MI) can lead to alterations in hemodynamic load conditions, thereby inducing right atrial hypertrophy and dilatation associated with phenotypic modulation of cardiomyocytes, electrical abnormalities, rhythm disturbances, and atrial fibrillation. However, there is limited information on the electrophysiological basis for these events. We investigated whether atrial stretch in the setting of chronic MI modulates the electrophysiological properties of cardiomyocytes via "mechano-electric feedback", providing a mechanism for atrial arrhythmia after ventricular infarction. Five weeks after left ventricular MI (n=37), action potentials (AP) were measured in right atrial tissue preparations using a current clamp scheme, and compared to sham-operated rats (SO, n=10). Contractile activity was recorded at a preload of 1 mN, and sustained stretch was applied via a micrometer. In SO, stretch of 1.75 mN shortened repolarization at 50% and prolonged it at 90%. In MI, mechanically-induced electrical alterations were observed at a significantly lower level of stretch than in SO (0.19 mN). Sustained stretch in MI prolonged AP at 90% repolarization giving rise to stretch-activated depolarizations (SAD) near 90% repolarization (SAD90). When reaching threshold for premature APs, electrical phenomena similar to atrial fibrillations were seen in some preparations. Moreover, we observed APs with prolonged duration at 25%, 50%, and 90% repolarization where stretch induced SAD near 50%. Gadolinium used at a concentration to inhibit stretch-activated channels (40microM) suppressed mechanically-induced electrical events. In conclusion, increased susceptibility after MI to mechanical stretch may predispose atrial cardiomyocytes to arrhythmia. These mechano-electrical alterations are sensitive to gadolinium suggesting involvement of stretch-activated ion channels. |
4,810 | Nitric oxide inhibition improved myocardial metabolism independent of tissue perfusion during ischemia but not during reperfusion. | Nitric oxide (NO) is one of the important regulators of cardiac metabolism and function as well as of tissue perfusion. Myocardial NO formation is increased during ischemia and reperfusion. We investigated the roles of endogenous NO in myocardial metabolism during ischemia and reperfusion independent of tissue perfusion changes. In an open-chest pig model, a bolus infusion of 20 mg/kg of N(G)-nitro l -arginine methyl ester (l -NAME), a NO synthase inhibitor, did not alter the regional myocardial perfusion compared with a control saline injection, as measured by colored microsphares. Using(31)P-nuclear magnetic resonance spectroscopy, we showed that the tissue levels of pH and adenosine triphosphate (ATP) but not those of creatine phosphate were significantly preserved in the l -NAME group compared with the placebo group during the subsequent 15-min regional ischemia. Thus, l -NAME reduced myocardial ATP utilization during ischemia, and the mechanism underlying these effects is independent of tissue perfusion changes. However, l -NAME did not accelerate the recovery of ATP levels following reperfusion, suggesting distinct roles of endogenous NO during reperfusion. |
4,811 | Systematic review of the management of atrial fibrillation in patients with heart failure. | To systematically review the management of atrial fibrillation (AF) in patients with heart failure.</AbstractText>Studies investigating the management of AF in patients with heart failure published between 1967 to 1998 were identified using MEDLINE, the Cochrane register and Embase databases. Reference lists from relevant papers and reviews were hand searched for further papers.</AbstractText>Eight studies pertaining to acute and twenty-four pertaining to chronic AF were identified. For patients with acute AF ventricular rate control, anticoagulation and treatment of heart failure should be pursued simultaneously before cardioversion is attempted. Digoxin is relatively ineffective at controlling ventricular response and for cardioversion. Intravenous diltiazem is rapidly effective in controlling ventricular rate and limited evidence suggests it is safe. Amiodarone controls ventricular rate rapidly and increases the rate of cardioversion. There are insufficient data to conclude that immediate anti-coagulation, trans-oesophageal echocardiography to exclude atrial thrombi followed by immediate cardioversion is an appropriate strategy. Patients with chronic AF should be anti-coagulated unless contra-indications exist. It is not clear whether the preferred strategy should be cardioversion and maintenance of sinus rhythm with amiodarone or ventricular rate control of AF combined with anticoagulation to improve outcome including symptoms, morbidity and survival. Electrical cardioversion has a high initial success rate but there is also a high risk of early relapse. Amiodarone currently appears the most effective and safest therapy for maintaining sinus rhythm post-cardioversion. Digoxin is fairly ineffective at controlling ventricular rate during exercise. Addition of a beta-blocker reduces ventricular rate and improves symptoms. Whether digoxin is required in addition to beta-blockade for the control of AF in this setting is currently under investigation. If pharmacological therapy is ineffective or not tolerated then atrio-ventricular node ablation and permanent pacemaker implantation should be considered.</AbstractText>There is a paucity of controlled clinical trial data for the management of AF among patients with heart failure. The interaction between AF and heart failure means that neither can be treated optimally without treating both. Presently treatment should be on a case by case basis.</AbstractText>Copyright 2000 The European Society of Cardiology.</CopyrightInformation> |
4,812 | The effects of graded doses of endothelin-1 on coronary perfusion pressure and vital organ blood flow during cardiac arrest. | Endothelin-1 (ET-1) is a potent vasoconstrictor and has been shown to improve coronary perfusion pressure (CPP) during arrest. The effects of ET-1 on organ blood flow during arrest have not been extensively studied.</AbstractText>To investigate the effects of ET-1 on myocardial and cerebral blood flow during cardiac arrest.</AbstractText>Sixty immature swine were anesthetized and instrumented. The animals were randomized to receive one of three doses of ET-1 (50, 150, or 300 microg) or placebo with/without standard-dose epinephrine (SDE) during cardiac arrest. After a 10-minute period of no-flow ventricular fibrillation (VF), cardiopulmonary resuscitation (CPR) was performed for 3 minutes, followed by drug administration. Placebo or SDE was given every 3 minutes. Myocardial and cerebral blood flow was measured using a fluorescent microsphere technique.</AbstractText>Prearrest and CPR variables were not different between groups. Beginning 4 minutes after giving 300 microg ET-1 with or without SDE, CPP was significantly increased compared with SDE alone. Total myocardial blood flow following ET-1 administration was no different than myocardial blood flow following SDE alone. Cerebral blood flow increased 3.5 minutes after administration of 300 microg ET-1 with SDE and reached significance 9.5 minutes after drug administration when compared with SDE alone [92.5 (48.8-117.9) vs 15.6 (7.7-23) mL/min/100 g].</AbstractText>Three hundred microg ET-1 with SDE increases CPP and improves cerebral blood flow but does not improve myocardial blood flow during cardiac arrest. The peripheral effects of ET-1 significantly improve CPP and cerebral blood flow, but myocardial blood flow is not increased due to coronary vasoconstriction.</AbstractText> |
4,813 | Azimilide. | Azimilide is a potassium channel antagonist that, in contrast to existing class III antiarrhythmic agents, blocks both the rapidly (I(Kr)) and slowly (I(Ks)) activating components of the delayed rectifier potassium current. In animal and clinical studies, azimilide prolonged repolarisation by increasing the action potential duration and effective refractory period. In animal models, azimilide was effective in terminating both atrial and ventricular arrhythmias. Azimilide also demonstrated antifibrillatory efficacy in a canine model of sudden cardiac death. In patients with a history of atrial fibrillation/flutter, oral azimilide controlled arrhythmias more effectively than placebo in a 6-month randomised double-blind study. At a dosage of 125 mg once daily, azimilide significantly increased the time to first symptomatic recurrence of atrial fibrillation/flutter. However, no significant difference between placebo and azimilide was found in another study. Oral azimilide 100 mg once daily demonstrated clinically significant treatment effects in patients with paroxysmal supraventricular tachycardia. In clinical trials, azimilide was generally well tolerated and headache was the most commonly occurring adverse event. Azimilide is associated with a low incidence of proarrhythmic events, such as torsades de pointes, and few serious adverse events have been reported. |
4,814 | Increased defibrillation threshold with right-sided active pectoral can. | The aim of this study was to identify the optimal position on the chest wall to place an implant able cardioverter defibrillator in a two-electrode system, consisting of a right ventricular electrode and active can.</AbstractText>Defibrillation thresholds (DFT) were measured in 10 anaesthetised pigs (weight 33-45 kg). An Angeflextrade mark lead was introduced transvenously to the right ventricular apex. The test-can (43 cc) was implanted submuscularly in each of four locations: left pectoral (LP), right pectoral (RP), left lateral (LL) and apex (A). The sequence in which the four locations were tested was randomized. Ventricular fibrillation (VF) was induced using 60 Hz alternating current. Rectangular biphasic shocks were delivered 10 seconds after VF induction. The DFT was measured using a modified four-reversal binary search. The results of the four configurations were: LP, 14.6+/- 4.0 J; RP, 18.8+/- 4.2 J; LL, 14.7+/- 4.1 J; A, 14.9+/- 3.1 J. Repeated measures analysis of variance showed that the DFT of RP was significantly higher than LP, LL and A (p < 0.05).</AbstractText>Implanting an active can in the RP position increases the DFT by 29% compared to LP, LL and A sites. The can position on the left thorax does not appear to have a significant influence on DFT.</AbstractText> |
4,815 | Endovascular neural stimulation via a novel basket electrode catheter: comparison of electrode configurations. | We previously showed that parasympathetic stimulation by a basket electrode catheter (BEC) positioned in the superior vena cava (SVC) can slow sinus rate (SR) or ventricular response (VR) during atrial fibrillation (AF). In 11 dogs, anesthetized with Na-pentobarbital, standard ECG leads II and aVR, blood pressure and right atrial electrograms were continuously monitored. Two different BEC configurations (B1, B2) were tested in the SVC. B1 consisted of five metal splines, each 3 cm in length. Stimulation was applied between adjacent splines. B2 consisted of 2 electrodes at opposite ends of each of 5 splines and a larger electrode at the middle of each spline. Stimulation was delivered between the two end electrodes and the middle electrode on the same arm. Stimulation consisted of square wave stimuli, each 0.1 msec duration, frequency 20 Hz at voltages from 1-40 V. Six dogs were studied with B1 and five were studied with the B2 configuration. The average voltage required to produce a 50% decrease in heart rate was 22+/- 12 V when stimulating between adjacent splines (B1) compared to 10+/- 5 V when stimulating along a single spline (B2), a 55% decrease (p</=0.05). During AF, the voltage required to reduce the average ventricular rate to 100 beats/min was 19+/- 13 V for B1 and 8+/- 5 V for B2, a 58% reduction (p</=0.05). Thus, the significant difference between B1 and B2 and in slowing SR or VR during AF was probably due to a greater current density delivered with B2 to the endovascular wall and adjacent neural elements. |
4,816 | Electrophysiological characterization of SCN5A mutations causing long QT (E1784K) and Brugada (R1512W and R1432G) syndromes. | Familial long QT syndrome (LQTS) and Brugada syndrome are two distinct human hereditary cardiac diseases known to cause ventricular tachyarrhythmias (torsade de pointes) and idiopathic ventricular fibrillation, respectively, which can both lead to sudden death.</AbstractText>In this study we have identified and electrophysiologically characterized, in patients having either LQTS or Brugada syndrome, three mutations in SCN5A (a cardiac sodium channel gene).</AbstractText>The mutant channels were expressed in a mammalian expression system and studied by means of the patch clamp technique.</AbstractText>The R1512W mutation found in our first patient diagnosed with Brugada syndrome produced a slowing of both inactivation and recovery from inactivation. The R4132G mutation found in our second patient who also presented Brugada syndrome, resulted in no measurable sodium currents. Both Brugada syndrome patients showed ST segment elevation and right bundle-branch block, and had experienced syncopes. The E1784K mutation found in the LQTS showed a persistent inward sodium current, a hyperpolarized shift of the steady-sate inactivation and a faster recovery from inactivation.</AbstractText>The different clinical manifestations of these three mutations most probably originate from the distinct electrophysiological abnormalities of the mutant cardiac sodium channels reported in this study.</AbstractText> |
4,817 | Pacing after shocks stronger than the upper limit of vulnerability: impact on fibrillation induction. | After upper-limit-of-vulnerability (ULV) shocks of the same strength and coupling interval (CI) during the T wave, (1) the epicardial activation pattern (EAP) for the first postshock cycle is indistinguishable between shocks that do (VF) and do not (NoVF) induce ventricular fibrillation (VF) and (2) >/=3 cycles in rapid succession always occur during VF but not during NoVF episodes. To study the role of these rapid cycles, rapid pacing was performed after a shock stronger than the ULV that by itself did not induce rapid cycles and VF.</AbstractText>A 504-electrode sock was sutured to the heart in 6 pigs to map EAPs. The S2 shock strength and S1-S2 CI at the ULV were determined by T-wave scanning with an up/down protocol. Ten shocks 50 to 100 V above the ULV (aULV) were delivered at the same S1-S2 CI to confirm that VF was not induced. Then, the postshock interval after aULV shocks was scanned with an S3 pacing stimulus from the LV apex until the shortest S2-S3 CI that captured was reached. This was repeated for S4, S5, etc, until VF was induced. To induce VF, 3 pacing stimuli (S3-S5) with progressively shorter CIs were required; S3 or S3, S4 never induced VF. After cycle S5, which induced VF, 2 EAP types occurred: focal (74%) and reentrant (26%).</AbstractText>At least 3 cycles with short CIs are necessary for VF induction after aULV shocks. Cycles S3-S4 may create the substrate for cycle S5 to initiate VF.</AbstractText> |
4,818 | Influence of postshock epicardial activation patterns on initiation of ventricular fibrillation by upper limit of vulnerability shocks. | Shocks of identical strength and timing sometimes induce ventricular fibrillation (VFI) and other times do not (NoVFI). To investigate this probabilistic behavior, a shock strength near the upper limit of vulnerability, ULV(50), was delivered to yield equal numbers of VFI and NoVFI episodes.</AbstractText>In 6 pigs, a 504-electrode sock was pulled over the ventricles. ULV(50) was determined by scanning the T wave. S(1) pacing was from the right ventricular apex. Ten S(2) shocks of approximate ULV(50) strength were delivered at the same S(1)-S(2) coupling interval. Intercycle interval (ICI) and wave front conduction time (WCT) were determined for the first 5 postshock cycles. ICI and the WCT of cycle 1 were not different for VFI versus NoVFI episodes (P=0.3). Beginning at cycle 2, ICI was shorter and WCT was longer for VFI than NoVFI episodes (P<0.05).</AbstractText>The first cycle after shocks of the same strength (ULV(50)) delivered at the same time has the same activation pattern regardless of shock outcome. During successive cycles, however, a progressive decrease in ICI and increase in WCT occur during VFI but not NoVFI episodes. These findings suggest shock outcome is (1) deterministic but exquisitely sensitive to differences in electrophysiological state at the time of the shock that are too small to detect or (2) probabilistic and not determined until after the first postshock cycle.</AbstractText> |
4,819 | Ventricular defibrillation with triphasic waveforms. | It has been reported that triphasic defibrillation waveforms cause less myocardial injury than biphasic waveforms. This study compared the defibrillation thresholds (DFTs) of triphasic and biphasic waveforms.</AbstractText>++DFTs were determined for a transvenous lead system and a 300-microF-capacitor defibrillator. In 8 pigs (group 1), DFTs were determined for 5 triphasic waveforms with tilts of 80%, 83%, and 86% and for 1 biphasic waveform. DFTs were determined in another 8 pigs (group 2) for 2 triphasic and 4 biphasic waveforms with tilts of 43%, 49%, and 56%. In both groups, a biphasic waveform from a 140-microF-capacitor defibrillator was also evaluated, and both shock polarities were tested for each waveform. In group 1, with the 300-microF-capacitor defibrillator, the leading-edge voltage and energy stored at DFT were significantly lower for triphasic waveforms with phase-duration ratios of 50/33/17 and an anode at the right ventricular electrode for phase 1 than for biphasic waveforms (P<0.001). In group 2, the stored energy of triphasic waveforms with 56% and 49% tilt was significantly lower than that of biphasic waveforms with the same tilts for anodal but not cathodal phase 1 at the right ventricular electrode. Electrode polarity significantly affected the DFT of triphasic waveforms for both studies.</AbstractText>Some 80% tilt triphasic waveforms defibrillate more efficiently than biphasic waveforms with a 300-microF-capacitor defibrillator. The triphasic waveforms for both groups were not superior to 140-microF-capacitor biphasic waveforms. The efficacy of triphasic waveforms depends on phase durations and electrode polarity.</AbstractText> |
4,820 | Canadian implantable defibrillator study (CIDS) : a randomized trial of the implantable cardioverter defibrillator against amiodarone. | Patients surviving ventricular fibrillation (VF) or sustained ventricular tachycardia (VT) are at a high risk of death due to a recurrence of arrhythmia. The implantable cardioverter defibrillator (ICD) terminates VT or VF, but it is not known whether this device prolongs life in these patients compared with medical therapy with amiodarone.</AbstractText>A total of 659 patients with resuscitated VF or VT or with unmonitored syncope were randomly assigned to treatment with the ICD or with amiodarone. The primary outcome measure was all-cause mortality, and the secondary outcome was arrhythmic death. A total of 328 patients were randomized to receive an ICD. A thoracotomy was done in 33, no ICD was implanted in 18, and the rest had a nonthoracotomy ICD. All 331 patients randomized to amiodarone received it initially. At 5 years, 85.4% of patients assigned to amiodarone were still receiving it at a mean dose of 255 mg/day, 28.1% of ICD patients were also receiving amiodarone, and 21.4% of amiodarone patients had received an ICD. A nonsignificant reduction in the risk of death was observed with the ICD, from 10.2% per year to 8.3% per year (19.7% relative risk reduction; 95% confidence interval, -7.7% to 40%; P=0.142). A nonsignificant reduction in the risk of arrhythmic death was observed, from 4.5% per year to 3.0% per year (32.8% relative risk reduction; 95% confidence interval, -7.2% to 57.8%; P=0.094).</AbstractText>A 20% relative risk reduction occurred in all-cause mortality and a 33% reduction occurred in arrhythmic mortality with ICD therapy compared with amiodarone; this reduction did not reach statistical significance.</AbstractText> |
