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Biomedical subjects

E N Prystowsky

Publications and source records attributed to E N Prystowsky.

At least 37 records · Page 2Linked to original sources
PubMed1999

Relation of atrial refractoriness to upper and lower limits of vulnerability for atrial fibrillation/flutter following implantable ventricular defibrillator shocks.

BACKGROUND: Implantable ventricular cardioverter defibrillator (ICD) shocks can cause atrial fibrillation/flutter (AF). This study investigated the pathogenesis of AF after ICD shocks in a canine model. METHODS AND RESULTS: The study was conducted in 8 dogs. In 5 dogs (group 1), truncated exponential (8 ms, 78% tilt) monophasic and biphasic shocks were delivered through a bipolar epicardial (patch) or endocardial lead. After the last S1 of atrial pacing at a cycle length of 350 ms, shocks of 0.1 to 7.6 A (0.005 to 27.7 J) were delivered, timed to the atrial effective refractory period (AERP). Ventricular defibrillation thresholds were also determined. In 3 dogs (group 2), the effect of the open versus closed chest technique on AF induction was tested in the endocardial biphasic shock configuration. AF was induced in all 8 dogs and in all waveforms and configurations. Mean AF duration was 11.5+/-6 s, with a mean ventricular rate of 184+/-37 bpm. Ventricular shocks could induce AF only if they were timed between an AERP of -60 to 40 ms, -40 to 60 ms, -40 to 60 ms, and -20 to 60 ms in the epicardial monophasic, epicardial biphasic, endocardial monophasic, and endocardial biphasic configurations, respectively. The mean+/-SD of the upper limit of vulnerability (ULV) for AF induction (in J) was 5. 2+/-0.6, 3.5+/-0.4, 5.2+/-1.2, and 2.5+/-0.1 for the epicardial monophasic, epicardial biphasic, endocardial monophasic, and endocardial biphasic configurations, respectively (P<0.05). The lower limit of vulnerability (LLV) was 0.8+/-0.1, 0.8+/-0.1, 0.9+/-0, and 0.6+/-0 for the epicardial monophasic, epicardial biphasic, endocardial monophasic, and endocardial biphasic configurations, respectively (P=NS). The ventricular defibrillation threshold (in J) for all wave forms and configurations was higher than the ULV (P<0. 05). CONCLUSIONS: (1) An atrial LLV and ULV exist for ventricular ICD shock-induced AF; (2) the shock-induced AF is related to both shock intensity and its timing to AERP; and (3) avoiding this atrial window of vulnerability may minimize the risk of post-ICD shock AF.

Animals↗
PubMed1999

Prevention of implantable-defibrillator shocks by treatment with sotalol. d,l-Sotalol Implantable Cardioverter-Defibrillator Study Group.

BACKGROUND: Patients with implantable cardioverter-defibrillators often receive adjunctive antiarrhythmic therapy to prevent frequent shocks. We tested the efficacy and safety of sotalol, a beta-blocker with class III antiarrhythmic effects, for this purpose. METHODS: In a multicenter trial, patients were stratified according to left ventricular ejection fraction (< or =0.30 or >0.30), randomly assigned to double-blind treatment with 160 to 320 mg of sotalol per day (151 patients) or matching placebo (151 patients), and followed for 12 months. Kaplan-Meier analyses of the time to an event were performed. Three end points were used: the delivery of a first shock for any reason or death from any cause, the first appropriate shock for a ventricular arrhythmia or death from any cause, and the first inappropriate shock for a supraventricular arrhythmia or death from any cause. RESULTS: Compliance with double-blind treatment was similar in the two groups. There were seven deaths in the placebo group and four in the sotalol group. As compared with placebo, treatment with sotalol was associated with a lower risk of death from any cause or the delivery of a first shock for any reason (reduction in risk, 48 percent; P<0.001 by the log-rank test), death from any cause or the delivery of a first appropriate shock (reduction in risk, 44 percent; P=0.007), or death from any cause or the delivery of a first inappropriate shock (reduction in risk, 64 percent; P=0.004). Sotalol also reduced the mean (+/-SD) frequency of shocks due to any cause (1.43+/-3.53 shocks per year, as compared with 3.89+/-10.65 in the placebo group; P=0.008). In the sotalol group, the reduction in the risk of death from any cause or the delivery of a first shock for any reason did not differ significantly between patients with ejection fractions of more than 0.30 and those with ejection fractions of 0.30 or less. CONCLUSIONS: Oral sotalol was safe and efficacious in reducing the risk of death or the delivery of a first defibrillator shock whether or not ventricular function was depressed.

