Use of disopyramide by arrhythmia specialists after Cardiac Arrhythmia Suppression Trial: patient selection and initial outcome.
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Arrhythmias, Cardiac↗
Biomedical subjects
E N Prystowsky
Publications and source records attributed to E N Prystowsky.
Electrophysiologic and anatomic characteristics of ventricular tachycardia induced at the right ventricular outflow tract but not at the apex.
The site of ventricular stimulation is an important variable in the initiation of ventricular tachycardia (VT) by programmed ventricular stimulation. Among 169 patients studied consecutively, 17 (10%) had ventricular tachycardia induced by programmed electrical stimulation from the right ventricular outflow tract but not from the apex. Fourteen of these 17 patients had had prior myocardial infarction (12 had inferior, and two had both inferior and anterior myocardial infarction), two had a dilated cardiomyopathy, and one had a localized cardiomyopathy. Fourteen patients had echocardiograms suitable for analysis. Of these, 12 had posterior/inferior ventricular wall motion abnormalities located at the base of the heart. The ventricular effective refractory periods from the right ventricular outflow tract and right ventricular apex were 237 +/- 4 and 244 +/- 5 msec, respectively (p less than 0.05, mean +/- SEM). Induced VT had a cycle length of 229 +/- 4 msec and had the morphology of right bundle branch block in 12 patients, of left bundle branch block in three patients, and had both morphologies in two patients. In 14 patients the axis was superior. VT was initiated with two extrastimuli in 15 patients and with burst right ventricular pacing in two patients. Similar pacing techniques with identical pacing intervals did not induce VT at the right ventricular apex in 14 of these 17 patients. Further, among the 15 patients whose VT was induced at the right ventricular outflow tract with two extrastimuli, neither burst pacing (n = 13) nor two extrastimuli introduced at faster paced rates (n = 12) induced VT at the right ventricular apex.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac Pacing, Artificial↗
Syncope secondary to paroxysmal high grade AV block in a heavily trained man.
J.B. is a well-trained male with syncope due to paroxysmal AV nodal heart block who ultimately required a permanent pacemaker despite an initial attempt at cessation of training only. Baseline sinus node function was normal, but AV nodal conduction remained abnormal even after autonomic blockade supporting intrinsic AV nodal dysfunction. This case illustrates that vigorous physical training may unmask previously unrecognized intrinsic dysfunction of AV nodal conduction or, as previously reported for physical training induced sinus node dysfunction, cause AV nodal dysfunction. Simple cessation of training to treat this problem is often recommended but may not be adequate for some patients who remain at risk for recurrent syncope during the deconditioning period.
Autonomic Nervous System↗
Effect of continuous enhanced vagal tone on atrioventricular nodal and sinoatrial nodal function in humans.
A constant intravenous infusion of phenylephrine (0.74 +/- 0.41 micrograms/kg/min) was given to 10 patients to cause a continuous augmentation in reflex vagal tone. After the infusion, the diastolic blood pressure increased from 76 +/- 7 to 89 +/- 11 mm Hg (p less than 0.01). The sinus cycle length and atrial-His (AH) interval were measured, and incremental atrial pacing was performed before and during phenylephrine infusion until atrioventricular (AV) nodal block was achieved. For each patient, the AV nodal function curve (i.e., the AH interval plotted as a function of the atrial pacing cycle length) was compared during both the control state and phenylephrine infusion; the AH intervals during each condition at chosen short (AHS) and long (AHL) cycle lengths were compared. The sinus cycle length increased during phenylephrine infusion from 941 +/- 294 to 1,115 +/- 347 msec (p = 0.013). The AH interval during sinus rhythm was not significantly prolonged (77 versus 82 msec, p = NS). The shortest atrial pacing cycle length yielding 1:1 AV nodal conduction increased during phenylephrine infusion from 412 +/- 120 to 575 +/- 211 msec (p less than 0.01). Of note, the degree of sinus cycle length prolongation did not correlate with the degree of prolongation in the shortest atrial pacing cycle length yielding 1:1 AV nodal conduction. The AV nodal function curve was shifted markedly to the right and only slightly upward.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Electrophysiology: the Wolff-Parkinson-White syndrome.