4,821 | Transthoracic cardioversion of atrial fibrillation: comparison of rectilinear biphasic versus damped sine wave monophasic shocks. | Clinical studies have shown that biphasic shocks are more effective than monophasic shocks for ventricular defibrillation. The purpose of this study was to compare the efficacy of a rectilinear biphasic waveform with a standard damped sine wave monophasic waveform for the transthoracic cardioversion of atrial fibrillation.</AbstractText>In this prospective, randomized, multicenter trial, patients undergoing transthoracic cardioversion of atrial fibrillation were randomized to receive either damped sine wave monophasic or rectilinear biphasic shocks. Patients randomized to the monophasic protocol (n=77) received sequential shocks of 100, 200, 300, and 360 J. Patients randomized to the biphasic protocol (n=88) received sequential shocks of 70, 120, 150, and 170 J. First-shock efficacy with the 70-J biphasic waveform (60 of 88 patients, 68%) was significantly greater than that with the 100-J monophasic waveform (16 of 77 patients, 21%, P<0.0001), and it was achieved with 50% less delivered current (11+/-1 versus 22+/-4 A, P<0.0001). Similarly, the cumulative efficacy with the biphasic waveform (83 of 88 patients, 94%) was significantly greater than that with the monophasic waveform (61 of 77 patients, 79%; P=0.005). The following 3 variables were independently associated with successful cardioversion: use of a biphasic waveform (relative risk, 4.2; 95% confidence intervals, 1.3 to 13.9; P=0.02), transthoracic impedance (relative risk, 0.64 per 10-Omega increase in impedance; 95% confidence intervals, 0.46 to 0.90; P=0.005), and duration of atrial fibrillation (relative risk, 0.97 per 30 days of atrial fibrillation; 95% confidence intervals, 0.96 to 0.99; P=0.02).</AbstractText>For transthoracic cardioversion of atrial fibrillation, rectilinear biphasic shocks have greater efficacy (and require less energy) than damped sine wave monophasic shocks.</AbstractText> |
4,822 | High-frequency periodic sources underlie ventricular fibrillation in the isolated rabbit heart. | The mechanism(s) underlying ventricular fibrillation (VF) remain unclear. We hypothesized that at least some forms of VF are not random and that high-frequency periodic sources of activity manifest themselves as spatiotemporal periodicities, which drive VF. Twenty-four VF episodes from 8 Langendorff-perfused rabbit hearts were studied using high-resolution video imaging in conjunction with ECG recordings and spectral analysis. Sequential wavefronts that activated the ventricles in a spatially and temporally periodic fashion were identified. In addition, we analyzed the lifespan and dynamics of wavelets in VF, using a new method of phase mapping that enables identification of phase singularity points (PSs), which flank individual wavelets. Spatiotemporal periodicity was found in 21 of 24 episodes. Complete reentry on the epicardial surface was observed in 3 of 24 episodes. The cycle length of discrete regions of spatiotemporal periodicity correlated highly with the dominant frequency of the optical pseudo-ECG (R(2)=0.75) and with the global bipolar electrogram (R(2)=0.79). The lifespan of PSs was short (14.7+/-14.4 ms); 98% of PSs existed for <1 rotation. The mean number of waves entering (6.50+/-0.69) exceeded the mean number of waves that exited our mapping field (4.25+/-0.56; P<0.05). These results strongly suggest that ongoing stable sources are responsible for the majority of the frequency content of VF and therefore play a role in its maintenance. In this model, multiple wavelets resulting from wavebreaks do not appear to be responsible for the sustenance of this arrhythmia, but are rather the consequence of breakup of high-frequency activation from a dominant reentrant source. |
4,823 | Development of a novel biomarker of free radical damage in reperfusion injury after cardiac arrest. | In a porcine model of cardiopulmonary resuscitation (CPR), we investigated changes in the plasma levels of 8-iso-PGF(2alpha), a marker for oxidative injury, and 15-keto-dihydro-PGF(2alpha), an inflammatory response indicator during the post-resuscitation period after cardiac arrest. Twelve piglets were subjected to either 2 or 5 min (VF2 and VF5 group) of ventricular fibrillation (VF) followed by 5 min of closed-chest CPR. Six piglets without cardiac arrest were used as controls. In VF5 group, 8-iso-PGF(2alpha) in the jugular bulb plasma (draining the brain) increased four-fold. Jugular bulb 8-iso-PGF(2alpha) in the control group remained unchanged. The 15-keto-dihydro-PGF(2alpha) also increased four-fold in the VF5 group. Thus, 8-iso-PGF(2alpha) and 15-keto-dihydro-PGF(2alpha) measurements in jugular bulb plasma may be used as biomarkers for quantification of free radical catalyzed oxidative brain injury and inflammatory response in reperfusion injury. |
4,824 | Opposite change with ischaemia in the antifibrillatory effects of class I and class IV antiarrhythmic drugs resulting from the alteration in ion transmembrane exchanges related to depolarization. | It is known that class I antiarrhythmic drugs lose their antifibrillatory activity with severe ischaemia, whereas class IV antiarrhythmic drugs acquire such activity. Tachycardia, which is also a depolarizing factor, has recently been shown to give rise to an alteration of ion transmembrane exchanges which is particularly marked in the case of calcium. This leads one to wonder if the change in antifibrillatory activity of antiarrhythmic drugs caused by ischaemia depends on the same process. The change in antifibrillatory activity was studied in normal conditions ranging to those of severe ischaemia with a class I antiarrhythmic drug, flecainide (1.00 mg x kg(-1) plus 0.04 mg x kg(-1)x min(-1), a sodium channel blocker, and a class IV antiarrhythmic drug, verapamil (50 microg x kg(-1) plus 2 microg x kg(-1) x min(-1)), a calcium channel blocker. The experiments were performed in anaesthetized, open-chest pigs. The resulting blockade of each of these channels was assessed at the end of ischaemic periods of increasing duration (30, 60, 120, 180, 300, and 420 s) by determining the ventricular fibrillation threshold (VFT). VFT was determined by means of trains of diastolic stimuli of 100 ms duration delivered by a subepicardial electrode introduced into the myocardium (heart rate 180 beats per min). Ischaemia was induced by completely occluding the left anterior descending coronary artery. The monophasic action potential was recorded concurrently for the measurement of ventricular conduction time (VCT). The monophasic action potential duration (MAPD) varied with membrane polarization of the fibres. The blockade of sodium channels by flecainide, which normally raises VFT (7.0 +/- 0.4 to 13.8 +/- 0.8 mA, p < 0.001) and lengthens VCT (28 +/- 3 to 44 +/- 5 ms, p < 0.001), lost its effects in the course of ischaemia. This resulted in decreased counteraction of the ischaemia-induced fall of VFT and decreased aggravation of the ischaemia-induced lengthening of VCT. The blockade of calcium channels, which normally does not alter VFT (between 7.2 +/- 0.6 and 8.4 +/- 0.7 mA, n.s.) or VCT (between 30 +/- 2 and 34 +/- 3 ms, n.s.), slowed the ischaemia-induced fall of VFT. VFT required more time to reach 0 mA, thus delaying the onset of fibrillation. Membrane depolarization itself was opposed as the shortening of MAPD and the lengthening of VCT were also delayed. Consequently there is a progressive decrease in the role played by sodium channels during ischaemia in the rhythmic systolic depolarization of the ventricular fibres. This reduces or suppresses the ability of sodium channel blockers to act on excitability or conduction, and increases the role of calcium channel blockers in attenuating ischaemia-induced disorders. |
4,825 | [The best of cardiac pacing in 1999]. | Since the first clinical application to man forty years ago, for the treatment of bradycardia, cardiac pacing has been the object of continuous technological innovation in parallel with those in electronics and computerisation. However, independently of these expected advances, there has been a surprising widening of the field of application of pacing into those of haemodynamics and rhythmology. The recent publication of the long-term results of the Pacing in Cardiomyopathy (PIC) study confirmed the sustained decrease of intraventricular pressure gradient, of NYHA functional stage and improved quality of life of patients with hypertrophic obstructive cardiomyopathy paced in the DDD mode. The investigators also underlined the placebo effect of the pacemaker. The decrease in risk of sudden death and the reduction in ventricular remodelling have not been demonstrated yet. More recently, biventricular pacing has been proposed for the treatment of dilated cardiomyopathy and a French study showed a long-term improvement in NYHA stage and effort capacity. Several prospective randomised trials are under way to validate this indication. Acute haemodynamic evaluations have confirmed the efficacy of biventricular stimulation but also underline the value of left ventricular pacing alone. The effects on mortality, the selection of patients and the optimal configuration of pacing remain to be defined. In the field of prevention of atrial arrhythmias, the results of the multicenter SYNBIAPACE study, investigating biatrial pacing in patients with interatrial conduction defects, only showed a tendency to an increase in the delay before recurrence of atrial fibrillation. The value of the memory functions of pacemakers and the algorithms of prevention of atrial arrhythmias are still under investigation. Haemodynamic transducers have been introduced in some recent pacemakers to assess myocardial contractility and have applications in the evaluation of different pacing modes and in the optimisation of the atrioventricular interval. Their value in the treatment of neurocardiogenic syncope is under evaluation. In conclusion, it is not overoptimistic to imagine that, in the near future, the cardiac pacemaker will be part of a "control and treatment system" well over the limits of treating patients with bradycardia. |
4,826 | [The best of arrhythmias in 1999]. | Recent studies of atrial fibrillation, or rather "atrial fibrillations", have been based on focal atrial fibrillation which seems to be one of the commonest forms of paroxysmal atrial fibrillation. This observation led to the possibility of ablative therapy, usually near the pulmonary veins. Technological advances are awaited before a wider diffusion of this therapy becomes possible. In the field of defibrillation, the MUSTT study demonstrated the value of implantable defibrillators in the prevention of sudden death, in this trial in the case of asymptomatic high risk patients after myocardial infarction, with a decreased ejection fraction and non-sustained ventricular tachycardia. Two large scale randomised controlled trials (MERIT-HF and CIBIS II) have confirmed the value of betablockers in preventing sudden death, in patients with moderate or severe cardiac failure in association with classical treatment by diuretics, ACE inhibitors and digitalis. Similarly, for spironolactone, the RALES study showed a reduced incidence of sudden death in cardiac failure, as its physiopathological modes of action suggested. New techniques of three-dimensional mapping have confirmed their value. Finally, significant progress has been made in the field of genetics of cardiac arrhythmias, indicating that, in years to come, it will be possible to identify most of the genes responsible for conditions predisposing to arrhythmias. |
4,827 | Potentialities and problems of a novel bilateral ventricular assist system without thoracotomy. | Mechanical cardiac assistance can be critical in saving the lives of patients with acute cardiac failure. However, currently used methods of ventricular assistance require advanced technical knowledge and equipment, and only small numbers of patients can be provided with them. Our aim was to develop new cannulas to construct a less invasive biventricular assist system that would permit easy application without thoracotomy. We prepared 2 centrifugal pumps and 4 uniquely shaped cannulas and conducted experiments to investigate the potential and problems of the system. In the first experiment, the system was attached to 6 dogs with ventricular fibrillation to confirm whether our system could maintain cardiac output. In the second experiment, the system was installed for 3 days in 3 goats, and changes in aminotransferases, BUN, creatinine, and plasma free hemoglobin levels were examined. In Experiment 1, it was demonstrated that the system was able to maintain circulation in dogs. In Experiment 2, although the flow rate of the pumps was maintained over 3 days, increased hemolysis and deteriorating renal function were observed. Although these problems need to be solved, the system was still helpful in the management of acute biventricular failure for short periods and may be clinically useful in the near future. |
4,828 | Resuscitation from fulminant myocarditis associated with refractory ventricular fibrillation. | Resuscitation was possible in a case of fulminant myocarditis with refractory ventricular fibrillation (Vf) using a percutaneous cardiopulmonary support system (PCPS). A 46-year old Japanese man suddenly experienced cardiopulmonary dysfunction shortly after the onset of flu symptoms, was promptly diagnosed as having fulminant myocarditis and PCPS was immediately initiated. On the second day in the hospital, refractory Vf occurred, which lasted for approximately 2h despite repeated efforts to terminate it. Finally, a large dose of steroids was administered. From the third day of hospitalization and onwards, the Vf disappeared totally. The patient completely recovered from such a serious state in 6 months. During the following 3 years, he has had no clinical symptoms of worsening. As in this case demonstrates, most myocarditis is curable and invasive measures are very helpful in rescuing patients from the fulminant type with refractory Vf. |
4,829 | Spatial heterogeneity in refractoriness as a proarrhythmic substrate: theoretical evaluation by numerical simulation. | Spatial heterogeneity in the refractoriness of the ventricular myocardium due to a regionally prolonged refractory period has often been observed in patients with cardiovascular disease as the substrate for functional reentrant tachyarrhythmias. The present study sought to determine how functional reentrant activity could occur due to the spatial heterogeneity, using numerical simulation. Spatial heterogeneity in the refractoriness was introduced into a two-dimensional array by the regionally prolonged refractory period expressed as a square cluster. Double stimulation, conducted from a single source, was introduced into 4 types of matrices, which differed in their level of spatial heterogeneity. A pseudoelectrocardiogram was calculated from these matrices. Spiral waves were initiated in all the matrices except for the lowest heterogeneous matrix. A vulnerable window of the coupling interval, which induced spiral waves, was observed and was wider in proportion to the level of the heterogeneity. A higher level of heterogeneity and more limited range of coupling intervals were required to sustain the spiral waves. Furthermore, in the pseudoelectrocardiogram, sustained spiral waves exhibited a waveform like that in torsades de pointes (TdP) and their transformation into ventricular fibrillation (VF). Spatial heterogeneity in refractoriness due to a regionally prolonged refractory period could be a substrate for functional reentrant tachyarrhythmias, possibly including TdP and VF. |
4,830 | Effect of beta-blocker therapy on severe ventricular arrhythmias in patients with idiopathic dilated cardiomyopathy. | Beta-blocker therapy has been shown to improve cardiac function and prognosis in patients with idiopathic dilated cardiomyopathy (DCM). However, whether beta-blockers reduce severe ventricular arrhythmias and sudden cardiac death has not been clarified. The present study was designed to investigate the effects of beta-blockers on non-sustained ventricular tachycardia (VT) and sudden cardiac death in patients with DCM. Sixty-five patients with DCM treated with diuretics, digitalis and angiotensin-converting enzyme inhibitors were assigned to receive beta-blockers (n = 33) or not (n = 32). Mean follow-up was 53+/-30 months. The echocardiographic indices of cardiac function, the incidence of non-sustained VT on Holter monitoring electrocardiograms, and sudden cardiac death rate were compared between the 2 groups. Comparable improvement in cardiac function on echocardiograms was found in the 2 treatment groups. The patient group treated with beta-blockers showed a significant reduction in the prevalence of VT (from 43 to 15%, p<0.05) and the development of new episodes of VT (5 vs. 16%) compared to the group without beta-blockers. The sudden cardiac death rate did not differ between the 2 groups. The results of the present study suggest that beta-blockers are effective in reducing severe ventricular arrhythmias in patients with DCM. |
4,831 | Comparative effects of pretreatment with captopril and losartan on cardiovascular protection in a rat model of ischemia-reperfusion. | We sought to assess the comparative effects of pretreatment with captopril and losartan on myocardial infarct size and arrhythmias in a rat model of ischemia-reperfusion.</AbstractText>Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) inhibit the renin-angiotensin system in different ways. However, the comparative effects of pretreatment with ACE inhibitors or ARBs on acute myocardial infarct size and arrhythmias are unknown.</AbstractText>We randomly assigned 117 female Sprague-Dawley rats into three groups: group N was the normal control; group C was given 40 mg/kg body weight per day of captopril in drinking water; and group L was given 40 mg/kg per day of losartan in drinking water. After 10 weeks of pretreatment, 25 rats in each group were subjected to 17 min of left anterior descending coronary artery occlusion and 2 h of reperfusion with hemodynamic and electrocardiographic monitoring. Fourteen rats in each group had blood samples drawn and aortic rings removed to study vascular reactivity.</AbstractText>Mortality during ischemia and reperfusion was lower in combined groups L and C than in group N (4.2% vs. 19.2%, p = 0.042). Rats treated with losartan had significantly higher levels of angiotensin II in their plasma. Hemodynamic variables were not significantly different among the three groups. The thresholds of ventricular fibrillation (VF) before occlusion and after reperfusion were significantly higher in groups L and C than in group N (1.99 +/- 0.24 and 1.93 +/- 0.27 vs. 1.23 + 0.17 mA, p = 0.04; 2.13 +/- 0.25 and 1.78 +/- 0.22 vs. 0.95 +/- 0.11 mA, p = 0.001). The average episodes of ventricular tachycardia (VT) and VF per rat were significantly less in groups L and C than in group N (0.96 +/- 0.2 and 1.2 +/- 0.3 vs. 2.8 + 0.4 mA, p < 0.001). Myocardial infarct size was significantly smaller in groups L and C than in group N (34 +/- 3% and 35 +/- 3% vs. 44 +/- 3%, p = 0.031, 0.043). Endothelium-dependent vasorelaxation induced by a calcium ionophore (A23187) was increased in both groups but was only statistically significant in group C (p = 0.020).</AbstractText>Losartan and captopril have similar cardiovascular protective effects in a rat model of ischemia-reperfusion. They increased the threshold of VF, decreased mortality and decreased episodes of VT and VF, as well as decreased myocardial infarct size.</AbstractText> |