Adrenergic beta-Antagonists↗
PubMed1999

Management of ventricular arrhythmias: detection, drugs, and devices.

OBJECTIVE: To review evaluation and treatment of patients with ventricular arrhythmias, based on recent studies, with an emphasis on randomized controlled trials. DATA SOURCES: MEDLINE search of English-language publications of ventricular arrhythmias and their references from 1966 through April 27, 1998. References to articles were also scanned to broaden the search. STUDY SELECTION: Randomized controlled trials and all large nonrandomized trials of arrhythmias and arrhythmia therapy were reviewed. In addition, studies that led to changes in approach to patients with arrhythmias were reviewed. DATA EXTRACTION: We reviewed articles jointly for pertinent studies and information. DATA SYNTHESIS: The goals of treatment of the patient with ventricular arrhythmias are to suppress symptoms and prevent a fatal event. The steps in providing such therapy include defining the cardiac anatomy, assessing arrhythmia risk through noninvasive or invasive testing, and prescribing treatment based on these results. Patients may be separated into high- and low-risk groups to help identify appropriate treatment. While low-risk groups may benefit from reassurance or medications such as beta-blockers or verapamil, high-risk groups have been more difficult to treat. Recent randomized trials of implantable cardioverter defibrillators for ventricular arrhythmias suggest that they may provide better protection for high-risk patients than do antiarrhythmic medications. CONCLUSIONS: Treatment and understanding of risk from ventricular arrhythmias have advanced substantially in recent years. Classifying patients as being at high or low risk for fatal arrhythmias allows the physician to identify appropriate treatments for the high-risk patient without exposing the low-risk patient to unnecessary treatment-related risks.

Algorithms↗
PubMed1999

A simple bedside test of 1-minute heart rate variability during deep breathing as a prognostic index after myocardial infarction.

BACKGROUND: We evaluate a simple, bedside test that measures 1-minute heart rate variability in deep breathing as a predictor of death after myocardial infarction. METHODS: Bedside heart rate variability was assessed in 185 consecutive patients 5.1 +/- 2.5 days after a first myocardial infarction. Patients were instructed to take 6 deep respirations in 1 minute while changes in heart rate were measured and calculated by an electrocardiographic recorder. An abnormal test result was defined as a difference of less than 10 beats/min between the shortest and longest heart rate interval. RESULTS: Heart rate variability <10 beats/min was found in 65 patients (35%) and was significantly lower (P <.05) in women, patients >60 years of age, patients with diabetes, patients with congestive heart failure, and patients taking angiotensin-converting enzyme inhibitors. Mean follow-up period was 16 months. Ten patients died during follow-up: 9 of cardiac causes and 1 of stroke. Nine of these 10 patients had heart rate variability <10 beats/min (P =.004). The sensitivity and specificity of this test for cardiovascular mortality is 90.0% and 68.0%, respectively. The negative predictive value is 99.2% and the relative risk is 16.6. Heart rate variability <10 beats/min remained a significant predictor of death after adjusting for clinical, demographic, and left ventricular function with an odds ratio of 1.38 (95% confidence interval, 1.13-1.63). CONCLUSIONS: This simple, brief bedside deep breathing test of heart rate variability in patients after myocardial infarction appears to be a good predictor for all-cause mortality and sudden death. It may be used as a clinical test for risk stratification after myocardial infarction.

Death, Sudden, Cardiac↗
PubMed1999

Sotalol: An important new antiarrhythmic.