Though tachyarrhythmias occur commonly in patients with the Wolff-Parkinson-White syndrome, many patients remain asymptomatic. Recent studies suggest that routine electrophysiologic testing in these individuals is of limited value. However, electrophysiologic testing remains very helpful in the symptomatic patient for predicting arrhythmia recurrence and for determining accessory pathway location and function. Unfortunately, noninvasive tests to predict high-risk WPW patients has not been proven helpful because of their low specificity. A number of recent studies have shown that autonomic function can markedly improve accessory pathway function and even counteract the effect of antiarrhythmic drugs. Given the frequent failure of antiarrhythmic therapy in the WPW syndrome, there has been increasing interest in nonpharmacologic therapies, including high-energy DC shock and radiofrequency catheter ablation of accessory pathways, which may prove to be more cost-effective than surgery.
Anti-Arrhythmia Agents↗
Occurrence of atrial fibrillation in patients with paroxysmal supraventricular tachycardia due to atrioventricular nodal reentry.
The occurrence of atrial fibrillation in patients with paroxysmal supraventricular tachycardia (PSVT) has been well documented when PSVT is secondary to atrioventricular reentry, but not when PSVT is secondary to atrioventricular nodal reentry (AVNRT). Seventeen patients with AVNRT were followed using transtelephonic electrocardiogram monitoring to document symptomatic tachycardias. The median length of telephone monitor surveillance was 357 days. Fifteen of 17 patients transmitted electrocardiograms that showed PSVT. Three of 17 patients (18%) transmitted electrocardiograms that showed atrial fibrillation. A transition from PSVT into atrial fibrillation was not recorded, but all three did have PSVT recorded on other days of follow-up. We report the occurrence of atrial fibrillation in patients with AVNRT and that its incidence is higher than expected for the general population.
Atrial Fibrillation↗
Critical decisions in arrhythmia management.
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Arrhythmias, Cardiac↗
Ventricular arrhythmias: risk stratification and approach to therapy after the Cardiac Arrhythmia Suppression Trial (CAST).
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Anilides↗
Nonpharmacologic treatment of the Wolff-Parkinson-White syndrome and other supraventricular tachycardias.
Nonpharmacologic treatment using surgery or intracardiac catheter ablation can be used for several forms of supraventricular tachycardia. Surgery is highly successful in preventing recurrent tachyarrhythmias in patients with the Wolff-Parkinson-White syndrome and can be recommended as first-line treatment in several situations. Catheter ablation of the atrioventricular conduction system combined with an implanted ventricular pacemaker can offer substantial relief to selected patients with drug-refractory atrial fibrillation. Technical advances in catheter ablation will undoubtedly lead to more widespread use of this form of therapy in supraventricular tachycardia.
Cardiac Catheterization↗
Importance of preexcited QRS morphology during induced atrial fibrillation to the diagnosis and localization of multiple accessory pathways.
The present investigation evaluates the ability of several electrocardiographic (ECG) and electrophysiologic methods to identify multiple accessory pathways in 47 patients in whom the presence and sites of multiple accessory pathways were confirmed intraoperatively. To establish ECG features that suggested the presence of multiple accessory pathways in these patients, we initially studied the 12-lead ECG during maximal preexcitation in 101 patients with single accessory pathways. Distinctive 12-lead ECG patterns were noted for six defined anatomic areas around the right and left atrioventricular groove. Multiple preexcited QRS morphologies, each typical for a separate accessory pathway, and atypical preexcited QRS morphologies were recorded during atrial fibrillation in 31 of 47 (66%) patients with multiple accessory pathways. By comparison, the ECG during sinus rhythm and rapid atrial pacing identified 14 (32%) and 26 (55%) of the patients, respectively. In 12 (26%) patients in whom evidence for multiple accessory pathways was absent from endocardial mapping data, atrial fibrillation provided the diagnosis. In five (11%) patients, atrial fibrillation was the only method that demonstrated the presence of multiple accessory pathways. A combination of ECG findings during atrial fibrillation and rapid atrial pacing plus endocardial mapping data identified 43 (91%) of the patients with multiple accessory pathways. There were two unique fusion patterns on the 12-lead ECG that were characteristic of specific multiple accessory pathway combinations.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Utility of introducing ventricular premature complexes during reciprocating tachycardia in specifying the location of left free wall accessory pathways.