4,832 | Combined assessment of T-wave alternans and late potentials used to predict arrhythmic events after myocardial infarction. A prospective study. | The aim of the present study was to determine whether the combination of two markers that reflect depolarization and repolarization abnormalities can predict future arrhythmic events after acute myocardial infarction (MI).</AbstractText>Although various noninvasive markers have been used to predict arrhythmic events after MI, the positive predictive value of the markers remains low.</AbstractText>We prospectively assessed T-wave alternans (TWA) and late potentials (LP) by signal-averaged electrocardiogram (ECG) and ejection fraction (EF) in 102 patients with successful determination results after acute MI. The TWA was analyzed using the power-spectral method during supine bicycle exercise testing. No antiarrhythmic drugs were used during the follow-up period. The study end point was the documentation of ventricular arrhythmias.</AbstractText>The TWA was present in 50 patients (49%), LP present in 21 patients (21%), and an EF <40% in 28 patients (27%). During a follow-up period of 13 +/- 6 months, symptomatic, sustained ventricular tachycardia or ventricular fibrillation occurred in 15 patients (15%). The event rates were significantly higher in patients with TWA, LP, or an abnormal EF. The sensitivity and the negative predictive value of TWA in predicting arrhythmic events were very high (93% and 98%, respectively), whereas its positive predictive value (28%) was lower than those for LP and EF. The highest positive predictive value (50%) was obtained when TWA and LP were combined.</AbstractText>The combined assessment of TWA and LP was associated with a high positive predictive value for an arrhythmic event after acute MI. Therefore, it could be a useful index to identify patients at high risk of arrhythmic events.</AbstractText> |
4,833 | Reversal of atrial electrical remodeling after cardioversion of persistent atrial fibrillation in humans. | Although atrial electrical remodeling has been studied extensively in animal models, the reversibility of this phenomenon after termination of clinical atrial fibrillation (AF) has not been demonstrated. We aimed to examine this important question of reversibility by using AF cycle length (AFCL) and coupling intervals of atrial premature beats after cardioversion as measures of atrial refractoriness.</AbstractText>We measured AFCL at the right atrial appendage and distal coronary sinus before attempting internal cardioversion in 39 patients with persistent AF. Patients were monitored by daily transtelephonic recordings after discharge and admitted rapidly for repeat internal cardioversion if there was spontaneous AF recurrence. Measurements of AFCL were repeated immediately before repeat cardioversions in the 17 patients who had recurrence of AF. There was an increase in AFCL from the initial cardioversion to that measured at the time of first AF recurrence at both the right atrial appendage (161+/-22 vs 167+/-26 ms, P=0.05) and distal coronary sinus (162+/-20 vs 168+/-22 ms, P=0.01) sites. The magnitude of increase in AFCL was positively correlated with duration of sinus rhythm before AF recurrence (r=0.524, P=0.001). Other measures of refractoriness (shortest coupling interval of atrial premature beats and directly measured refractory periods after cardioversion) also increased from initial to subsequent cardioversions.</AbstractText>These findings demonstrate that changes in atrial electrophysiology associated with chronic AF in humans are reversible after cardioversion and that the extent of this reversal is dependent on the duration of sinus rhythm after cardioversion.</AbstractText> |
4,834 | Clinical outcomes after ablation and pacing therapy for atrial fibrillation : a meta-analysis. | Radiofrequency ablation of the atrioventricular node and permanent pacing are used for symptomatic relief in patients with medically refractory atrial fibrillation. In this study, meta-analysis was used to clarify clinical outcomes and survival after ablation and pacing therapy using data from the published literature.</AbstractText>We used 21 studies with a total of 1181 patients in the meta-analysis. All patients had medically refractory atrial tachyarrhythmias, primarily atrial fibrillation (97%). Nineteen measures of clinical outcome, encompassing quality of life, ventricular function, exercise duration, and healthcare use, were derived from the studies. The meta-analysis demonstrated significant improvement after ablation and pacing therapy in all outcome measures except fractional shortening, which demonstrated a trend toward improvement (P=0.08). Ejection fraction did show significant improvement (P<0.001). The calculated 1-year total and sudden death mortality rates after ablation and pacing therapy were 6.3% and 2.0%, respectively.</AbstractText>Ablation and pacing therapy improves a broad range of clinical outcomes for patients with medically refractory atrial fibrillation. The calculated 1-year mortality rates after this therapy are low and comparable with medical therapy.</AbstractText> |
4,835 | Terminal warm blood cardioplegia improves the recovery of myocardial electrical activity. A retrospective and comparative study. | The effect of terminal warm blood cardioplegia was analyzed in 191 patients undergoing either coronary artery bypass grafting (CABG) or prosthetic heart valve replacement between Jan. 1990 and Dec. 1995.</AbstractText>Patients were subdivided into 3 historical cohorts based on the method of myocardial protection: Group A (n = 106), multidose cold crystalloid glucose-potassium cardioplegia, alone; Group B (n = 37), cold crystalloid glucose-potassium cardioplegia plus terminal warm blood cardioplegia, Group C (n = 48), cardioplegia induction with cold crystalloid glucose-potassium cardioplegia, maintenance with multidose cold blood cardioplegia, and terminal warm blood cardioplegia.</AbstractText>Of patients undergoing CABG, 5.6% of group A, 70.4% of group B, and 86.7% of group C spontaneously resumed sinus rhythm after aortic declamping, as did 9.1% of group A, 60.0% of group B, and 55.6% of group C of patients undergoing prosthetic heart valve replacement. The incidence of spontaneous recovery was significantly better in groups B and C than in group A (p < 0.05). Over 90% of patients without terminal warm blood cardioplegia developed ventricular fibrillation or tachycardia requiring electrical cardioversion (p < 0.05). Postoperatively, patients without terminal warm blood cardioplegia required temporary epicardial pacing more frequently than those with terminal warm blood cardioplegia (p < 0.05). In patients undergoing prosthetic heart valve replacement, groups B and C, the incidence of postoperative atrial fibrillation was significantly lower than in group A.</AbstractText>Terminal warm blood cardioplegia thus promoted better postoperative electrophysiological cardiac recovery.</AbstractText> |
4,836 | [Diagnostic usefulness of KL-6 measurements in patients with pulmonary complications after administration of amiodarone]. | Amiodarone-induced pulmonary toxicity is one of the major complications in patients receiving administration of amiodarone. KL-6 is a useful indicator to evaluate the activity of interstitial pneumonitis. We studied the clinical utility of KL-6 as a marker for amiodarone-induced pulmonary toxicity. We investigated 6 patients in whom chest radiography revealed abnormal consolidations after administration of amiodarone from 1997 to 1999. All patients were male aged 56 to 76 years (mean 66 +/- 7 years). The indications for amiodarone included sustained ventricular tachycardia in 5 patients and atrial fibrillation in one patient with refractory heart failure. The mean left ventricular ejection fraction was 31 +/- 12% (22-52%). KL-6 levels were measured by a sandwich type enzyme immunoassay using a murine monoclonal antibody (KL-6 antibody), and the cutoff level was determined at 520 U/ml. Complications occurred from 17 days to 45 months after treatment with amiodarone. The KL-6 levels were abnormally high (2,100 and 3,000 U/ml) in 2 patients with amiodarone-induced pneumonitis but under the cutoff level in the non-pneumonitis patients. In one patient with amiodarone-induced pneumonitis, the KL-6 level increased from 695 to 2,100 U/ml concurrently with worsening interstitial changes shown by high resolution computed tomography. We conclude that KL-6 has practical uses as a marker for the detection and evaluation of amiodarone-induced pulmonary toxicity. |
4,837 | Safety, hemodynamic profile, and feasibility of dobutamine stress technetium myocardial perfusion single-photon emission CT imaging for evaluation of coronary artery disease in the elderly. | Cardiovascular disease is the leading cause of morbidity and mortality in the elderly. The evaluation of coronary artery disease by exercise stress testing is frequently limited by the patient's inability to exercise. Although pharmacologic stress testing with dobutamine is an alternative, the safety of dobutamine myocardial perfusion scintigraphy in the elderly has not been previously studied.</AbstractText>We studied the safety and feasibility of dobutamine (up to 40 microg/kg/min)-atropine (up to 1 mg) stress myocardial perfusion scintigraphy using technetium single-photon emission CT imaging in 227 patients > or = 70 years old (mean +/- SD age, 75 +/- 4 years). A control group of 227 patients < 70 years old (mean age, 55 +/- 11 years; matched for gender, prevalence of previous infarction, beta-blocker therapy, and severity of resting perfusion abnormalities) was studied to assess age-related differences in the safety and the hemodynamic response. A feasible test was defined as the achievement of the target heart rate and/or an ischemic end point (angina, ST-segment depression, or reversible perfusion abnormalities).</AbstractText>No myocardial infarction or death occurred during the test. The target heart rate was achieved more frequently in the elderly patients (87% vs 79%; p < 0.05). The elderly patients had a higher prevalence of supraventricular tachycardia (7% vs 1%; p < 0.005) and premature ventricular contraction (74% vs 32%; p < 0.005) during the test, as compared to the younger patients. There was a trend to a higher prevalence of ventricular tachycardia (5% vs 2%) and atrial fibrillation (3% vs 0.4%) in the elderly patients. Arrhythmias were terminated spontaneously by termination of dobutamine infusion or by administration of metoprolol. Independent predictors of supraventricular tachyarrhythmias and ventricular tachycardia were older age (p < 0.001; chi(2), 9.8) and myocardial perfusion defect score at rest (p < 0.01; chi(2), 6.8) respectively, by using a multivariate analysis of clinical and stress test variables. Elderly patients had a higher prevalence of systolic BP drop > 20 mm Hg during the test (37% vs 12%; p < 0.05). The test was terminated due to hypotension in 2% of the elderly patients and in 1% of the control group. Age was the most powerful predictor of hypotension (p < 0.005; chi(2), 10.3). The test was considered feasible in 216 elderly patients (95%) and in 209 patients of the control group (92%).</AbstractText>Dobutamine-atropine stress myocardial perfusion scintigraphy is a highly feasible method for the evaluation of coronary artery disease in the elderly. Elderly patients have a higher risk for developing hypotension and supraventricular tachyarrhythmias during a dobutamine stress test. However, dobutamine-induced hypotension is often asymptomatic and rarely necessitates the termination of the test.</AbstractText> |
4,838 | Brugada syndrome and sudden cardiac death in children. | In five children from the same family who died after unexplained cardiac arrest, Brugada syndrome syndrome was suspected based on the transient manifestation of the typical electrocardiogram pattern in one of them. A mutation in the cardiac sodium-channel confirmed the diagnosis of Brugada syndrome, which suggests that this disease may cause sudden death in children. |
4,839 | Influence of positive airway pressure on the pressure gradient for venous return in humans. | To study the effect of positive airway pressure (Paw) on the pressure gradient for venous return [the difference between mean systemic filling pressure (Pms) and right atrial pressure (Pra)], we investigated 10 patients during general anesthesia for implantation of defibrillator devices. Paw was varied under apnea from 0 to 15 cmH(2)O, which increased Pra from 7.3 +/- 3.1 to 10.0 +/- 2.3 mmHg and decreased left ventricular stroke volume by 23 +/- 22%. Episodes of ventricular fibrillation, induced for defibrillator testing, were performed during 0- and 15-cmH(2)O Paw to measure Pms (value of Pra 7.5 s after onset of circulatory arrest). Positive Paw increased Pms from 10.2 +/- 3.5 to 12.7 +/- 3.2 mmHg, and thus the pressure gradient for venous return (Pms - Pra) remained unchanged. Echocardiography did not reveal signs of vascular collapse of the inferior and superior vena cava due to lung expansion. In conclusion, we demonstrated that positive Paw equally increases Pra and Pms in humans and alters venous return without changes in the pressure gradient (Pms - Pra). |
4,840 | Altered transient outward current in human atrial myocytes of patients with reduced left ventricular function. | Electrophysiologic remodeling is involved in the self-perpetuation of atrial fibrillation. To define whether differences in atrial electrophysiology already are present in patients with increased susceptibility for atrial fibrillation, we compared patients in sinus rhythm with and without heart failure.</AbstractText>Atrial specimens were obtained from patients with reduced left ventricular ejection fraction (LVEF; n = 10) and normal LVEF (n = 16) who were undergoing aortocoronary bypass surgery and from donor hearts (n = 4). Enzymatically isolated atrial myocytes were investigated by whole cell, patch clamp techniques. Total outward current was significantly larger in myocytes of hearts with low LVEF than normal LVEF (19.4 +/- 1.3 vs 15.1 +/- 1.2 pA/pF at pulses to +60 mV, respectively). Analysis of inactivation time courses of different outward current components revealed that the observed current difference is due to the transient calcium-independent outward current I(to1) which is twice as large in the low LVEF group than in the normal LVEF group (9.4 +/- 0.9 vs 4.7 +/- 0.4 pA/pF at pulses to +60 mV, respectively). I(to1) recovery from inactivation was significantly more rapid in myocytes of hearts with low LVEF, and action potential plateau in these cells was significantly shorter. The results of I(to1) and action potential measurements in atrial myocytes of donor hearts were very similar to the results of patients with preserved heart function.</AbstractText>I(to1) in human atrial myocytes of patients with reduced LVEF has an increased density and altered kinetics in sinus rhythm. These differences in outward current may explain the reduced plateau phase of action potentials.</AbstractText> |
4,841 | Signal-averaged isoharmonic body surface maps of patients with ischemic cardiomyopathy. | Prevention of sudden arrhythmic cardiac death depends on accurate identification of individuals at high risk. Previous studies of signals recorded directly from arrhythmogenic tissue suggested that the predictive value of the signal-averaged ECG could be enhanced by expanded temporal, spectral, and spatial analysis. Accordingly, we performed a prospective study of 192-lead signal-averaged body surface maps from 43 patients with ischemic cardiomyopathy referred for electrophysiologic study. Three groups were included: 15 patients with clinical ventricular tachycardia (VT), 12 patients with inducible VT, and 16 patients with non-VT.</AbstractText>The patients were well matched with regard to age, gender, infarct location, ejection fraction (28% +/- 9%), QRS duration, and incidence of nonsustained VT (96%). Isoharmonic maps of the entire cardiac cycle were constructed for each patient. The peaks of the 1-7 Hz isoharmonic maps distinguished patients with clinical VT from non-VT and inducible VT patients (1,152 +/- 273, 852 +/- 283, and 808 +/- 272, respectively; P = 0.003). After prospective observation for 22 +/- 16 months, the combined endpoint of spontaneous sustained VT, ventricular fibrillation, appropriate defibrillator therapy, and death was predicted by inducibility of VT (relative risk 3.8, P = 0.008) and by the signal-averaged isoharmonic body surface map (relative risk 3.1, P = 0.02).</AbstractText>These results confirm the diagnostic utility of signal-averaged isoharmonic body surface maps in a rigorously defined patient population.</AbstractText> |
4,842 | Are routine arrhythmia inductions necessary in patients with pectoral implantable cardioverter defibrillators? | The value of ventricular arrhythmia inductions as part of routine implantable cardioverter defibrillator (ICD) follow-up in new-generation pectoral ICDs is unknown.</AbstractText>We performed a retrospective analysis of a prospectively collected database analyzing data from 153 patients with pectoral ICDs who had routine arrhythmia inductions at predismissal, and 3 months and 1 year after implantation. Routine predismissal ventricular fibrillation (VF) induction yielded important findings in 8.8% of patients, all in patients with implantation defibrillation threshold (DFT) > or = 15 J or with concomitant pacemaker systems. At 3 months and 1 year, routine VF induction yielded important findings in 5.9% and 3.8% of tested patients, respectively, all in patients who had high DFT on prior testing. Ventricular tachycardia (VT) induction at predismissal, and 3 months and 1 year after implantation resulted in programming change in 37.4%, 28.1%, and 13.8% of tested patients, almost all in patients with inducible VT on baseline electrophysiologic study and clinical episodes since implantation.</AbstractText>Although helpful in identifying potentially important ICD malfunctions, routine arrhythmia inductions during the first year after ICD implantation may not be necessary in all cases. VF inductions have a low yield in patients with previously low DFTs who lack concomitant pacemakers. VT inductions have a low yield in patients without baseline inducible VT and in the absence of clinical events. Definite recommendations regarding patient selection must await larger prospective studies as well as consensus in the medical community about what comprises an acceptable risk justifying avoidance of the costs and inconveniences of routine arrhythmia inductions.</AbstractText> |
4,843 | Clinical trials of pacing mode selection. | Current recommendations in favor of dual-chamber over single-chamber ventricular pacing for patients with sinus node dysfunction or AV conduction disorders were made largely based on observational data and expert opinions. The first randomized pacing mode selection study was relatively small and suggested survival advantage with physiologic pacing only after an extended follow-up duration of 5.5 years. Preliminary results of the first large-scale multicenter randomized pacing mode selection trial revealed only modest reduction in atrial fibrillation without survival advantage after 3 years of physiologic pacing. Two other large-scale multicenter randomized trials comparing physiologic versus ventricular pacing are currently ongoing. They may provide further scientific evidence based on which more objective recommendations can be made with respect to pacing mode selection. |
4,844 | Catheter ablation of atrioventricular junction via retrograde route in a patient with single ventricle. | Radiofrequency catheter ablation of the atrioventricular junction (AVJ) was performed by the retrograde route in a 19-year-old woman with atrial fibrillation and single ventricle following the bidirectional Glenn procedure. Two energy applications resulted in complete atrioventricular block and dependence on an epicardial ventricular pacemaker. |