Sotalol, the most recently approved oral antiarrhythmic drug, has a unique pharmacologic profile. Its electrophysiology is explained by nonselective beta-blocking action as well as class III antiarrhythmic activity (including fast-activating cardiac membrane-delayed rectifier current blockade), which leads to increases in action potential duration and refractory period throughout the heart and in QT interval on the surface electrocardiogram. Its better hemodynamic tolerance than other beta-blockers may be a result of enhanced inotropy associated with class III activity. Sotalol's ability to suppress ventricular ectopy is similar to that of class I agents and better than that of standard beta-blockers. Unlike class I agents, its use in a postinfarction trial was not associated with increased mortality rate. Therapeutically, it has shown superior efficacy for prevention of recurrent ventricular tachycardia and ventricular fibrillation, which was the basis for its approval. In a randomized study, the Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) trial, sotalol was associated with an increased in-hospital efficacy prediction rate (by Holter monitor or electrophysiologic study), reduced long-term arrhythmic recurrence rate with superior tolerance, and lower mortality rate than class I ("standard") antiarrhythmic drugs. Sotalol was 1 of 2 drugs selected for comparison with implantable defibrillators in the recent National Institutes of Health Antiarrhythmics versus Implantable Defibrillator (AVID) study. Sotalol appears to be a preferred drug for use with implantable defibrillators; unlike some other agents (eg, amiodarone) it does not elevate and, indeed, may lower defibrillation threshold. Although unapproved for this use, sotalol is active against atrial arrhythmias. It has shown efficacy equivalent to propafenone and quinidine in preventing atrial fibrillation recurrence, but it is better tolerated than quinidine and provides excellent rate control during recurrence. Sotalol's major side effects are related to beta-blockade and the risk of torsades de pointes (acceptably small if appropriate precautions are taken). Unlike several other antiarrhythmics (eg, amiodarone), it has no pharmacokinetic drug-drug interactions, is not metabolized, and is entirely renally excreted. Initial dose is 80 mg twice daily, with gradual titration to 240 to 360 mg/day as needed. The daily dose must be reduced in renal failure. On the basis of favorable clinical trials and practice experience, sotalol has shown a steadily growing impact on the treatment of arrhythmias during its 5 years of market availability, a trend that is likely to continue.

Action Potentials↗
PubMed1999

Implantable defibrillator event rates in patients with unexplained syncope and inducible sustained ventricular tachyarrhythmias: a comparison with patients known to have sustained ventricular tachycardia.

OBJECTIVES: To assess the clinical significance of inducible ventricular tachyarrhythmias among patients with unexplained syncope. BACKGROUND: Induction of sustained ventricular arrhythmias at electrophysiology study in patients with unexplained syncope and structural heart disease is usually assigned diagnostic significance. However, the true frequency of subsequent spontaneous ventricular tachyarrhythmias in the absence of antiarrhythmic medications is unknown. METHODS: In a retrospective case-control study, the incidence of implantable cardiac defibrillator (ICD) therapies for sustained ventricular arrhythmias among patients with unexplained syncope or near syncope (syncope group, n = 22) was compared with that of a control group of patients (n = 32) with clinically documented sustained ventricular tachycardia (VT). Sustained ventricular arrhythmias were inducible in both groups and neither group received antiarrhythmic medications. All ICDs had stored electrograms or RR intervals. Clinical variables were similar between groups except that congestive cardiac failure was more common in the syncope group. RESULTS: Kaplan-Meier analysis of the time to first appropriate ICD therapy for syncope and control groups produced overlapping curves (p = 0.9), with 57 +/- 11% and 50 +/- 9%, respectively, receiving ICD therapy by one year. In both groups, the induced arrhythmia was significantly faster than spontaneous arrhythmias, but the cycle lengths of induced and spontaneous arrhythmias were positively correlated (R = 0.6, p < 0.0001). During follow-up, three cardiac transplantations and seven deaths occurred in the syncope group, and two transplantations and five deaths occurred in the control group (36-month survival without transplant 52 +/- 11% and 83 +/- 7%, respectively, p = 0.03). CONCLUSIONS: In patients with unexplained syncope, structural heart disease and inducible sustained ventricular arrhythmias, spontaneous sustained ventricular arrhythmias occur commonly and at a similar rate to patients with documented sustained VT. Thus, electrophysiologic testing in unexplained syncope can identify those at risk of potentially life-threatening tachyarrhythmias, and aggressive treatment of these patients is warranted.

Aged↗
PubMed1998

Perspectives and controversies in atrial fibrillation.