The usefulness of the response to single and double ventricular premature complexes (VPCs) introduced during reciprocating tachycardia (RT) in predicting the location of a left free wall accessory pathway was studied in 55 patients with the Wolff-Parkinson-White syndrome. One VPC introduced from the right ventricle into narrow QRS RT when the His bundle was refractory resulted in retrograde atrial preexcitation in 25 of 55 (45%) patients, while 30 (55%) showed no preexcitation. Double VPCs produced retrograde atrial preexcitation in 9 of 26 patients not responding to a single VPC. No difference in RT cycle length, AH, HV or ventriculoatrial intervals was found between those patients who did or did not show retrograde atrial preexcitation. The response to single and double VPCs during RT was related to the location of the AP. The average distance of the AP from the crux determined by intraoperative epicardial mapping in the 41 patients who underwent surgery was 2.7 +/- 0.7 mapping units (left posterolateral region) in patients showing retrograde atrial preexcitation with a single VPC, 3.6 +/- 0.7 units (at the lateral left ventricular margin) in those responding to double VPCs and 4.3 +/- 0.8 units (beyond the LV margin) in those showing no response. Left bundle--branch block (LBBB) aberrancy during RT resulted in an average 60 +/- 14 ms prolongation of the ventriculoatrial interval in 40 patients, including 5 in whom LBBB was seen only after procainamide infusion. VPCs introduced into LBBB RT resulted in significant retrograde atrial preexcitation in 6 additional patients in whom no response during normal QRS RT was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
Bundle-Branch Block↗
The electrophysiologic effects of enoximone in patients with preexisting ventricular tachyarrhythmias.
Electrophysiologic and hemodynamic effects of intravenous enoximone were studied in 15 male patients, mean age 62.2 years, with New York Heart Association classes II to IV congestive heart failure (coronary artery disease in 10 and idiopathic dilated cardiomyopathy in five patients; mean ejection fraction, 0.19). All patients had spontaneous ventricular tachyarrhythmias; eight had sustained ventricular tachycardia (VT), one had ventricular fibrillation, and six had nonsustained VT. Hemodynamic and electrophysiologic parameters including VT induction were determined before and during an intravenous infusion of enoximone. The cardiac index increased (2.49 +/- 0.89 to 2.96 +/- 0.78), and the pulmonary capillary wedge pressure decreased (22.4 +/- 13.2 to 10.0 +/- 9.0) after enoximone per predefined protocol endpoints. There was a significant decrease in spontaneous sinus cycle length, corrected sinus nodal recovery time, AH interval during atrial pacing, shortest cycle length at which 1:1 atrioventricular nodal conduction occurred, and refractory periods of the atrium, ventricle, and atrioventricular node. Enoximone did not alter the cycle length of induced VT, and there was no consistent change in the number of extrastimuli required for VT induction. A baseline 24-hour ECG recording was obtained on 14 patients (while receiving a long-term antiarrhythmic drug regimen, if needed) and repeated after 1 week and 1 month of oral enoximone therapy. There was no significant increase in the number of premature ventricular complexes per hour or VT episodes per 24 hours after 1 week or 1 month of therapy with enoximone. However, if four patients who received amiodarone and may not yet have reached steady state were excluded from analysis, there was a significant increase in the frequency of premature ventricular complexes per hour 1 month after initiation of enoximone. We conclude that intravenous enoximone reduces pulmonary capillary wedge pressure and increases cardiac output in most patients. Intravenous enoximone in doses sufficient to have hemodynamic effects shortens atrial, ventricular, and atrioventricular nodal refractoriness and decreases AV nodal conduction time but has no consistent effect on VT induction or VT cycle length. The frequency of spontaneous ventricular ectopy may increase in some patients after oral enoximone, but its clinical significance is undefined. Enoximone may be administered cautiously to patients with congestive heart failure and preexisting ventricular tachyarrhythmias.