4,845 | Effect of underlying heart disease on the frequency content of ventricular fibrillation in the dog heart. | Although prior studies have examined the frequency content of local electrogram characteristics during fibrillation, little is know about the effects of underlying heart disease on these parameters. This study was designed to compare the frequency content of local electrograms during VF in canine models of acute ischemia, subacute infarction, and chronic myocardial infarction (MI) to those in control animals to test the hypothesis that underlying heart disease can alter the basic characteristics of VF. VF was induced using burst pacing in three groups of mongrel dogs. Five dogs were evaluated 8 weeks after LAD occlusion MI, five were evaluated 5 days after experimental MI, and 5 had VF induced before (control) and immediately after LAD occlusion (ischemia). During VF, unipolar electrograms were recorded from 112 sites on the anterior LV and electrograms were evaluated 15 and 30 seconds after VF initiation in each group. Electrograms were analyzed by fast Fourier transform. No significant time dependent changes in VF characteristics were noted. The peak frequency was highest in control animals and 8-week MI, intermediate in 5-day MI, and lowest in acute ischemia (P < 0.01 for pairwise comparisons). In contrast, the fractional of energy within a bandwidth of 25% peak amplitude was highest in acute ischemia, (P < 0.001) and similar in the other three groups. Infarction decreased total energy by approximately 50%. In conclusion, the pressure of ischemia or infarction alters the frequency content of VF in a complex fashion. In addition to decreasing the peak frequency, the shape of the power spectral curve is altered in models of structural heart disease. These results suggest that the electrophysiological changes produced by infarction or ischemia alter the structural organization of ventricular fibrillation. |
4,846 | Scaling structure of electrocardiographic waveform during prolonged ventricular fibrillation in swine. | Ventricular fibrillation (VF) is the most common arrhythmia causing sudden cardiac death. However, the likelihood of successful defibrillation declines with increasing duration of VF. Because the morphology of the electrocardiogram (ECG) waveform during VF also changes with time, this study examined a new measure that describes the VF waveform and distinguishes between early and late VF. Surface ECG recordings were digitized at 200 samples/s from nine swine with induced VF. A new measure called the scaling exponent was calculated by examining the power-law relationship between the summation of amplitudes of a 1,024-point (5.12 second) waveform segment and the time scale of measurement. The scaling exponent is a local estimate of the fractal dimension of the ECG waveform. A consistent power-law relationship was observed for measurement time scales of 0.005-0.040 seconds. Calculation of the scaling exponent produced similar results between subjects, and distinguished early VF (< 4-minute duration) from late VF (> or = 4-minute duration). The scaling exponent was dependent on the order of the data, supporting the hypothesis that the surface ECG during VF is a deterministic rather than a random signal. The waveform of VF results from the interaction of multiple fronts of depolarization within the heart, and may be described using the tools of nonlinear dynamics. As a quantitative descriptor of waveform structure, the scaling exponent characterizes the time dependent organization of VF. |
4,847 | Prospective evaluation of pulmonary edema. | To describe the clinical profile and hospital outcome of successive unselected patients with pulmonary edema hospitalized in an internal medicine department.</AbstractText>Prospective, consecutive, unsolicited patients diagnosed with pulmonary edema.</AbstractText>An internal medicine department in a 900 tertiary care center.</AbstractText>A total of 150 consecutive unselected patients (90 males, 60 females; median age, 75 yrs).</AbstractText>Ischemic heart disease, hypertension, various valvular lesions and diabetes mellitus were present in 85%, 70%, 53%, and 52% of patients, respectively. Acute myocardial infarction at admission was observed in 15% of patients. The most common precipitating factors associated with the development of pulmonary edema included: high blood pressure (29%), rapid atrial fibrillation (29%,) unstable angina pectoris (25%), infection (18%), and acute myocardial infarction (15%). Twenty-two patients (15%) were mechanically ventilated. Eighteen patients (12%) died while in the hospital, and the cause of death was cardiac pump failure in 82%. The median hospital stay was 10 days. Predictors for increase rate of in-hospital mortality included: diabetes (p<.05), orthopnea (p<.05), echocardiographic finding of moderate-to-severely depressed global left ventricular systolic function (p<.001), acute myocardial infarction during hospital stay (p<.001), hypotension/shock (p<.05), and the need for mechanical ventilation (p<.001).</AbstractText>Most patients with pulmonary edema in the internal medicine department are elderly, having ischemic heart disease, hypertension, diabetes, and a previous history of pulmonary edema. The overall mortality is high (in-hospital, 12%) and the predictors associated with high in-hospital mortality are related to left ventricular myocardial function. The long median hospital stay (10 days) and the need for many cardiovascular drugs, impose a considerable cost in the management and health care of these patients.</AbstractText> |
4,848 | Stroke in a hospital-derived cohort of patients with chronic Chagas' disease. | The aim of this study was to determine the prevalence of stroke in a hospital-derived cohort of patients with chronic Chagas' disease. Seventy-nine patients with chronic Chagas' disease were prospectively followed at the Cardiomyopathy Clinic of the Santa Casa Hospital from January 1990 to June 1993 (mean follow up = 17 +/- 12 months). Mean New York Heart Association functional class was 2.42 +/- 1.24. Fifty-six (70%) patients were on angiotensin-converting enzyme inhibitors at maximum tolerated doses, but no patient was on anticoagulation therapy. Atrial fibrillation was detected on the resting ECG in twelve (15%) patients. On echocardiography, mean left ventricular ejection fraction was 49.07 +/- 17.96% and mean left ventricular diastolic dimension 60.12 +/- 10.97 mm; mitral regurgitation was detected in 20 (29%) patients. Left ventricular thrombus was seen in three (4%) patients; all of them were in sinus rhythm and had left ventricular dysfunction on echocardiography. No thromboembolic event, however, was detected during the follow-up. One patient (1%) had a fatal stroke during the study period; she was in sinus rhythm on the resting ECG, and had mild mitral regurgitation, normal left ventricular function and no intracavitary thrombus on Doppler echocardiography. The prevalence of stroke is low in a hospital-derived cohort of patients with mild to moderate heart failure due to chronic Chagas' disease. Routine prophylactic anticoagulation, therefore, seems not to be warranted. |
4,849 | Economic outcomes of implantable cardioverter-defibrillators. | We reviewed the literature pertaining to the cost-effectiveness of implantable cardioverter-defibrillator (ICD) therapy in the management of ventricular fibrillation and tachycardia. Discussed are the methodology, advantages, and limitations of economic-outcomes analyses as related to ICD therapy; the impact of new technology and physician practice patterns; and methodological recommendations for future studies.</AbstractText>Articles published between 1990 and 1997 were screened for cost-effectiveness analyses of ICD versus antiarrhythmic drug therapy. Randomized clinical trials, prospective and retrospective studies, and economic models were included. These studies report incremental cost-effectiveness ratios ranging from cost savings of $13 975 per life-year saved (LYS) to an incremental cost of $114 917 per LYS for ICD therapy. Differences were due to study type, cost-reporting methodology, ICD technology used, and length of follow-up. Assuming current technology and physician practice patterns, we find that ICD total therapy costs may break even in 1 to 3 years.</AbstractText>Recent literature suggests that ICDs are a cost-effective therapy for management of life-threatening ventricular tachyarrhythmias. The advent of new technology and patient management practices should further improve the cost-effectiveness of ICD therapy. Future studies of ICD cost-effectiveness should address the implications of truncated follow-up periods and quality of life.</AbstractText> |
4,850 | [Multiple changes of the morphology of ST segment in a patient with Brugada syndrome]. | The Brugada syndrome is characterized by in a electrocardiographic pattern of right bundle branch block and ST-segment elevation in the right precordial leads, absence of any structural heart disease and syncope episodes or sudden death. We report the case of a 50 year-old men with Brugada syndrome and manifold changes of the precordial morphology of ST segment. |
4,851 | Distribution of excitation frequencies on the epicardial and endocardial surfaces of fibrillating ventricular wall of the sheep heart. | Tissue heterogeneities may play an important role in the mechanism of ventricular tachycardia (VT) and fibrillation (VF) and can lead to a complex spatial distribution of excitation frequencies. Here we used optical mapping and Fourier analysis to determine the distribution of excitation frequencies in >20 000 sites of fibrillating ventricular tissue. Our objective was to use such a distribution as a tool to quantify the degree of organization during VF. Fourteen episodes of VT/VF were induced via rapid pacing in 9 isolated, coronary perfused, and superfused sheep ventricular slabs (3x3 cm(2)). A dual-camera video-imaging system was used for simultaneous optical recordings from the entire epi- and endocardial surfaces. The local frequencies of excitation were determined at each pixel and displayed as dominant frequency (DF) maps. A typical DF map consisted of several (8.2+/-3.6) discrete areas (domains) with a uniform DF within each domain. The DFs in adjacent domains were often in 1:2, 3:4, or 4:5 ratios, which was shown to be a result of an intermittent Wenckebach-like conduction block at the domain boundaries. The domain patterns were relatively stable and could persist from several seconds to several minutes. The complexity in the organization of the domains, the number of domains, and the dispersion of frequencies increased with the rate of the arrhythmia. Domain patterns on the epicardial and endocardial surfaces were not correlated. Sustained epicardial or endocardial reentry was observed in only 3 episodes. Observed frequency patterns during VT/VF suggest that the underlying mechanism may be a sustained intramural reentrant source interacting with tissue heterogeneities. |
4,852 | Incidence, duration and survival of ventricular fibrillation in out-of-hospital cardiac arrest patients in sweden. | The chance of survival from ventricular fibrillation (VF) is up to ten times higher than those with other cardiac arrest rhythms. To calculate the effect of out-of-hospital resuscitation organisations on survival, it is necessary to know the percentage of cardiac arrest patients initially in VF and the relationship between delay time to defibrillation and survival.</AbstractText>To study the incidence of VF at the time of cardiac arrest and on first ECG, the duration of VF and the relation between time to defibrillation and survival.</AbstractText>The Swedish Cardiac Arrest Registry has collected standardised reports on out-of-hospital cardiac arrests from ambulance organisations in Sweden, serving 60% of the Swedish population.</AbstractText>In 14065 cases of out-of-hospital cardiac arrest collected between 1990 and 1995, resuscitation was attempted in 10966 cases.</AbstractText>The first ECG showed VF in 43% of all patients. The incidence of VF at the time of cardiac arrest was estimated to be 60-70% in all patients and 80-85% in the cases with probable heart disease.</AbstractText>The estimated disappearance rate of VF was slow. Thirty minutes after collapse approximately 40% of the patients were in VF.</AbstractText>Overall survival to 1 month was only 1.6% for patients with non-shockable rhythms and 9.5% for patients found in VF. With increasing time to defibrillation, the survival rate fell rapidly from approximately 50% with a minimal delay to 5% at 15 min.</AbstractText>This study suggests a high initial incidence of VF among out-of-hospital cardiac arrest patients and a slow rate of transformation into a non-shockable rhythm. The survival rate with very short delay times to defibrillation was approximately 50%, but decreased rapidly as the delay increased.</AbstractText> |
4,853 | Percutaneous transluminal septal myocardial ablation for hypertrophic obstructive cardiomyopathy: long term follow up of the first series of 25 patients. | To determine the long term outcome in patients treated with percutaneous transluminal septal myocardial ablation (PTSMA) for hypertrophic obstructive cardiomyopathy (HOCM).</AbstractText>Observational, single centre study.</AbstractText>25 patients (13 women, 12 men, mean (SD) age 54.7 (15.0) years) with drug treatment resistant New York Heart Association (NYHA) class 2.8 (0. 6) symptoms attributed to a high left ventricular outflow gradient (LVOTG) and a coronary artery anatomy suitable for intervention.</AbstractText>PTSMA by injection of 4.1 (2.6) ml of alcohol (96%) into 1.4 (0.6) septal perforator arteries to ablate the hypertrophied interventricular septum.</AbstractText>During in-hospital follow up, enzyme rise, the frequency of atrioventricular conduction lesions requiring permanent DDD pacing, and in-hospital mortality were assessed. Long term follow up (30 (4) months, range 24-36 months) included symptoms, echocardiographic measurements of left atrial and left ventricular dimensions and function, and LVOTG.</AbstractText>Mean postinterventional creatine kinase rise was 780 (436) U/l. During PTSMA 13 patents developed total heart block, permanent pacing being necessary in five of them. One 86 year old patient died from ventricular fibrillation associated with intensive treatment (beta mimetic and theophylline) for coexistent severe obstructive airway disease. After three months, three patients underwent re-PTSMA because of a dissatisfactory primary result, leading to LVOTG elimination in all of them. During long term follow up, LVOTG showed sustained reduction (3 (6) mm Hg at rest and 12 (19) mm Hg with provocation) associated with stable symptomatic improvement (NYHA class 1.2 (1.0)) and without significant global left ventricular dilatation.</AbstractText>PTSMA is an effective non-surgical technique for reduction of symptoms and LVOTG in HOCM. Prospective, long term observations of larger populations are necessary in order to determine the definitive significance of the procedure.</AbstractText> |
4,854 | Antiarrhythmic management and implantable defibrillator use in survivors of prehospital cardiac arrest without myocardial infarction in West Yorkshire. | To explore the current use of secondary preventive treatment in survivors of out of hospital cardiac arrest without myocardial infarction (primary ventricular tachycardia/ventricular fibrillation (VT/VF)) in West Yorkshire, and assess the implications of recent studies on the benefits of implantable cardioverter-defibrillators (AICD) in this context.</AbstractText>Retrospective analysis of an ambulance service based database of outcome after resuscitation of out of hospital cardiac arrest and the Leeds AICD implantation database.</AbstractText>Mortality, rate of referral for specialist investigation, antiarrhythmic treatment.</AbstractText>Twelve month mortality following successful discharge after primary VF arrest was 15%. Of 53 patients with primary VF/VT, 29 apparently did not see a cardiologist during the initial admission. Amiodarone was the most widely used antiarrhythmic agent. Six patients (15%) received an AICD. During the same period 22 patients from the same catchment area received an AICD following an in-hospital cardiac arrest.</AbstractText>Mortality among survivors of non-infarct related prehospital cardiac arrest remains significant, with few patients being referred for specialist investigation. The implementation of recent guidelines on AICD use in cardiac arrest survivors would have resulted in an approximate 60% increase in the total numbers of defibrillators implanted in the West Yorkshire area.</AbstractText> |
4,855 | Arrhythmias in heart failure: current concepts of mechanisms and therapy. | About one half of deaths in patients with heart failure are sudden, mostly due to ventricular tachycardia (VT) degenerating to ventricular fibrillation or immediate ventricular fibrillation. In severe heart failure, sudden cardiac death also may occur due to bradyarrhythmias. Other dysrhythmias complicating heart failure include atrial and ventricular extrasystoles, atrial fibrillation (AF), and sustained and nonsustained ventricular tachyarrhythmias. The exact mechanism of the increased vulnerability to arrhythmias is not known. Depending on the etiology of heart failure, different preconditions, including ischemia or structural alterations such as fibrosis or myocardial scarring, may be prominent. Reentrant mechanisms around scar tissue, afterdepolarizations, and triggered activity due to changes in calcium metabolism significantly contribute to arrhythmogenesis. Furthermore, alterations in potassium currents leading to action potential prolongation and an increase in dispersion of repolarization play a significant role. Treatment of arrhythmias is necessary either because patients are symptomatic or to reduce the risk for sudden cardiac death. The individual history, left ventricular function, electrophysiologic testing, and the signal-averaged ECG give useful information for identifying patients at risk for sudden cardiac death. The implantable cardioverter defibrillator (ICD) has evolved as a promising therapy for life-threatening arrhythmias. A potential role may exist for antiarrhythmic drugs, mainly amiodarone. There is growing evidence that patients with sustained VT or a history of resuscitation have the best outcome with ICD therapy regardless of the degree of heart failure. Many of these patients require additional antiarrhythmic therapy because of AF or nonsustained VTs that may activate the device. Catheter ablation or map-guided endocardial resection are additional options in selected patients but seldom represent the only therapeutic strategy. |
4,856 | Ventricular fibrillation in a patient with prominent J (Osborn) waves and ST segment elevation in the inferior electrocardiographic leads: a Brugada syndrome variant? | Recurrent ventricular fibrillation was observed in a 29-year-old Vietnamese man who did not exhibit structural heart disease. The patient's ECG showed prominent J (Osborn) waves and ST segment elevation in the inferior leads that were not associated with hypothermia, serum electrolyte disturbance, or myocardial ischemia. Rate-dependent change in the amplitude of J waves and ST segment elevation also were observed. An implantable cardioverter defibrillator (ICD) was implanted. Adjunctive treatment with amiodarone reduced J wave amplitude, preventing ventricular fibrillation and ICD shocks. Prominent J waves and ST segment elevation in the inferior leads may serve as an important diagnostic sign to detect high-risk individuals with a history of unexplained syncope. ICD implantation plus amiodarone is the treatment of choice. |