Atrial fibrillation (AF) is the most common sustained arrhythmia in humans. The 3 basic tenets of therapy are (1) restoration and maintenance of sinus rhythm; (2) ventricular rate control; and (3) prevention of thromboembolism. Maintenance of sinus rhythm appears preferable to rate control alone in patients with significant symptoms caused by AF. Complete suppression of AF with drug therapy for >6 months is unusual, but it is not the sole criterion of success. As with other chronic cardiac disorders such as angina and heart failure, a marked reduction in frequency and duration of episodes of AF will likely translate into an excellent clinical outcome. The major risk of antiarrhythmic drug therapy is ventricular proarrhythmia, which is seen most frequently in patients with substantial left ventricular dysfunction. Torsade de pointes is the most frequent proarrhythmia that occurs with antiarrhythmic agents that prolong ventricular repolarization and the QT interval. To minimize the risk of proarrhythmia, antiarrhythmic drugs are started in-hospital in patients with significant heart disease, and agents are selected based on certain patient characteristics. For example, the drugs initially selected for patients with heart failure and coronary artery disease are amiodarone and sotalol, respectively. Two approaches may be used to decrease the thromboembolic risk associated with cardioversion of AF to sinus rhythm. In the conventional method, warfarin is given (INR 2.0-3.0) for 3 weeks before and at least 4 weeks after cardioversion. An alternative approach employs transesophageal echocardiography to rule out left atrial thrombi before cardioversion. Both methods appear reasonable and safe, and I prefer the conventional and transesophageal echocardiography-guided approaches for outpatients and in-hospital patients, respectively.

Atrial Fibrillation↗
PubMed1998

Drug treatment of atrial fibrillation in the managed care era.

There are many reasons why one might wish to suppress atrial fibrillation (AFib) and attempt to maintain sinus rhythm. This article assumes that the clinical decision to maintain sinus rhythm has been made. That being the case, antiarrhythmic drug therapy is generally the first line of treatment of AFib. Currently in the United States, there are 8 available antiarrhythmic drugs that have demonstrated efficacy for preventing AFib. The drugs are quinidine, procainamide, disopyramide, flecainide, propafenone, moricizine, sotalol, and amiodarone. Because AFib tends to recur regardless of the drug selected, recurring in at least one-half of the patients being treated, no drug is clearly better than any other for suppression of AFib. Furthermore, because AFib is rarely life-threatening, occasional recurrence should be anticipated and should not be considered failure per se. The measure of drug efficacy is the frequency of recurrence. Before initiating drug therapy, the presence or absence of structural heart disease must be determined, because in the absence of structural heart disease, antiarrhythmic drugs generally can be given rather safely, but in the presence of structural heart disease, especially when associated with ventricular dysfunction, there is an important risk of developing ventricular proarrhythmia. Considerations for specific drug selection are discussed and an algorithm for therapy is suggested.

Anti-Arrhythmia Agents↗
PubMed1997

Utility and cost of event recorders in the diagnosis of palpitations, presyncope, and syncope.

In 184 patients given an event recorder for the evaluation of palpitations, syncope or presyncope, we found that event recorders are useful and relatively inexpensive in the initial evaluation of patients with palpitations regardless of the presence of heart disease, and of syncopal or presyncopal patients without heart disease. In patients with presyncope or syncope who have heart disease and a negative electrophysiology evaluation, event recorders have less utility and are more costly.

Adult↗
PubMed1997

Atrioventricular node reentry: physiology and radiofrequency ablation.

Atrioventricular (AV) node reentry has been recognized as a clinical arrhythmia for many years. Earlier basic investigations identified a dual AV conduction system, and atrial echo beats occurred when the refractory period of the slow conduction pathway was shorter than the fast pathway. Subsequent studies in humans confirmed the concept of dual AV node physiology and AV node reentry. Slow-fast AV node reentry (anterograde conduction over the slow pathway and retrograde conduction over the fast pathway) occurs most frequently. The fast-slow and intermediate varieties are much less common. A high (> 95%) cure rate occurs with radiofrequency catheter ablation with experienced electrophysiologists. Most electrophysiologists prefer the posterior approach, which results in absence or very poor conduction over the slow AV node pathway: the PR interval is minimally changed. This approach is highly successful for all three forms of AV node reentry and associated with a 1%-2% incidence of heart block in most experienced laboratories.

Animals↗
PubMed1997

Atrial fibrillation/flutter induced by implantable ventricular defibrillator shocks: difference between epicardial and endocardial energy delivery.