Administration, Oral↗
Arrhythmogenic effects of antiarrhythmic drugs: a study of 506 patients treated for ventricular tachycardia or fibrillation.
Antiarrhythmic therapy in 506 consecutive patients undergoing 1,268 antiarrhythmic drug trials for ventricular tachycardia or ventricular fibrillation was reviewed for evidence of arrhythmogenic drug effect defined as the occurrence of a new form of ventricular tachyarrhythmia temporally associated with initiation of drug therapy or dosage increase. Arrhythmogenic effects occurred in 6.9% of patients and 3.4% of drug trials. This ranged from a high of 11.8% caused by encainide to none occurring with procainamide, tocainide or beta-adrenergic blocking drugs. The incidence of arrhythmogenesis was significantly greater in patients whose presenting arrhythmia was sustained ventricular tachycardia than it was in those who presented with nonsustained ventricular tachycardia or ventricular fibrillation (p = 0.02). Decreased systolic function measured echocardiographically at the base of the left ventricle was associated with an increased incidence of arrhythmogenic effects (p = 0.006) whereas global left ventricular ejection fraction was not. Age, gender, cardiac diagnosis, location of prior myocardial infarction and New York Heart Association functional class for heart failure were not related to the occurrence of drug-induced arrhythmias. These findings emphasize the need for in-hospital cardiac monitoring during initiation of antiarrhythmic drug therapy for ventricular tachyarrhythmias.
Adolescent↗
Asymptomatic Wolff-Parkinson-White. Should we intervene?
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Death, Sudden↗
Encainide for treatment of atrioventricular reciprocating tachycardia in the Wolff-Parkinson-White syndrome.
Oral encainide, varying from 75 to 300 mg/day (mean 174 mg/day), was administered to 52 patients with drug-resistant atrioventricular reciprocating tachycardia (AVRT) associated with the Wolff-Parkinson-White syndrome. Electrophysiologic studies were performed before and during drug treatment. Encainide resulted in anterograde accessory pathway block in 15 of 37 (41%) and retrograde accessory pathway block in 11 of 46 (24%) patients. In patients with residual accessory pathway conduction, encainide significantly prolonged the shortest pacing cycle length maintaining anterograde (261 +/- 26 to 404 +/- 85 ms) and retrograde (279 +/- 46 to 436 +/- 87 ms) accessory pathway conduction, as well as the anterograde accessory pathway effective refractory period (271 +/- 32 to 329 +/- 73 ms). AVRT could not be induced during encainide therapy in 20 of 49 patients (41%). In the remaining patients, AVRT cycle length increased (319 +/- 44 to 426 +/- 90 ms, p less than 0.001) due to prolongation of HV and ventriculoatrial intervals. During follow-up (mean 38.5 months), 30 patients continued to take the drug and 7 patients with favorable drug response subsequently elected to undergo surgical accessory pathway ablation (71% overall favorable response). Encainide was ineffective in 11 patients, was discontinued because of drug intolerance in 2 patients and exacerbated ventricular tachycardia in 2 patients. Lack of AVRT inducibility at encainide electrophysiologic study did not always predict recurrence-free follow-up. Encainide is an effective and well-tolerated drug to prevent recurrence of AVRT in patients with Wolff-Parkinson-White syndrome.
Administration, Oral↗
Encainide for atrial fibrillation associated with Wolff-Parkinson-White syndrome.