4,857 | Effect of atrial radiofrequency ablation designed to cure atrial fibrillation on atrial mechanical function. | The effects of linear radiofrequency lesions in the atria for cure of atrial fibrillation on atrial contraction have not previously been quantified.</AbstractText>Atrial function was measured before and 30 +/- 24 days after a biatrial ablation procedure designed to cure atrial fibrillation in eight dogs and after a sham procedure in three dogs. Atrial mechanical function was assessed using Doppler diastolic blood flow velocities, atrial systolic pressure wave amplitude, and assessment of atrial contribution to cardiac output estimated by comparison of AV sequential pacing to ventricular pacing at the same heart rate. The mitral Doppler A/E velocity ratio was 1.03 +/- 0.45 before and 0.72 +/- 0.43 after ablation (P = 0.048). The tricuspid A/E ratio was 0.88 +/- 0.17 before and 0.71 +/- 0.12 after ablation (P = 0.04). The estimated atrial contribution to cardiac output was 18% +/- 9% before and 5% +/- 4% after ablation (P < 0.01). The left atrial systolic pressure wave amplitude was 2.8 +/- 1.5 mmHg before and 1.7 +/- 1.0 mmHg after ablation (P = 0.1). These changes were not observed in control dogs. Lesions covered 25% +/- 6% of the atrial endocardial surface.</AbstractText>Multiple linear radiofrequency lesions in the atria designed to cure atrial fibrillation may impair atrial contractility. Reduced atrial function is partly due to loss of atrial myocardial mass, but regional delays in atrial activation and splinting of the atria by scarring also may contribute.</AbstractText> |
4,858 | Transvenous parasympathetic nerve stimulation in the inferior vena cava and atrioventricular conduction. | In previous reports, we demonstrated a technique for parasympathetic nerve stimulation (PNS) within the superior vena cava, pulmonary artery, and coronary sinus to control rapid ventricular rates during atrial fibrillation (AF). In this report, we describe another vascular site, the inferior vena cava (IVC), at which negative dromotropic effects during AF could consistently be obtained. Moreover, stimulation at this site also induced dual AV nodal electrophysiology.</AbstractText>PNS was performed in ten dogs using rectangular stimuli (0.1 msec/20 Hz) delivered through a catheter with an expandable electrode basket at its tip. Within 3 minutes and without using fluoroscopy, the catheter was positioned at an effective PNS site in the IVC at the junction of the right atrium. AF was induced and maintained by rapid atrial pacing. During stepwise increase of the PNS voltage from 2 to 34 V, a graded response of ventricular rate slowing during AF was observed (266 +/- 79 msec without PNS vs 1,539 +/- 2,460 msec with PNS at 34 V; P = 0.005 by analysis of variance), which was abolished by atropine and blunted by hexamethonium. In three animals, PNS was performed during sinus rhythm. Dual AV nodal electrophysiology was present in 1 of 3 dogs in control, whereas with PNS, dual AV nodal electrophysiology was observed in all three dogs. PNS did not significantly change sinus rate or arterial blood pressure during ventricular pacing.</AbstractText>Stable and consistent transvenous electrical stimulation of parasympathetic nerves innervating the AV node can be achieved in the IVC, a transvenous site that is rapidly and readily accessible. The proposed catheter approach for PNS can be used to control ventricular rate during AF in this animal model.</AbstractText> |
4,859 | Optimization of transvenous coil position for active can defibrillation thresholds. | Lead systems that include an active pectoral pulse generator are now standard for initial defibrillator implantations. However, the optimal transvenous lead system and coil location for such active can configurations are unknown. The purpose of this study was to evaluate the benefit and optimal position of a superior vena cava (SVC) coil on defibrillation thresholds with an active left pectoral pulse generator and right ventricular coil.</AbstractText>This prospective, randomized study was performed on 27 patients. Each subject was evaluated with three lead configurations, with the order of testing randomized. Biphasic shocks were delivered between the right ventricular coil and an active can alone (unipolar), or an active can in common with the proximal coil positioned either at the right atrial/SVC junction (low SVC) or in the left subclavian vein (high SVC). Stored energies at defibrillation threshold were higher for the single-coil, unipolar configuration (11.2 +/- 6.6 J) than for the high (8.9 +/- 4.2 J) or low (8.5 +/- 4.2 J) SVC configurations (P < 0.01). Moreover, 96% of subjects had low (< or = 15 J) thresholds with the SVC coil in either position compared with 81% for the single-coil configuration. Shock impedance (P < 0.001) was increased with the unipolar configuration, whereas peak current was reduced (P < 0.001).</AbstractText>The addition of a proximal transvenous coil to an active can unipolar lead configuration reduces defibrillation energy requirements. The position of this coil has no significant effect on defibrillation thresholds.</AbstractText> |
4,860 | Oral anticoagulant therapy for heart disease: results in actual cardiology practice. | To determine whether the success and complication rates of oral anticoagulation obtained in large, well controlled trials, upon which recommendations are based, are comparable with routine cardiology practice.</AbstractText>An observational, prospective cohort study collected data on all patients followed at an anticoagulant clinic over one calendar year.</AbstractText>One thousand and seventy-eight patients anticoagulated for cardiovascular indications, mainly atrial fibrillation, prosthetic valves and ventricular dysfunction, were followed for 804 patient-years of treatment. No patient was lost to follow-up.</AbstractText>Telephone conversations and regular verification of medical files were used to record and classify all bleeding and thromboembolic events according to severity. International normalized ratios (INR) were compared with target ranges.</AbstractText>One hundred and twelve bleeding events, ie, 13.9/100 patient-years (% p-y), were recorded, of which 61 required medical attention. Major hemorrhages, defined as those requiring treatment or hospital observation for more than 24 h, occurred in 15 instances (1.9% p-y). Among these, 9 (1.1% p-y) were classified as life threatening, with four being fatal (0,5% p-y). Twenty-two thromboembolic events (2.7% p-y) occurred, of which 10 were major (1.2% p-y), leaving three patients (0.4% p-y) with long term sequelae and causing two deaths (0.25% p-y). INRs were within target range 62.3% of the time, with 2.2% of values recorded above 5 and 0.3% above 10.</AbstractText>The low failure and complication rates obtained in large, controlled trials are similar to those observed in actual cardiology practice.</AbstractText> |
4,861 | Detection of atrial fibrillation and flutter by a dual-chamber implantable cardioverter-defibrillator. For the Worldwide Jewel AF Investigators. | To distinguish prolonged episodes of atrial fibrillation (AF) that require cardioversion from self-terminating episodes that do not, an atrial implantable cardioverter-defibrillator (ICD) must be able to detect AF continuously for extended periods. The ICD should discriminate between atrial tachycardia/flutter (AT), which may be terminated by antitachycardia pacing, and AF, which requires cardioversion.</AbstractText>We studied 80 patients with AT/AF and ventricular arrhythmias who were treated with a new atrial/dual-chamber ICD. During a follow-up period lasting 6+/-2 months, we validated spontaneous, device-defined AT/AF episodes by stored electrograms in all patients. In 58 patients, we performed 80 Holter recordings with telemetered atrial electrograms, both to validate the continuous detection of AT/AF and to determine the sensitivity of the detection of AT/AF. Detection was appropriate in 98% of 132 AF episodes and 88% of 190 AT episodes (98% of 128 AT episodes with an atrial cycle length <300 ms). Intermittent sensing of far-field R waves during sinus tachycardia caused 27 inappropriate AT/AF detections; these detections lasted 2.6+/-2.0 minutes. AT/AF was detected continuously in 27 of 28 patients who had spontaneous episodes of AT/AF (96%). The device memory recorded 90 appropriate AT/AF episodes lasting >1 hour, for a total of 2697 hours of continuous detection of AT/AF. During Holter monitoring, the sensitivity of the detection of AT/AF (116 hours) was 100%; the specificity of the detection of non-AT/AF rhythms (1290 hours) was 99.99%. Of 166 appropriate episodes detected as AT, 45% were terminated by antitachycardia pacing.</AbstractText>A new ICD detects AT/AF accurately and continuously. Therapy may be programmed for long-duration AT/AF, with a low risk of underdetection. Discrimination of AT from AF permits successful pacing therapy for a significant fraction of AT.</AbstractText> |
4,862 | Permanent, direct His-bundle pacing: a novel approach to cardiac pacing in patients with normal His-Purkinje activation. | Direct His-bundle pacing (DHBP) produces synchronous ventricular depolarization and improved cardiac function relative to apical pacing. Although it has been performed transiently in the electrophysiology laboratory and persistently in open-chested canines, permanent DHBP in humans has not been achieved.</AbstractText>A total of 18 patients aged 69+/-10 years who had a history of chronic atrial fibrillation, dilated cardiomyopathy, and normal activation (ie, QRS< or =120 ms) were screened for permanent DHBP using an electrophysiology catheter. In 14 patients, the His bundle could be reliably stimulated. Of these 14, permanent DHBP using a fixed screw-in lead was successful in 12 patients. Radiofrequency atrioventricular node ablation was performed in patients exhibiting a fast ventricular response. All patients received single-chamber rate-responsive pacemakers. Acute pacing thresholds were 2.4+/-1.0 V at a pulse duration of 0.5 ms. Lead complications included exit block requiring reoperative adjustment and gross lead dislodgment. Echocardiographic improvement in heart function was shown by reductions in the left ventricular end-diastolic dimension from 59+/-8 to 52+/-6 mm (P</=0.01) and in the end-systolic dimension from 51+/-10 to 43+/-8 mm (P<0.01), with an accompanying increase in fractional shortening from 14+/-7% to 20+/-10% (P=0.05). The left ventricular ejection fraction improved from 20+/-9% to 31+/-11% (P<0. 01), and the cardiothoracic ratio decreased from 0.61+/-0.06 to 0. 57+/-0.07 (P<0.01). Despite DHBP, 2 patients died at 8 and 36 months. Conclusions-Permanent DHBP is feasible in select patients who have chronic atrial fibrillation and dilated cardiomyopathy. Long-term, DHBP results in a reduction of left ventricular dimensions and improved cardiac function.</AbstractText> |
4,863 | A novel wavelet transform based analysis reveals hidden structure in ventricular fibrillation. | We report a new method of interrogating the surface ECG signal using techniques developed in the field of wavelet transform analysis. Previously unreported structure within the ECG during ventricular fibrillation (VF) is found using a high-resolution decomposition of the signal employing the continuous wavelet transform. We believe that wavelet transform methods could lead to the development of powerful tools for use in the resuscitation of patients with cardiac arrest. |
4,864 | The evidence regarding the drugs used for ventricular rate control. | Our goal was to determine what drugs are most efficacious for controlling the ventricular rate in patients with atrial fibrillation.</AbstractText>We conducted a systematic review of the literature published before May 1998, beginning with searches of The Cochrane Collaboration's CENTRAL database and MEDLINE.</AbstractText>We included English-language articles describing randomized controlled trials of drugs used for heart rate control in adults with atrial fibrillation.</AbstractText><AbstractText Label="DATA COLLECTION/ANALYSIS" NlmCategory="METHODS">Abstracts of trials were reviewed independently by 2 members of the study team. We reviewed English-language abstracts of non-English-language publications to assess qualitative consistency with our results.</AbstractText>Forty-five articles evaluating 17 drugs met our criteria for review. In the 5 trials of verapamil and 5 of diltiazem, heart rate was reduced significantly (P <.05), both at rest and with exercise, compared with placebo, with equivalent or improved exercise tolerance in 6 of 7 comparisons. In 7 of 12 comparisons of a beta-blocker with placebo, the beta-blocker was efficacious for control of resting heart rate, with evidence that the effect is drug specific, as nadolol and atenolol proved to be most efficacious. All 9 comparisons demonstrated good heart rate control with beta-blockers during exercise, although exercise tolerance was compromised in 3 of 9 comparisons. In 7 of 8 trials, digoxin administered alone slowed the resting heart rate more than placebo, but it did not significantly slow the rate during exercise in 4 studies. The trials evaluating other drugs yielded insufficient evidence to support their use, but those drugs may yet be promising.</AbstractText>The calcium-channel blockers verapamil or diltiazem, or select beta-blockers are efficacious for heart rate control at rest and during exercise for patients with atrial fibrillation without a clinically important decrease in exercise tolerance. Digoxin is useful when rate control during exercise is less a concern.</AbstractText> |
4,865 | Histamine H(3)-receptors: a new frontier in myocardial ischemia. | In protracted myocardial ischemia, sympathetic nerve endings undergo ATP depletion, hypoxia and pH(i) reduction. Consequently, norepinephrine (NE) accumulates in the axoplasm, because it is no longer stored in synaptic vesicles, and intraneuronal Na(+) concentration increases, as the Na(+)/H(+) exchanger (NHE) is activated. This forces the reversal of the Na(+)- and Cl(-)-dependent NE transporter, triggering a massive carrier-mediated release of NE and thus, arrhythmias. Indeed, NE overflow in myocardial ischemia directly correlates with the severity of arrhythmias. Histamine H(3)-receptors (H(3)R) have been identified as inhibitory heteroreceptors in adrenergic nerve endings of the heart. In addition to inhibiting NE exocytosis from sympathetic nerve endings, selective H(3)R agonists attenuate carrier-mediated release of NE in both animal and human models of protracted myocardial ischemia. Whereas H(3)R-mediated attenuation of exocytotic NE release involves an inhibition of N-type Ca(2+)-channels, H(3)R-mediated reduction of carrier-mediated NE release is associated with diminished NHE activity. In addition to inhibiting NE release, H(3)R stimulation significantly attenuates the incidence and duration of ventricular fibrillation. Although other presynaptic receptors also modulate NE release from sympathetic nerve endings, H(3)R stimulation reduces both exocytotic and carrier-mediated NE release, whereas alpha(2)-adrenoceptor agonists attenuate NE exocytosis but enhance carrier-mediated NE release. Furthermore, unlike adenosine A(1)-receptors, whose activation reduces both exocytotic and carrier-mediated NE release, H(3)R stimulation is devoid of negative chronotropic and dromotropic effects (i.e., sinoatrial and atrioventricular nodal functions are unaffected). Because excess NE release can trigger severe arrhythmias and sudden cardiac death, negative modulation of NE release by H(3)R agonists may offer a novel therapeutic approach to myocardial ischemia. |
4,866 | Pharmacological management of atrial fibrillation: an update. | Therapy of atrial fibrillation remains difficult in many patients. There is increasing awareness that antiarrhythmic drug therapy instituted to maintain sinus rhythm after successful cardioversion of atrial fibrillation may pose a substantial risk to the patient. Therefore, results of prospective randomized trials are needed to allow a more evidence-based approach to the treatment of this common arrhythmia. Two recently published studies have shown superiority of amiodarone over conventional antiarrhythmic drugs in maintaining sinus rhythm. The largest such study published today, the Canadian Trial in Atrial Fibrillation (CTAF), has randomized 403 patients to amiodarone or to sotalol or propafenone. At the end of the observation period, amiodarone-treated patients were significantly more likely to remain in sinus rhythm than conventionally treated patients. A number of new antiarrhythmic drugs, mainly class III substances, are currently developed for the treatment of atrial fibrillation or atrial flutter. Ibutilide has recently been released for intravenous administration, attempting pharmacological cardioversion of atrial fibrillation/atrial flutter. It has been evaluated in a number of prospective trials, which showed a higher conversion rate in patients with atrial flutter. Dofetilide is another new compound developed mainly for maintenance of sinus rhythm after restoration of sinus rhythm. It has been evaluated in two prospective, randomized, placebo-controlled trials; moreover, analysis of the DIAMOND trials showed effectiveness of dofetilide in maintaining sinus rhythm in patients with depressed left ventricular function without increased mortality when compared with placebo. Finally, several ongoing studies compare the therapeutic strategy of controlling ventricular rate in atrial fibrillation compared with the strategy of maintaining sinus rhythm. These trials will help to optimize therapy in atrial fibrillation, the most commonly encountered arrhythmia. |
4,867 | The effects of Z13752A, a combined ACE/NEP inhibitor, on responses to coronary artery occlusion; a primary protective role for bradykinin. | The effects on the responses to coronary artery occlusion of a combined ACE/NEP inhibitor (Z13752A) were examined in anaesthetized dogs. A 1 h infusion of Z13752A (128 microgram kg(-1) min(-1) intravenously) decreased arterial blood pressure (by 11+/-3%; P<0. 05) and increased coronary blood flow (by 12+/-4%, P<0.05). There were no other significant haemodynamic changes. Z13752A inhibited both NEP and ACE enzymes both in dog plasma and in tissue (lung ACE; kidney NEP). Pressor responses to angiotensin I in vivo were inhibited and systemic vasodilator responses to bradykinin were potentiated. When the left anterior descending coronary artery was occluded for 25 min, Z13752A markedly reduced the severity of the resultant ventricular arrhythmias. No ventricular fibrillation (VF) occurred (compared to 7/16 in the controls; P<0.05), and ventricular tachycardia (VT) was reduced (VT in 2/9 dogs treated with Z13752A cp. 16/16 of controls; episodes of VT 0.2+/-0.1 c.p. 10.7+/-3.3; P<0. 05). Reperfusion of the ischaemic myocardium led to VF in all control dogs but occurred less frequently in dogs given Z13752A (survival from the combined ischaemia-reperfusion insult 67% c.p. 0% in controls; P<0.05). Z13752A reduced two other indices of ischaemia severity; epicardial ST-segment elevation and inhomogeneity of electrical activation. These protective effects of Z13752A during ischaemia and reperfusion were abolished by the administration of icatibant (0.3 mg kg(-1), i.v.) a selective antagonist of bradykinin at B(2) receptors; the ischaemic changes in dogs given both icatibant and Z13752A were similar to those in the controls. We conclude that this ACE/NEP inhibitor is effective at reducing the consequences of coronary artery occlusion in this canine model and that this protection is primarily due to potentiation of released bradykinin. British Journal of Pharmacology (2000) 129, 671 - 680 |