INTRODUCTION: We evaluated the incidence and energy dependence of atrial fibrillation/flutter (AF) induced by implantable ventricular defibrillator shocks in 63 patients tested in the operating room or electrophysiology laboratory. METHODS AND RESULTS: Defibrillator shocks were epicardial monophasic in 32 patients, and through an Endotak lead endocardial monophasic in 19 and biphasic in 12 patients. The epicardial and endocardial patient groups had similar clinical characteristics. A total of 517 defibrillator shocks were given. The epicardial group received 336 total defibrillator shocks and 10 +/- 6 shocks (mean +/- SD) per patient compared with the endocardial group, which received 181 total shocks and 6 +/- 4 defibrillator shocks per patient (P = 0.004). In the epicardial group, AF occurred in 13 (41%) patients and in 17 (5%) of the 336 shocks. No AF was induced with endocardial defibrillator shocks. The epicardial mean energy was 16 +/- 9 J, lower than the endocardial mean energy of 20 +/- 9 J (P < 0.004). In the epicardial monophasic group, energy correlated with AF induction. Each patient received 7 +/- 6 defibrillator shocks < 15 J and 4 +/- 2 shocks > or = 15 J, yet AF occurred in only 2.3% versus 9.6% (P < 0.05) of defibrillator shocks < 15 J and > or = 15 J, respectively. Of note, AF was not induced with energy < 4 J or > 31 J. CONCLUSIONS: In the epicardial configuration, AF induction is energy dependent, with an apparent lower and upper limit of vulnerability. AF induction by defibrillator shocks delivered through an Endotak lead is very rare, possibly related to an apparent upper limit of vulnerability of less energy, avoidance of thoracotomy, or different energy field distribution.

Adult↗
PubMed1996

Proarrhythmia during drug treatment of supraventricular tachycardia: paradoxical risk of sinus rhythm for sudden death.

The purpose of this review is to summarize available data concerning proarrhythmia during drug therapy for supraventricular tachycardia. Patients were included in this review if 4 elements of treatment were available from the citation: (1) presence or absence of heart disease; (2) type of supraventricular tachycardia; (3) type of antiarrhythmic drug; and (4) type of proarrhythmic event. Citations spanning the years 1922-1995 yielded 56 reports and 195 events meeting the inclusion criteria. Atrial fibrillation was the most common arrhythmia and occurred alone in 76% of patients. Heart disease was present in 96% of patients. Proarrhythmic events were associated with 8 antiarrhythmic drugs in a total of 195 administered regimens. An adverse arrhythmic event was reported most frequently with quinidine (72%). Torsades de pointes was the most common of the documented proarrhythmic events (61%). Although supraventricular tachycardias are rarely in themselves life-threatening, symptoms may be disabling for many patients, and their lifestyle may be measurably improved by the maintenance of sinus rhythm. An algorithm is presented that takes into account the factors that predispose to proarrhythmia; it attempts to minimize the risk of treating these patients with antiarrhythmic drugs.

Anti-Arrhythmia Agents↗
PubMed1996

Differential effects of changes in local myocardial refractoriness on atrial and ventricular latency.

BACKGROUND: Assessment of myocardial refractoriness and conduction properties, critical to development and propagation of reentrant arrhythmias, is an integral part of the investigation of atrial and ventricular tachycardias through the use of programmed electrical stimulation. Local conduction itself, however, may be affected by myocardial refractoriness. METHODS AND RESULTS: We studied the effects of changes in myocardial refractoriness on local conduction in right atrial and ventricular myocardium in 19 patients. Changes in effective, functional, and relative refractoriness were accomplished with the use of four pacing protocols, including drive train pacing cycle lengths (PCLs) of 600 and 400 milliseconds (ms) and drive train durations (DTDs) of 8 and 50 stimuli. Unipolar cathodal stimulation was performed from the distal electrode, and unipolar electrograms were recorded from the proximal three poles of quadripolar catheters with 5-mm interelectrode spaces. Atrial and ventricular effective and relative refractory periods (ERPs and RRPs) were significantly shortened by both the reduction in PCL and the increase in DTD. The reduction in the PCL shortened atrial and ventricular refractory periods significantly more than did the increase in the DTD. Changes in ventricular refractory periods were significantly greater compared with atrial refractory periods. The ratio of RRP to ERP was reduced in the atrium but significantly increased in the ventricle with reduction in PCL and increase in DTD. For all premature intervals, the conduction interval from stimulus to the first recording electrode pole was significantly greater than conduction intervals measured between subsequent electrode poles. The greatest increase in conduction interval with closely coupled premature complexes occurred between the stimulus artifact and the first recording electrode pole. Reduction in ventricular but not atrial ERP was associated with significantly increased local conduction interval. CONCLUSIONS: First, most of the conduction delay after the stimulus artifact occurs within 5 mm from the pacing site. Second, closely coupled premature complexes delay conduction primarily by prolonging latency in the first 5 mm from the pacing site. Third, fundamental differences occur between the atrium and ventricle regarding changes in local conduction as a function of changes in ERP, suggesting that factors involved in sudden changes in refractoriness (eg, heart rate acceleration) could produce divergent effects on atrial and ventricular arrhythmogenesis.