Thirty-six patients with a history of atrial fibrillation and Wolff-Parkinson-White syndrome were treated with oral encainide, 175 +/- 44 mg/day, after undergoing baseline drug-free electrophysiologic studies. The mean age was 38 +/- 15 years, with structural heart disease present in only 3 patients. Nine patients had only paroxysmal atrial fibrillation and 27 patients had both atrial fibrillation and atrioventricular reciprocating tachycardia (AVRT). Symptoms were present for a mean of 195 +/- 168 months and were treated with an average of 2.7 +/- 1.6 drugs before encainide. Anterograde block in the accessory pathway occurred in 12 of 30 patients (40%) and retrograde block accessory pathway occurred in 10 of 24 patients in whom comparison could be made. AVRT was initiated in 29 of 36 patients during the control study and could be initiated in 19 of 29 patients while receiving encainide. Drug efficacy was determined by the clinical response judged completely effective, partially effective or ineffective. During a mean follow-up of 30.1 +/- 25 months, 24 patients (67%) continued to take encainide. Encainide was completely effective in 14 of 24 patients and partially effective in another 7 patients. Noncardiac side effects were mild and generally resolved, and required discontinuance in only 1 patient. More frequent AVRT occurred in 2 patients, but was managed with dose reduction and the addition of a beta blocker. Three patients had ventricular tachycardia requiring discontinuance; however 2 of 3 patients had a history of ventricular tachycardia before receiving encainide. Encainide is an effective and safe agent for treating atrial fibrillation in patients with Wolff-Parkinson-White syndrome.
Adolescent↗
Nonpharmacologic treatment of supraventricular tachycardia.
During the last 2 decades, more than 1,000 patients have undergone surgical division of an accessory pathway; many refinements in epicardial mapping and surgical techniques have been made. In institutions where the procedure is routinely performed, the rate of successful accessory pathway interruption now approaches 98%. Concomitant risk of complete heart block among patients with posteroseptal pathways has declined to less than 5%. Among patients with other organic heart disease, myocardial preservation techniques result in mortality rates within 1 to 2%; among those with significant cardiac abnormalities, the mortality rate is 4 to 6%. Two techniques are generally used to ablate an accessory pathway: the endocardial and the epicardial. The aim of both approaches is to identify the site of the accessory pathway and disarticulate the atrioventricular groove or expose and ablate the atrioventricular junction to interrupt accessory pathway conduction. Although each technique has its advantages, the choice of technique is far less important than the skill of the surgeon and clinical electrophysiologist performing the procedure. Newer surgical techniques include application of external epicardial shocks in the area of the accessory pathway and use of a cryosurgical probe in the sinus to ablate accessory pathways. Whereas our current thought is that surgery should be limited to those adults who fail to respond to pharmacologic therapy, advances in atrial endocardial and epicardial mapping, as well as surgical techniques, may expand the role of surgery in the treatment of ectopic atrial tachycardia.
Heart Conduction System↗
Clinical characteristics of patients with ventricular fibrillation during antiarrhythmic drug therapy.
We retrospectively studied 28 patients with 38 episodes of newly occurring ventricular fibrillation during antiarrhythmic drug therapy. Twenty-six of these patients, who had ventricular fibrillation during single-drug therapy with quinidine, procainamide, or disopyramide, were compared with a control group of 62 patients who had been treated similarly for ventricular arrhythmias but did not have ventricular fibrillation during treatment. The median duration of therapy before ventricular fibrillation was three days. The left ventricular ejection fraction of the study group was lower than that of the control group (0.29 vs. 0.43; P less than 0.0001), and concomitant treatment with digitalis and diuretic agents was more common in the study group. The base-line QT interval (corrected for heart rate) was slightly longer in the study group than in the controls (0.47 vs. 0.44; P less than 0.005), although both groups had similar degrees of QT prolongation during drug therapy. Four of 13 patients (31 percent) who underwent multiple trials of antiarrhythmic drugs had recurrent episodes of ventricular fibrillation. Six patients died suddenly after a mean follow-up of 18 months--four who were receiving antiarrhythmic therapy and two who were not. We conclude that drug-associated ventricular fibrillation is an early event, that there may be an increased risk of its recurrence with subsequent trials of antiarrhythmic drugs, and that left ventricular dysfunction and concomitant therapy with digitalis and diuretic agents may predispose patients to this complication.
Anti-Arrhythmia Agents↗