4,868 | Survival with full neurologic recovery and no cerebral pathology after prolonged cardiopulmonary resuscitation with vasopressin in pigs. | We sought to determine the effects of vasopressin and saline placebo in comparison with epinephrine on neurologic recovery and possible cerebral pathology in an established porcine model of prolonged cardiopulmonary resuscitation (CPR).</AbstractText>It is unknown whether increased cerebral blood flow during CPR with vasopressin is beneficial with regard to neurologic recovery or detrimental owing to complications such as cerebral edema after return of spontaneous circulation.</AbstractText>After 4 min of cardiac arrest, followed by 3 min of basic life support CPR, 17 animals were randomly assigned to receive every 5 min either vasopressin (0.4, 0.4 and 0.8 U/kg; n = 6), epinephrine (45, 45 and 200 microg/kg; n = 6) or saline placebo (n = 5). The mean value +/- SEM of aortic diastolic pressure was significantly (p < 0.05) higher 90 s after each of three vasopressin versus epinephrine versus saline placebo injections (60 +/- 3 vs. 45 +/- 3 vs. 29 +/- 2 mm Hg; 49 +/- 5 vs. 27 +/- 3 vs. 23 +/- 1 mm Hg; and 50 +/- 6 vs. 21 +/- 3 vs. 16 +/- 3 mm Hg, respectively). After 22 min of cardiac arrest, including 18 min of CPR, defibrillation was attempted to achieve return of spontaneous circulation.</AbstractText>All the pigs that received epinephrine and saline placebo died, whereas all pigs on vasopressin survived (p < 0.05). Neurologic evaluation 24 h after successful resuscitation revealed only an unsteady gait in all vasopressin-treated animals; after 96 h, magnetic resonance imaging revealed no cerebral pathology.</AbstractText>During prolonged CPR, repeated vasopressin administration, but not epinephrine or saline placebo, ensured long-term survival with full neurologic recovery and no cerebral pathology in this porcine CPR model.</AbstractText> |
4,869 | High dispersion of ventricular repolarization after an implantable defibrillator shock predicts induction of ventricular fibrillation as well as unsuccessful defibrillation. | To test the hypothesis that post-shock dispersion of repolarization (PSDR) is higher in T wave shocks that induce ventricular fibrillation (VF) than in those that do not, as well as in implantable cardioverter defibrillator (ICD) defibrillation shocks which fail to terminate VF when compared with those that are successful.</AbstractText>Ventricular fibrillation has been linked to the presence of dispersion of repolarization, which facilitates reentry. Most of the studies have been done in animals, and the mechanism underlying the generation and termination of VF in humans is speculative and remains to be determined.</AbstractText>Monophasic action potentials (MAPs) were recorded simultaneously from the right ventricular outflow tract (RVOT) and the right ventricular apex (RVA) in 27 patients who underwent implantation and testing of an ICD. T wave shocks were used to induce VF while the termination was attempted using internal defibrillator shocks. The post-shock repolarization time (PSRT) was measured in both the RVA and RVOT MAPs, and the difference between the two recordings was defined as the PSDR. The averages of PSDR were compared between the successful and unsuccessful inductions and terminations of VF.</AbstractText>T wave shocks that induced VF generated a greater PSDR (93.4 +/- 85.1 ms) than the unsuccessful ones (45.1 +/- 55.9 ms, p < 0.001). On the other hand, shocks that failed to terminate VF were associated with a greater PSDR (59.9 +/- 41.2 ms) than shocks that terminated VF (21.1 +/- 20.1 ms), p < 0.001.</AbstractText>A high PSDR following a T wave shock is associated with induction of VF; while following a defibrillating shock, it is associated with its failure and the continuation of VF. Conversely, a low PSDR is associated with failure of a T wave shock to induce VF and successful termination of VF by a defibrillating shock.</AbstractText> |
4,870 | Prediction of paroxysmal atrial fibrillation in patients with congestive heart failure: a prospective study. | We sought to prospectively determine whether patients with congestive heart failure (CHF) at risk for paroxysmal atrial fibrillation (PAF) could be identified by clinical and study variables including the P-wave signal-averaged electrocardiogram (P-SAECG).</AbstractText>Although it is important to assess the risk of developing PAF in patients with CHF, it still remains difficult to predict the PAF appearance in patients with CHF clinically.</AbstractText>The study group consisted of 75 patients in sinus rhythm without a history of PAF, whose left ventricular ejection fraction, as measured by radionuclide angiography, was <40%. These patients underwent P-SAECG, echocardiography and 24-h Holter monitoring; in addition, the plasma concentration of atrial natriuretic peptide (ANP) was measured at study entry.</AbstractText>An abnormal P-SAECG was found at study entry in 29 of 75 patients. In the follow-up period of 21 +/- 9 months, the PAF attacks documented on the ECG significantly more frequently occurred in patients with (32%) rather than without an abnormal P-SAECG (2%) (p = 0.0002). The plasma ANP level was significantly higher in patients with rather than without PAF attacks (75 +/- 41 vs. 54 +/- 60 pg/ml, p = 0.01), although there were no significant differences in age, left atrial dimension or high grade atrial premature beats between the groups. The multivariate Cox analysis identified that the variables significantly associated with PAF development were an abnormal P-SAECG (hazard ratio 19.1, p = 0.0069) and elevated ANP level > or =60 pg/ml (hazard ratio 8.6, p = 0.018).</AbstractText>An abnormal P-SAECG and elevated ANP level could be predictors of PAF development in patients with CHF.</AbstractText> |
4,871 | Dofetilide: a class III-specific antiarrhythmic agent. | To review published reports on the pharmacology and clinical use of dofetilide in the management of cardiac dysrhythmias.</AbstractText>A MEDLINE search (January 1966-June 1999) was performed using dofetilide and UK-68,798 as key words. English-language articles were identified, and the references of these articles were used to further identify pertinent articles.</AbstractText>All acquired studies and reviews discussing the pharmacology, pharmacokinetics, chemistry, and clinical efficacy of dofetilide were reviewed.</AbstractText>Articles were selected based on quality of review of the pharmacology and clinical use of dofetilide. Given the paucity of data on the clinical pharmacology and use of dofetilide, most articles obtained were used, including abstracts when full reports were not available.</AbstractText>Dofetilide is a relatively specific class III antiarrhythmic agent. It increases action potential duration and effective refractory period without impacting conduction velocity. These actions of dofetilide are explained by its ability to inhibit the rapid component of the delayed, outward-rectifying potassium current, thus blocking the efflux of potassium during repolarization. Introductory investigations suggest that dofetilide may be of use in treating and preventing atrial dysrhythmias such as atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia. Dofetilide may also have a role in preventing ventricular tachycardia from occurring. Some data also suggest that dofetilide may improve the morbidity of heart failure patients. Currently, the most troublesome adverse effect of dofetilide is its propensity to induce ventricular proarrhythmias, especially torsade de pointes.</AbstractText>Based on the data currently available, dofetilide should have a role in the pharmacotherapy of cardiac dysrhythmias, especially those of atrial origin. More data on its efficacy and tolerability are needed, however, to fully delineate dofetilide's role amid currently available antiarrhythmic agents.</AbstractText> |
4,872 | Adenosine induced atrial fibrillation precipitating polymorphic ventricular tachycardia. | An 86-year-old female developed supraventricular tachycardia 36 hours after a myocardial infarction (MI). She developed atrial fibrillation and polymorphic ventricular tachycardia (PVT) following administration of 12 mg of adenosine. The PVT caused hemodynamic instability with no response to cardioversion, but termination with procainamide. The heart is vulnerable to hemodynamically unstable, possibly lethal, PVT early after MI under some circumstances. This vulnerability may be exposed following administration of adenosine. Extra caution is warranted when using adenosine in the post-MI period. |
4,873 | Electrophysiologist-implanted transvenous cardioverter defibrillators using local versus general anesthesia. | With the advent of smaller biphasic transvenous implantable cardioverter defibrillators (ICDs) and the experience gained over the years, it is now feasible for electrophysiologists to implant them safely in the abdominal or pectoral area without surgical assistance. Throughout the years, general anesthesia has been used as the standard technique of anesthesia for these procedures. However, use of local anesthesia combined with deep sedation only for defibrillation threshold (DFT) testing might further facilitate and simplify these procedures. The purpose of this study was to test the feasibility of using local anesthesia and compare it with the standard technique of general anesthesia, during implantation of transvenous ICDs performed by an electrophysiologist in the electrophysiology laboratory. For over 4 years in the electrophysiology laboratory, we have implanted transvenous ICDs in 90 consecutive patients (84 men and 6 women, aged 58 +/- 15 years). Early on, general anesthesia was used (n = 40, group I), but in recent series (n = 50, group II) local anesthesia was combined with deep sedation for DFT testing. Patients had coronary (n = 58) or valvular (n = 4) disease, cardiomyopathy (n = 25) or no organic disease (n = 3), a mean left ventricular ejection fraction of 35%, and presented with ventricular tachycardia (n = 72) or fibrillation (n = 16), or syncope (n = 2). One-lead ICD systems were used in 74 patients, two-lead systems in 10 patients, and an AVICD in 6 patients. ICDs were implanted in abdominal (n = 17, all in group I) or more recently in pectoral (n = 73) pockets. The DFT averaged 9.7 +/- 3.6 J and 10.2 +/- 3.6 J in the two groups, respectively (P = NS) and there were no differences in pace-sense thresholds. The total procedural duration was shorter (2.1 +/- 0.5 hours) in group II (all pectoral implants) compared with 23 pectoral implants of group I (2.9 +/- 0.5 hours) (P < 0.0001). Biphasic devices were used in all patients and active shell devices in 67 patients; no patient needed a subcutaneous patch. There were six complications (7%), four in group I and two in group II: one pulmonary edema and one respiratory insufficiency that delayed extubation for 3 hours in a patient with prior lung resection, both probably related to general anesthesia, one lead insulation break that required reoperation on day 3, two pocket hematomas, and one pneumothorax. There was one postoperative arrhythmic death at 48 hours in group I. No infections occurred. Patients were discharged at a mean time of 3 days. All devices functioned well at predischarge testing. Thus, it is feasible to use local anesthesia for current ICD implants to expedite the procedure and avoid general anesthesia related cost and possible complications. |
4,874 | The comparative effects of drive and test stimulus intensity on myocardial excitability and vulnerability. | The number and intensity of stimuli that set basic cycle length in cardiac electrophysiological studies can influence the electrical properties assessed by extrastimuli. The relative contribution of drive (S1) and test (S2) stimulus intensity in defining myocardial excitability and vulnerability has not been reported. The purpose of this investigation was to assess this interaction and to determine whether atrial and ventricular findings differed. The effects of S1 and S2 intensity on atrial and ventricular stimulus-intensity-refractory-period curves were determined in open-chest dogs: comparisons were made between curves with S1 intensity varied between diastolic threshold (DT) and 10 mA and S2 intensity maintained at DT and those with S1 intensity maintained at DT and S2 intensity varied between DT and 10 mA. S1-S1 was held constant and S1-S2 varied. The effects of different stimulation sites, cycle length, number of stimulations, and neural blockade were assessed. S1 intensity amplification shifted atrial stimulus-intensity-refractory period curves in the direction of increased excitability and vulnerability; the changes were more pronounced than those obtained by modulating S2 intensity. The changes produced by increasing S1 intensity were evident at different cycle lengths and were enhanced by an increased number of stimulations, but were not evident when S1 and S2 were delivered at different atrial sites. Although beta-blockade attenuated the effects of increasing S1 intensity somewhat, the addition of cholinergic blockade virtually abolished it. Ventricular refractoriness was also changed by modulation of S1 intensity, but the changes were less striking. In the atrium, modulation of S1 intensity has greater effects of stimulus-intensity-refractory-period relations than modulation of S2 intensity; in the ventricule, the converse is true. |
4,875 | Importance of ventricular rate after mode switching during low intensity exercise as assessed by clinical symptoms and ventilatory gas exchange. | Automatic mode switching from DDD(R) to DDI(R) or VVI(R) pacing modes has improved dual chamber pacing in patients at high risk for supraventricular tachyarrhythmias. However, little is known about the effect of ventricular pacing rate adaptation after mode switching. We conducted a single-blinded, crossover study in 15 patients (58 +/- 21 years) with a DDD pacemaker who had AV block and normal sinus node function to investigate the influence of pacing rate adaptation to intrinsic heart rate during low intensity exercise. Patients performed two tests (A/B) of low intensity treadmill exercise (0.5 W/kg) in randomized order. They initially walked for 6 minutes while paced in DDD mode. The pacing mode was then switched to VVI with a pacing rate of either 70 beats/min (test A) or matched to the intrinsic heart rate (95 +/- 11 beats/min test B). Respiratory gas exchange variables were determined and patients classified the effort before and after mode switching on a Borg scale from 6 to 20. Percentage changes of respiratory gas exchange measurements were significantly larger (O2 consumption: -8.2 +/- 5.0% vs. -0.6 +/- 7.2%; ventilatory equivalent of CO2 exhalation: 5.3 +/- 4.9% vs. 1.5 +/- 4.3%; respiratory exchange ratio: 7.0 +/- 2.2% vs. 3.5 +/- 3.0%; end-tidal CO2: -5.7 +/- 2.9% vs. -1.8 +/- 2.7%; all P < 0.01) and the increase in subjective assessment of the effort tended to be higher (mean increase on Borg scale: 1.6 +/- 1.9 vs. 1.1 +/- 1.8, P = 0.07) after heart rate unadjusted than after adjusted mode switching. Mode switching from DDD to VVI pacing is better tolerated and gas exchange measurements are less influenced if ventricular pacing rate is adjusted to the level of physical activity. Thus, pacing rate adjustment should be considered as part of automatic mode switch algorithms. |
4,876 | Amiodarone: clinical trials. | Amiodarone is an antiarrhythmic agent commonly used in the treatment of supraventricular and ventricular tachyarrhythmias. This article reviews the results and clinical implications of primary and secondary prevention trials in which amiodarone was used in one of the treatment arms. Key post-myocardial infarction primary prevention trials include the European Myocardial Infarct Amiodarone Trial (EMIAT) and the Canadian Amiodarone Myocardial Infarction Trial (CAMIAT), both of which demonstrated that amiodarone reduced arrhythmic but not overall mortality. In congestive heart failure patients, amiodarone was studied as a primary prevention strategy in two pivotal trials: Grupo de Estudio de la Sobrevida en la Insuficiencia Cardiac en Argentina (GESICA) and Amiodarone in Patients With Congestive Heart Failure and Asymptomatic Ventricular Arrhythmia (CHF-STAT). Amiodarone was associated with a neutral overall survival and a trend toward improved survival in nonischemic cardiomyopathy patients in CHF/STAT and improved survival in GESICA. In post-myocardial infarction patients with nonsustained ventricular tachycardia and a depressed ejection fraction, the Multicenter Automatic Defibrillator Implantation Trial (MADIT) demonstrated that implantable cardioverter-defibrillators (ICD) statistically improved survival compared to the antiarrhythmic drug arm, most of whose patients were taking amiodarone. In patients with histories of sustained ventricular tachycardia or ventricular fibrillation, the Cardiac Arrest Study in Seattle: Conventional Versus Amiodarone Drug Evaluation (CASCADE) trial demonstrated that empiric amiodarone lowered arrhythmic recurrence rates compared to other drugs guided by serial Holter or electrophysiologic studies. However, arrhythmic death rates were high in both treatment arms of the study. Several secondary prevention trials, including the Antiarrhythmics Versus Implantable Defibrillators Study (AVID), the Canadian Implantable Defibrillator Study (CIDS), and the Cardiac Arrest Study Hamburg (CASH), have demonstrated the superiority of ICD therapy compared to empiric amiodarone in improving overall survival. Based on the above findings, amiodarone is safe to use in post-myocardial infarction and congestive heart failure patients that need antiarrhythmic therapy. Although amiodarone is effective in treating malignant arrhythmias, high-risk patients should be considered for an ICD as frontline therapy. |
4,877 | Clinical implication of antiembolic trials in atrial fibrillation and role of transesophageal echocardiography in atrial fibrillation. | Risk for stroke in patients with atrial fibrillation (AF) is highly heterogeneous. Increasing age, history of diabetes, hypertension, previous transient ischemic attack or stroke, and poor ventricular function are independent risk factors for stroke in patients with AF. Accordingly, some groups of patients with AF have low risk and some have high risk. In general, patients at high risk benefit most from anticoagulation therapy with warfarin. In general, if a patient is younger than 65 years of age and has none of the defined risk factors, the stroke rate without prophylaxis (aspirin or warfarin) is low. In patients 65 to 75 years of age with no risk factors, the risk for stroke is low with either aspirin or warfarin therapy; the choice is left to the caretaking physician. All patients older than 75 years and all patients of any age who have risk factors obtain striking benefit from the use of anticoagulation with warfarin. This benefit far outweighs any risk for major hemorrhage. |
4,878 | New advances in class III antiarrhythmic drug therapy. | In the past 2 years, significant advances have been made in class III antiarrhythmic drug therapy. In patients with ventricular arrhythmias and implantable cardioverter defibrillators (ICDs), antiarrhythmic agents are increasingly being used as adjunct therapy to decrease the frequency of ICD discharges. Sotalol was recently shown to be effective in reducing tachyarrhythmias in patients with ICDs. Intravenous amiodarone is being used for the acute treatment of unstable ventricular arrhythmia and is being investigated for the treatment of acute out-of-hospital cardiac arrest. Class III agents are increasingly being used for prophylaxis in patients who have atrial fibrillation or atrial flutter, and data point to an important role for these agents in reducing supraventricular tachyarrhythmias after cardiac surgery. Future studies will need to directly compare these agents with pure anti-adrenergic maneuvers in postoperative patients. In addition to terminating atrial fibrillation and atrial flutter, ibutilide significantly reduces human atrial defibrillation thresholds and increases the percentage of patients who can be cardioverted from atrial fibrillation to sinus rhythm. The US Food and Drug Administration is expected to approve dofetilide for clinical use soon, and it is currently reviewing azimilide (which seems to be devoid of frequency-dependent effects on repolarization) for prophylaxis against atrial fibrillation and atrial flutter. Dronedarone, tedisamal, and trecetilide are now under active study intended to determine their usefulness in patients with cardiac arrhythmias. Experimental studies are ongoing to identify pharmacologic agents that will selectively prolong repolarization in the atria without exerting electrophysiologic effects in the ventricles. |