Adult↗
PubMed1996

Nonsustained ventricular tachycardia in coronary artery disease: relation to inducible sustained ventricular tachycardia. MUSTT Investigators.

BACKGROUND: Many physicians believe that electrocardiographic characteristics of nonsustained ventricular tachycardia correlate with the risk for sudden death in survivors of myocardial infarction. Sustained ventricular tachycardia induced by programmed electrical stimulation has also been shown to predict sudden death. OBJECTIVE: To determine whether electrocardiographic characteristics of spontaneous nonsustained ventricular tachycardia can predict the inducibility of sustained ventricular tachycardia by programmed electrical stimulation in patients with coronary artery disease having abnormal ventricular function. DESIGN: Observational cohort study. SETTING: 70 clinical electrophysiology laboratories in the United States and Canada. PATIENTS: 1480 consecutive patients with coronary artery disease, left ventricular ejection fraction of 0.40 or less, and asymptomatic nonsustained ventricular tachycardia. INTERVENTION: Electrophysiologic study attempting to induce sustained monomorphic ventricular tachycardia. MEASUREMENTS: Daily frequency, duration, and cycle length of spontaneous episodes of nonsustained ventricular tachycardia, measured by standard electrocardiographic recordings. RESULTS: No statistically significant difference in the frequency or duration of spontaneous nonsustained ventricular tachycardia was seen between patients with and those without inducible sustained ventricular tachycardia. Rates of spontaneous tachycardia were slightly slower in patients with inducible ventricular tachycardia than in patients without inducible ventricular tachycardia (P = 0.047), but the difference was not clinically significant. CONCLUSION: Electrocardiographic characteristics of spontaneous nonsustained ventricular tachycardia do not predict which patients with coronary artery disease will have inducible sustained ventricular tachycardia.

Coronary Disease↗
PubMed1996

Effect of continuous vagal enhancement on concealed conduction and refractoriness within the atrioventricular node.

This study examined the complex interaction between vagal enhancement and how a concealed atrial impulse alters atrioventricular (AV) nodal function. In theory, vagal augmentation could increase or decrease the effect that a premature atrial beat has on the subsequent beat. In 10 patients we established the AV nodal effective refractory period (ERP) without and with a conditioning atrial stimulus (Sc); the stimulation protocol was then repeated after enhancing reflex vagal tone with a continuous phenylephrine infusion. During phenylephrine infusion, the sinus cycle length prolonged from 827 +/- 99 to 1,029 +/- 223 ms (p < 0.001) and AV nodal ERP increased from 331 +/- 51 to 425 +/- 64 ms (p < 0.005). At control, AV nodal ERP in the presence of Sc prolonged to 536 +/- 69 ms (p < 0.001), and during phenylephrine infusion increased to 579 +/- 57 ms (p < 0.01), a change significantly less than during control (58 +/- 14% vs 31 +/- 14%, respectively, p < 0.01). Further experiments suggest that the effect of Sc was reduced because it occurred earlier relative to the vagally prolonged AV nodal ERP. In conclusion, this study demonstrates a complex relation between the timing of a premature atrial beat causing concealed conduction and the degree of vagal tone. The concealed beat, as related to the AV node ERP, has a substantial effect on subsequent AV nodal conduction. These data give insights into clinical AV nodal function.

Adrenergic beta-Agonists↗