4,879 | Effects of zatebradine and propranolol on canine ischemia and reperfusion-induced arrhythmias. | 1,3,4,5-Tetrahydro-7,8-dimethoxy-3[3-[[2-(3, 4-dimethoxyphenyl)-ethyl]methylamino]propyl]-2H-3-benzazepin-2-one -hy drochloride (Zatebradine) is a specific bradycardiac agent, blocking the hyperpolarization-activated pacemaker current (I(f)), and thus has no negative inotropic effect. The purpose of this study was to examine whether zatebradine is effective against ischemia and reperfusion-induced arrhythmias in dogs compared to propranolol. Arrhythmia was induced by ligation of the left anterior descending coronary artery followed by reperfusion. Ischemia-induced biphasic arrhythmias were suppressed in both zatebradine and propranolol groups. During ischemia, fatal ventricular fibrillation occurred in four dogs in the control group, 0 in the zatebradine group, and two dogs in the propranolol group. Of the 31 dogs subjected to reperfusion, mortality rates in the zatebradine, propranolol, and control groups were 56%, 75%, and 86%, respectively, and there were no significant differences. In the heart beating 10 beats/min faster than the predrug heart rate by atrial pacing, both zatebradine and propranolol attenuated ischemia-induced arrhythmias but did not affect reperfusion arrhythmias. Our results suggest that I(f) and/or beta-adrenoceptors rather than the bradycardiac action might be related to the antiarrhythmic effects during ischemia, but that they do not play a role in the generation of the reperfusion-induced ventricular arrhythmias. |
4,880 | Efficacy of implantable cardioverter-defibrillators for the prevention of sudden death in patients with hypertrophic cardiomyopathy. | Hypertrophic cardiomyopathy is a genetic disease associated with a risk of ventricular tachyarrhythmias and sudden death, especially in young patients.</AbstractText>We conducted a retrospective multicenter study of the efficacy of implantable cardioverter-defibrillators in preventing sudden death in 128 patients with hypertrophic cardiomyopathy who were judged to be at high risk for sudden death.</AbstractText>At the time of the implantation of the defibrillator, the patients were 8 to 82 years old (mean [+/-SD], 40+/-16), and 69 patients (54 percent) were less than 41 years old. The average follow-up period was 3.1 years. Defibrillators were activated appropriately in 29 patients (23 percent), by providing defibrillation shocks or antitachycardia pacing, with the restoration of sinus rhythm; the average age at the time of the intervention was 41 years. The rate of appropriate defibrillator discharge was 7 percent per year. A total of 32 patients (25 percent) had episodes of inappropriate discharges. In the group of 43 patients who received defibrillators for secondary prevention (after cardiac arrest or sustained ventricular tachycardia), the devices were activated appropriately in 19 patients (11 percent per year). Of 85 patients who had prophylactic implants because of risk factors (i.e., for primary prevention), 10 had appropriate interventions (5 percent per year). The interval between implantation and the first appropriate discharge was highly variable but was substantially prolonged (four to nine years) in six patients. In all 21 patients with stored electrographic data and appropriate interventions, the interventions were triggered by ventricular tachycardia or fibrillation.</AbstractText>Ventricular tachycardia or fibrillation appears to be the principal mechanism of sudden death in patients with hypertrophic cardiomyopathy. In high-risk patients with hypertrophic cardiomyopathy, implantable defibrillators are highly effective in terminating such arrhythmias, indicating that these devices have a role in the primary and secondary prevention of sudden death.</AbstractText> |
4,881 | Safety and prognostic value of early dobutamine-atropine stress echocardiography in patients with spontaneous chest pain and a non-diagnostic electrocardiogram. | To risk stratify and shorten hospital stay in patients with spontaneous (resting) chest pain and a non-diagnostic electrocardiogram (ECG).</AbstractText>The study comprised 102 patients (mean age 58+/-12 years, 67 men) with spontaneous chest pain and a non-diagnostic ECG. Forty-three patients had suspected coronary artery disease and 59 had known (but of unknown actual significance) coronary artery disease. All patients underwent serial creatine kinase enzyme measurements, continuous ECG monitoring for at least 12 h and early dobutamine-atropine stress echocardiography in patients with negative creatine kinase enzymes and normal findings at ECG monitoring. Dobutamine-atropine stress echocardiography was considered positive in patients with new or worsening wall thickening abnormalities. Patients with negative dobutamine-atropine stress echocardiography were discharged after the test. In-hospital and 6 month follow-up events noted were cardiac death, non-fatal myocardial infarction, unstable angina, and coronary artery bypass surgery or angioplasty. Thirteen patients had evidence of evolving myocardial infarction by elevated creatine kinase enzymes, or unstable angina by ECG monitoring. In the remaining 89 patients, dobutamine-atropine stress echocardiography was performed after a median observation period of 31 h (range 12-68 h). During dobutamine-atropine stress echocardiography no serious complications (death, non-fatal myocardial infarction, sustained ventricular tachycardia or ventricular fibrillation) occurred. Dobutamine-atropine stress echocardiography results were of poor quality in three, non-diagnostic in six, negative in 44 and positive in 36 patients. In the 80 patients with diagnostic dobutamine-atropine stress echocardiography, variables associated with in-hospital events (n=7) were history of exertional angina (P<0. 005), chest pain score (P<0.005), stress-induced angina (P<0.001) and positive dobutamine-atropine stress echocardiography (P<0.005). Variables associated with follow-up events (n=11) were history of exertional angina (P<0.05), chest pain score (P<0.001), stress-induced angina (P<0.01) and positive dobutamine-atropine stress echocardiography (P<0.01). At multivariate analysis the only significant predictor of events was positive dobutamine-atropine stress echocardiography (P<0.01).</AbstractText>Early dobutamine-atropine stress echocardiography may safely distinguish between low- and high-risk subsets for subsequent cardiac events in patients with spontaneous chest pain and a non-diagnostic ECG.</AbstractText>Copyright 2000 The European Society of Cardiology.</CopyrightInformation> |
4,882 | SCN5A mutation (T1620M) causing Brugada syndrome exhibits different phenotypes when expressed in Xenopus oocytes and mammalian cells. | Brugada syndrome is a hereditary cardiac disease causing abnormal ST segment elevation in the ECG, right bundle branch block, ventricular fibrillation and sudden death. In this study we characterized a new mutation in the SCN5A gene (T1620M), causing the Brugada syndrome. The mutated channels were expressed in both Xenopus leavis oocytes and in mammalian tsA201 cells with and without the beta-subunit and studied using the patch clamp technique. Opposite phenotypes were observed depending on the expression system. T1620M mutation led to a faster recovery from inactivation and a shift of steady-state inactivation to more positive voltages when expressed in Xenopus oocytes. However, using the mammalian expression system no effect on steady-state inactivation was observed, but this mutation led to a slower recovery from inactivation. Our finding supports the idea that the slower recovery from inactivation of the cardiac sodium channels seen in our mammalian expression system could decrease the density of sodium channels during the cardiac cycle explaining the in vivo arrhythmogenesis in patients with Brugada syndrome. |
4,883 | Emergency repair of type A aortic dissection in type IV Ehlers-Danlos syndrome. | Ehlers-Danlos syndrome type IV is a distinctive syndrome in which thin and fragile skin, premature ageing, bruising and scarring are combined with lethal or life-threatening arterial weakness. Aortic rupture either at the aortic root and arch, or sometimes lower down the artery, are particularly characteristic. Even quite minor injury can produce dangerous vascular tearing and damage. Technical difficulties encountered in arterial repair or venous ligature are particularly worrying. The authors report the treatment of a ruptured type A aortic dissection associated with Ehlers-Danlos syndrome where the extreme fragility of the tissues and tendency to bleed posed a difficult task for the surgeon. |
4,884 | A simple HPLC-fluorescence method for the measurement of R,S-sotalol in the plasma of patients with life-threatening cardiac arrhythmias. | R,S-sotalol, a ss-blocker drug with class III antiarrhythmic properties, is prescribed to patients with ventricular, atrial and supraventricular arrhythmias. A simple and sensitive method based on HPLC-fluorescence is described for the quantification of R,S-sotalol racemate in 500 microl of plasma. R,S-sotalol and its internal standard (atenolol) were eluted after 5.9 and 8.5 min, respectively, from a 4-micron C18 reverse-phase column using a mobile phase consisting of 80 mM KH2PO4, pH 4.6, and acetonitrile (95:5, v/v) at a flow rate of 0.5 ml/min with detection at lambdaex = 235 nm and lambdaem = 310 nm, respectively. This method, validated on the basis of R,S-sotalol measurements in spiked blank plasma, presented 20 ng/ml sensitivity, 20-10,000 ng/ml linearity, and 2.9 and 4.8% intra- and interassay precision, respectively. Plasma sotalol concentrations were determined by applying this method to investigate five high-risk patients with atrial fibrillation admitted to the Emergency Service of the Medical School Hospital, who received sotalol, 160 mg po, as loading dose. Blood samples were collected from a peripheral vein at zero, 0.5, 1.0, 1.5, 2.0, 3.0, 4. 0, 6.0, 8.0, 12.0 and 24.0 h after drug administration. A two-compartment open model was applied. Data obtained, expressed as mean, were: C MAX = 1230 ng/ml, T MAX = 1.8 h, AUC T = 10645 ng h-1 ml-1, Kab = 1.23 h-1, alpha = 0.95 h-1, ss = 0.09 h-1, t((1/2))ss = 7.8 h, ClT/F = 3.94 ml min-1 kg-1, and Vd/F = 2.53 l/kg. A good systemic availability and a fast absorption were obtained. Drug distribution was reduced to the same extent in terms of total body clearance when patients and healthy volunteers were compared, and consequently elimination half-life remained unchanged. Thus, the method described in the present study is useful for therapeutic drug monitoring purposes, pharmacokinetic investigation and pharmacokinetic-pharmacodynamic sotalol studies in patients with tachyarrhythmias. |
4,885 | Atrial fibrillation after cardiac operation: risks, mechanisms, and treatment. | Atrial fibrillation (AF) is a common complication of cardiac operations that leads to increased risk for thromboembolism and excessive health care resource utilization. Advanced age, previous AF, and valvular heart operations are the most consistently identified risk factors for this arrhythmia. Dispersion of repolarization leading to reentry is believed to be the mechanism of postoperative AF, but many questions regarding the pathophysiology of AF remain unanswered. Treatment is aimed at controlling heart rate, preventing thromboembolic events, and conversion to sinus rhythm. Multiple investigations have examined methods of preventing postoperative AF, but the only firm conclusions that can be drawn is to avoid beta-blocker withdrawal after operation and to consider beta-blocker therapy for other patients who may tolerate these drugs. Preliminary investigations showing sotalol and amiodarone to be effective in preventing postoperative AF are encouraging, but early data have been limited to selective patient populations and have not adequately evaluated safety. Newer class III antiarrhythmic drugs under development may have a role in the treatment of postoperative AF, but the risk of drug-induced polymorphic ventricular tachycardia must be considered. Nonpharmacologic interventions under consideration for the treatment of AF in the nonsurgical setting, such as automatic atrial cardioversion devices and multisite atrial pacing, may eventually have a role for selected cardiac surgical patients. |
4,886 | Cardiac arrest witnessed by emergency medical services personnel: descriptive epidemiology, prodromal symptoms, and predictors of survival. | The Utstein guidelines recommend that emergency medical services (EMS)-witnessed cardiac arrests be considered separately from other out-of-hospital cardiac arrest cases. The objective of this study was to assess EMS-witnessed cardiac arrest and to determine predictors of survival in this group.</AbstractText>This prospective cohort included all adults with an EMS-witnessed cardiac arrest in the 21 communities of the Ontario Prehospital Advanced Life Support (OPALS) study. Systems provided a basic life support with defibrillation (BLS-D) level of care. Case and survival definitions followed the Utstein style. Descriptive and univariate methods (χ2</sup> and t test) were used to characterize EMS-witnessed cardiac arrest. Multivariate logistic regression was undertaken to assess predictors of survival to hospital discharge.</AbstractText>From January 1, 1991, to December 31, 1996, there were 9,072 cardiac arrest cases in the study communities. Of these, 610 (6.7%) were EMS-witnessed. The majority had preexisting cardiac or respiratory disease (81.5%) and experienced prodromal symptoms before EMS personnel arrived (91.4%). An initial rhythm of pulseless electrical activity was present in 50.1% of the patients, ventricular fibrillation/ventricular tachycardia in 34.2%, and asystole in 15.7%. Survival to discharge was 12.6%. Multivariate analysis identified the following as independent predictors of survival (odds ratio with 95% confidence intervals [CIs]): nitroglycerin use before EMS arrival: 2.3 (95% CI 1.2 to 4.5), prodromal symptoms of chest pain: 2.5 (95% CI 1.4 to 4.5) or dyspnea: 0.5 (95% CI 0.3 to 1.0), and unconsciousness on EMS arrival: 0.5 (95% CI 0.2 to 0.9). Patients with chest pain were more likely than dyspneic patients to experience ventricular fibrillation/ventricular tachycardia (62% versus 17%, P <.0001), and were 5 times more likely to survive (30.6% versus 6.3%, P <.0001).</AbstractText>EMS-witnessed cases are clearly an important subset of out-of-hospital cardiac arrest and are characterized by 2 distinct symptom groups: chest pain and dyspnea. These symptoms are important predictors of survival and may also help determine underlying mechanisms before patient collapse. A later phase of the OPALS study will prospectively evaluate the impact of out-of-hospital advanced life support on the survival of victims of EMS-witnessed cardiac arrest. [De Maio VJ, Stiell IG, Wells GA, Spaite DW, for the OPALS Study Group. Cardiac arrest witnessed by emergency medical services personnel: descriptive epidemiology, prodromal symptoms, and predictors of survival. Ann Emerg Med. February 2000;35:138-146.].</AbstractText>Copyright © 2000 American College of Emergency Physicians. Published by Elsevier Inc. All rights reserved.</CopyrightInformation> |
4,887 | The relation between mitral annulus motion and left ventricular ejection fraction in atrial fibrillation. | Mitral annulus motion (MAM) has recently been introduced as an index of left ventricular function. Previous studies have shown a good agreement between MAM (mm) x 5 and ejection fraction in middle-aged and elderly patients. These studies only included patients with sinus rhythm, while patients with atrial fibrillation were excluded. In the present study, MAM was reduced in patients with atrial fibrillation while ejection fraction (EF) did not differ from age-matched control patients with sinus rhythm. The 'conversion factor' (EF/MAM) was 7.2 in the group with atrial fibrillation and 5. 1 in controls with sinus rhythm. This difference must be taken into account when MAM is used to estimate left ventricular function in patients with atrial fibrillation. Patients with atrial fibrillation had lower stroke volume and higher heart rate than patients with sinus rhythm. A decreased systolic long-axis shortening was found (P<0.005) compared to patients with sinus rhythm, but no difference in short-axis diameter shortening. |
4,888 | Long-term low-dose cibenzoline in patients with chronic renal failure undergoing hemodialysis. | Because most anti-arrhythmic drugs are eliminated from the kidney, anti-arrhythmic drug therapy is largely restricted in patients undergoing hemodialysis (HD). Cibenzoline is a widely used antiarrhythmic drug excreted mainly from the kidney. The present study evaluated the safety and efficacy of reduced doses of cibenzoline (25 and 50 mg/day chronically) in 8 patients with maintenance HD. Cibenzoline was administered for more than 3 months without any problems in 7 of the 8 patients, although the medication was discontinued in 1 patient due to nausea and anorexia. With cibenzoline administration, the incidence and duration of atrial fibrillation decreased or disappeared in 6 of 7 patients and the frequency of complex ventricular arrhythmias was also reduced in 3 of 4 patients. No adverse side effects were noted. Plasma concentration of cibenzoline ranged from 169 to 220 ng/ml with the 25-mg/day dosage, and from 408 to 500 ng/ml with the 50-mg/day dosage. The concentrations remained stable during the study. In conclusion, low doses of cibenzoline are safe and effective in patients undergoing maintenance HD. However, intermittent monitoring is essential to ensure therapeutic drug concentrations. |
4,889 | Characteristics and outcomes in patients with acute myocardial infarction with ST-segment depression on initial electrocardiogram. | Acute myocardial infarction (AMI) with nonreciprocal ST-segment depression is said to have a poor prognosis, and early diagnosis and treatment are problematic. The aim of this study was to determine the proportion of unselected consecutive patients admitted to a university center with AMI with nonreciprocal ST-segment depression and to characterize these patients in terms of clinical features, treatment, and short- and long-term prognoses.</AbstractText>Admission electrocardiographic data on 852 consecutive admissions with AMI were analyzed. Nonreciprocal ST-depression was an admitting feature in 95 (11%) patients, the majority of whom had ST depression >3 mm. These were older (70.3 vs 66.8 years, P <.05), more likely to have had myocardial infarction (40% vs 25%, P <.01), and to have left ventricular failure (56% vs 42%, P <.5), cardiogenic shock (15% vs 9% P =.06), and atrial fibrillation (34% vs 19%, P <.01). Hospital mortality rate was significantly higher (31% vs 17%, P <.01). Patients were less likely to undergo thrombolysis (17% vs 31%, P <.01), angiography (22% vs 35%, P <.05), or percutaneous revascularization (5% vs 9%, P <.01). Patients with ST depression undergoing coronary angiography were more likely to have 3-vessel disease (71% vs 47%, P <.05). Mortality rate at follow-up (median 36 months) was significantly higher in patients with ST depression (56% vs 32%, P <.001). Analysis by individual electrocardiography demonstrated ST-segment depression to be the third most frequent presentation after ST elevation (n = 327) and T-wave changes (n = 258), in whom hospital mortality rates were 24% and 9%, respectively. In multivariate analysis, previous myocardial infarction was an independent predictor of nonreciprocal ST depression at initial examination (odds ratio 2.04 [1.25 to 3.34], P <.005). No electrocardiographic presentation was an independent predictor of death in the hospital after AMI.</AbstractText>In unselected cases of AMI, patients with ST-segment depression make up a significant minority (11%), who are likely to be older with a high prevalence of previous myocardial infarction and multivessel disease, and who have a poor prognosis.</AbstractText> |
4,890 | Cardiac arrest witnessed by emergency medical services personnel: descriptive epidemiology, prodromal symptoms, and predictors of survival. OPALS study group. | The Utstein guidelines recommend that emergency medical services (EMS)-witnessed cardiac arrests be considered separately from other out-of-hospital cardiac arrest cases. The objective of this study was to assess EMS-witnessed cardiac arrest and to determine predictors of survival in this group.</AbstractText>This prospective cohort included all adults with an EMS-witnessed cardiac arrest in the 21 communities of the Ontario Prehospital Advanced Life Support (OPALS) study. Systems provided a basic life support with defibrillation (BLS-D) level of care. Case and survival definitions followed the Utstein style. Descriptive and univariate methods (chi(2) and t test) were used to characterize EMS-witnessed cardiac arrest. Multivariate logistic regression was undertaken to assess predictors of survival to hospital discharge.</AbstractText>From January 1, 1991, to December 31, 1996, there were 9,072 cardiac arrest cases in the study communities. Of these, 610 (6.7%) were EMS-witnessed. The majority had preexisting cardiac or respiratory disease (81.5%) and experienced prodromal symptoms before EMS personnel arrived (91.4%). An initial rhythm of pulseless electrical activity was present in 50.1% of the patients, ventricular fibrillation/ventricular tachycardia in 34.2%, and asystole in 15.7%. Survival to discharge was 12.6%. Multivariate analysis identified the following as independent predictors of survival (odds ratio with 95% confidence intervals [CIs]): nitroglycerin use before EMS arrival: 2.3 (95% CI 1.2 to 4.5), prodromal symptoms of chest pain: 2.5 (95% CI 1.4 to 4.5) or dyspnea: 0.5 (95% CI 0.3 to 1.0), and unconsciousness on EMS arrival: 0.5 (95% CI 0.2 to 0.9). Patients with chest pain were more likely than dyspneic patients to experience ventricular fibrillation/ventricular tachycardia (62% versus 17%, P<.0001), and were 5 times more likely to survive (30.6% versus 6.3%, P<.0001).</AbstractText>EMS-witnessed cases are clearly an important subset of out-of-hospital cardiac arrest and are characterized by 2 distinct symptom groups: chest pain and dyspnea. These symptoms are important predictors of survival and may also help determine underlying mechanisms before patient collapse. A later phase of the OPALS study will prospectively evaluate the impact of out-of-hospital advanced life support on the survival of victims of EMS-witnessed cardiac arrest.</AbstractText> |
4,891 | Induction of atrial fibrillation with rapid high voltage ventricular pacing for ventricular fibrillation conversion testing. The Ventak AV II DR Study. | To assess whether rapid high voltage ventricular pacing can also induce atrial fibrillation, and whether the induction of atrial fibrillation during ventricular fibrillation conversion testing is related to the patient's heart disease.</AbstractText>Prospective study of 50 patients who received the dual chamber implantable cardioverter-defibrillator (ICD) Ventak AV II DR (Guidant) as a first implant. This device can record atrial activity even during a ventricular fibrillation episode and can induce atrial fibrillation by rapid atrial bursts.</AbstractText>Frequency of atrial fibrillation after induction of ventricular fibrillation; clinical characteristics of patients with and without induced atrial fibrillation; frequency of atrial fibrillation induced by rapid atrial bursts during predischarge testing.</AbstractText>Atrial fibrillation was observed in 40 of the 217 ventricular fibrillation episodes (18%) that could be detected immediately after delivery of high voltage pacing. The biphasic ICD shock for termination of ventricular fibrillation also terminated the atrial fibrillation in all cases. The 40 episodes of simultaneous atrial and ventricular fibrillation occurred in 18 patients (36%). The distribution of the clinical characteristics of the patients and the inducibility of atrial fibrillation during predischarge testing were similar in those with and without induced atrial fibrillation.</AbstractText>Rapid high voltage ventricular pacing frequently induces atrial fibrillation, which was terminated by the subsequent biphasic ICD shock. The induction of atrial fibrillation seems to be a non-specific phenomenon, unrelated to the clinical status of the patient.</AbstractText> |
4,892 | Long term prognosis after CABG in relation to preoperative left ventricular ejection fraction. | To evaluate the mortality rate, risk indicators for death, mode of death and symptoms of angina pectoris during 5 years after coronary artery by pass grafting (CABG) in relation to the preoperative left ventricular ejection fraction (LVEF).</AbstractText>All patients in western Sweden who underwent CABG without concomitant valve surgery and without previously performed CABG between June 1988 and June 1991.</AbstractText>In all 1904 patients were included in the analysis, of whom 173 (9%) had a LVEF < 40%. Patients with LVEF > or = 40% had a 5-year mortality of 12.5%. LVEF < 40% was associated with an increased risk of death (RR 2.3; 95% cl 1.7-3.1). There was no significant interaction between age, sex or any other factor in terms of clinical history and LVEF. However, left main stenosis was a strong independent predictor of death among patients with LVEF < 40% but not in those with a higher LVEF. Patients with a low LVEF more frequently died a cardiac death and a death associated with myocardial infarction (AMI). Furthermore they more frequently died in association with congestive heart failure and ventricular fibrillation. Among survivors, symptoms of angina pectoris were similar regardless of the preoperative LVEF.</AbstractText>Patients with a low preoperative LVEF have a more than two-fold increased risk of death during 5 years after CABG. Their increased risk of death includes cardiac death, death associated with AMI, congestive heart failure and ventricular fibrillation.</AbstractText> |
4,893 | Kallikrein gene delivery attenuates myocardial infarction and apoptosis after myocardial ischemia and reperfusion. | The tissue kallikrein-kinin system is present in the heart, and kinin has been shown to have cardioprotective effects. In this study, we investigated the potential role of tissue kallikrein in myocardial ischemia/reperfusion injury through adenovirus-mediated human kallikrein gene delivery. One week after gene delivery, the rats were subjected to a 30-minute coronary occlusion followed by a 2-hour reperfusion. Kallikrein gene delivery caused significant decreases in the ratio of infarct size to ischemic area at risk (from 69.6% to 44.5%, n=10 and 8, P<0.01) and in the incidence of ventricular fibrillation (from 64.3% to 16.7%, n=14 and 24, P<0.01) compared with the group injected with control adenovirus. Kallikrein gene delivery also attenuated programmed cell death in the ischemic area compared with the control area as assessed with the terminal deoxynucleotidyl transferase-mediated nick end labeling assay (n=6, P<0.01). Icatibant, a specific bradykinin B(2) receptor antagonist, abolished these kallikrein-mediated beneficial effects. The expression of human tissue kallikrein mRNA was identified in rat heart, kidney, lung, liver, and adrenal gland. After kallikrein gene delivery, cardiac kinin and cGMP levels were significantly elevated compared with the control (29.6+/-12.7 versus 6.1+/-2.1 pg/mg protein, n=7, P<0.01; 1.30+/-0.06 versus 0.86+/-0.09 pmol/mg protein, n=5, P<0.05). These results indicate that kallikrein gene delivery protects against myocardial infarction, ventricular arrhythmias, and apoptosis in ischemia/reperfusion injury via kinin-cGMP signal pathway. The successful application of this technology may have potential therapeutic value in the treatment of coronary artery diseases. |
4,894 | Serum troponins T and I after elective cardioversion. | To describe the pattern of release of five myocardial proteins after elective cardioversion.</AbstractText>We measured serum levels of the myocardial proteins creatine kinase, creatine kinase MB mass, myoglobin, troponin T and troponin I serially from baseline to 24 h after 72 elective cardioversion attempts. The total energy used for attempted cardioversion was 408+/-318 J (range 50 to 1280 J). Maximal creatine kinase levels (median 232 IU x l(-1), interquartile range 91 to 1152 IU x l(-1)) occurred at 24 h and correlated with the total energy delivered (r=0.75, P<0.0001). The peak creatine kinase MB mass levels exceeded the discrimination level for myocardial injury (>/=5 microg x l(-1)) in seven patients (10%). The peak myoglobin levels were elevated (>85 microg x l(-1)) in 40 patients (56%) and correlated with the peak creatine kinase levels (r=0.83, P<0.0001). Troponin T reached the discrimination level (0.10 microg x l(-1)) in one patient with a serum creatinine level of 0.16 mmol x l(-1)and severe left ventricular impairment. Twelve patients had baseline troponin I levels above our prespecified discrimination level of 0.4 microg x l(-1)(range 0.4 to 3.1 microg x l(-1)), which did not increase after cardioversion. In two patients the levels rose from <0.4 microg x l(-1) to 0.5 microg x l(-1) and 0.6 microg x l(-1) respectively.</AbstractText>Troponin T levels do not rise after elective cardioversion. The minor increases in troponin I may reflect our choice of discrimination level. Cardiac troponins are useful in determining whether arrhythmias requiring emergency cardioversion are primary or secondary to myocardial infarction.</AbstractText>Copyright 2000 The European Society of Cardiology.</CopyrightInformation> |
4,895 | Is there a need for routine testing of ICD defibrillation capacity? Results from more than 1000 studies. | Benefits and complications of postoperative implantable cardioverter-defibrillator tests are controversial matters. This study sought to assess the necessity of defibrillation function tests after implantation.</AbstractText>We retrospectively analysed 1007 implantable cardioverter-defibrillator tests in 587 systems and 556 patients. Nine hundred and thirty implantable cardioverter-defibrillator tests (89.4%) were routinely performed. Seventy-one tests (7%) were performed after a change in the antiarrhythmic drug regimen and six tests (0.60%) because of a suspected dysfunction of the implantable cardioverter-defibrillator. During routine tests, four systems (0.4%) failed to defibrillate the patient. However, in all but one test, abnormalities of the system had been observed before the test. After the addition of antiarrhythmic drugs, two of 71 implantable cardioverter-defibrillator systems (2.8%) failed to defibrillate the patient. One of six systems tested due to a suspected dysfunction failed to defibrillate the patient. During 16 tests (1.6%), complications occurred.</AbstractText>Our experience demonstrates that postoperative tests of the defibrillation function of implantable cardioverter-defibrillators rarely reveal dysfunctions. As testing is unpleasant for the patient and not free of complications, tests might be restricted to those patients in whom a dysfunction is suspected and to those patients in whom class I or class III antiarrhythmic drugs have been added to the antiarrhythmic drug regimen.</AbstractText>Copyright 2000 The European Society of Cardiology.</CopyrightInformation> |
4,896 | Out-of-hospital ventricular fibrillation in patients with acute myocardial infarction: coronary angiographic determinants. | The study intended to compare the acute coronary anatomy of patients with acute myocardial infarction (AMI) complicated by out-of-hospital ventricular fibrillation (VF) versus patients with AMI without this complication.</AbstractText>More than half of the deaths associated with AMI occur out of the hospital and within 1 h of symptom onset. The angiographic determinants of out-of-hospital VF in patients with AMI have not been investigated in detail.</AbstractText>Acute coronary angiographic findings of 72 consecutive patients with AMI complicated by out-of-hospital VF were compared with findings from 144 matched patients with AMI without this complication.</AbstractText>Patients with an acute occlusion of the left anterior descending coronary artery (LAD) or left circumflex coronary artery (LCx) had a higher risk for out-of-hospital VF compared with patients with an acute occlusion of the right coronary artery (RCA) (odds ratio and 95% confidence interval, respectively, 4.82 [2.35 to 9.92] and 4.92 [2.34 to 10.39]). With regard to extent of coronary artery disease (CAD), the location of the culprit lesion in the coronary arteries (proximal vs. mid or distal), the flow in the infarct related artery (IRA), the presence or absence of collaterals to the IRA and chronic occlusions, there were no differences between the two groups.</AbstractText>Acute myocardial infarction due to occlusion in the left coronary artery (LCA) is associated with greater risk for out-of-hospital VF compared to the RCA. The location of occlusion within LCA (LAD, LCx, proximal or distal), amount of myocardium at risk for necrosis and extent of CAD are not related to out-of-hospital VF.</AbstractText> |
4,897 | Cost-effectiveness analysis of a rural/urban first-responder defibrillation program. | To analyze the cost-effectiveness of a proposed first-responder defibrillation program in a small rural area in comparison with a recently initiated first-responder program in an adjoining urban center in southwestern Ontario. The purpose of the analysis was to quantify the expected benefits of the proposed program to determine whether the costs are justified.</AbstractText>This analysis was conducted on the city of Waterloo (population 80,000 over 25 square miles) and the adjoining rural township of Wellesley (population 8,000 over 105 square miles). The township has volunteer fire department first responders with basic life support (BLS), and basic life support/defibrillation (BLS-D) ambulances as the second tier; whereas the city's full-time fire department has recently adopted a first-responder defibrillation (BLS-D) program backed up by the same BLS-D ambulance service. The most relevant costs identified were the capital costs of the defibrillators, ancillary equipment, and biomedical service for preventive maintenance and routine nonwarranty work. Response intervals and percentage of patients found in ventricular fibrillation were projected and sensitivity analysis was applied.</AbstractText>The projected cost per life saved is $6,776 (C) in the urban area and $49,274 (C) in the rural area using an incremental save rate of 6%. Applying sensitivity analysis to the data, the save rate varied from 2% to 10%, resulting in a cost per life saved of $20,328 (C) and $4,066 (C), respectively, in the urban community. For the rural area, the cost per life saved ranged from $147,821 (C) (2%) to $29,564 (C) (10%). Even the worst-case save rate for the urban center [2%; $20,328 (C)] is significantly less than the best-case save rate [10%; $29,564 (C)] for the rural area.</AbstractText>The cost per life saved for a rural first-responder defibrillation program is significantly more expensive than one for an urban center. However, the cost per life saved is still economical compared with common treatments for other life-threatening illnesses.</AbstractText> |
4,898 | Combination pharmacotherapy with delayed countershock vs standard advanced cardiac life support after prolonged ventricular fibrillation. | To test the hypothesis that combination pharmacotherapy with delayed countershock would produce higher rates of return of spontaneous circulation (ROSC) and one-hour survival when compared with standard Advanced Cardiac Life Support (ACLS) therapy.</AbstractText>A prospective, block-randomized, blinded, laboratory experiment was conducted in an established swine model of prolonged ventricular fibrillation (VF). Fifty-six female domestic swine were anesthetized, instrumented, and shocked into VF with a bipolar pacing catheter. The VF was untreated for 8 minutes, then basic CPR was done mechanically for 1 minute. At 9 minutes of VF, the animals were randomized to treatment with one of seven therapies: group 1, combination pharmacotherapy with epinephrine (0.20 mg/kg), lidocaine (1.0 mg/kg), bretylium (5.0 mg/kg), propranolol (1.0 mg), and U-74389G (3.0 mg/kg); group 2, epinephrine (0.20 mg/kg); group 3, lidocaine (1.0 mg/kg) and bretylium (5.0 mg/kg); group 4, propranolol (1.0 mg); group 5, U-74389G (3.0 mg/kg); group 6, normal saline solution (volume equal to that for group 1); and group 7, standard ACLS (first countershock at 9 minutes of VF). Initial countershocks for groups 1-6 were given after 11 minutes of VF. Data were analyzed with two-tailed Fisher's exact test, with alpha set at 0.05.</AbstractText>Return of spontaneous circulation occurred in group 1 = 8/8 (100%); group 2 = 7/8 (88%); group 3 = 3/8 (38%); group 4 = 3/8 (38%); group 5 = 5/8 (63%); group 6 = 4/8 (50%); and group 7 = 3/8 (38%). One-hour survival occurred in group 1 = 8/8 (100%); group 2 = 5/8 (63%); group 3 = 2/8 (25%); group 4 = 2/8 (25%); group 5 = 3/8 (38%); group 6 = 2/8 (25%); and group 7 = 1/8 (13%).</AbstractText>Combination pharmacotherapy with delayed countershock (group 1) produced significantly higher rates of ROSC (p = 0.03) and one-hour survival (p = 0.001) when compared with standard ACLS in this porcine model of prolonged VF.</AbstractText> |
4,899 | Intravenous AMP 579, a novel adenosine A(1)/A(2a) receptor agonist, induces a delayed protection against myocardial infarction in minipig. | The aim of the study was to probe if acute administration of [1S-[1a, 2b,3b, 4a(S*)]]-4-[7-[[2-(3-chloro-2-thienyl)-1-methylpropyl]amino]-3H-imida zo[4,5-b] pyridin-3-yl] cyclopentane carboxamide (AMP 579) could provide a delayed protection against myocardial ischemia-reperfusion injury after 24 h. Anesthetized Yucatan minipigs were given an intravenous (i.v.) loading dose (3 microg/kg) of AMP 579 in 2 min followed by a 68-min infusion (0.3 microg/kg/min) and were allowed to recover. After 24 h, the animals were subjected to an open-chest operation and the left anterior descending coronary artery was occluded for 40 min, followed by 3 h of reperfusion. Results indicated that there were no significant differences in hemodynamic parameters between vehicle- and drug-treated groups either during drug infusion or ischemia-reperfusion. Both groups had similar area at risk (24.9% for vehicle and 25.1% for AMP 579-treated). However, the infarct size was 36.5% of area at risk in vehicle group (n=8) and 12.5% in AMP 579 group (n=8), representing a 66% reduction of infarct size by AMP 579 (p=0.011). This is the first report to demonstrate that in a large animal model, a hemodynamically silent, single i.v. dose of an adenosine receptor agonist can result in a delayed protection against myocardial infarction. |
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