Paired comparisons of efficacy of intravenous and oral procainamide in patients with inducible sustained ventricular tachyarrhythmias.

Thirty-eight patients who had inducible sustained ventricular tachycardia during baseline programmed electrical stimulation underwent electrophysiologic testing after both intravenous and oral administration of procainamide. Each had presented clinically with documented sustained ventricular tachycardia or out of hospital cardiac arrest not associated with acute myocardial infarction. In 23 patients (61%) (Group I) the arrhythmia became noninducible during an intravenous infusion of procainamide. Oral procainamide was subsequently administered and retesting was carried out after dose titration to match plasma concentration at the end of the intravenous study. Among the 23 patients in Group I the mean (+/- SD) plasma procainamide level was 7.2 +/- 2.8 micrograms/ml after intravenous dosing and 7.9 +/- 2.5 micrograms/ml after oral dosing (p = 0.09). In 15 (65%) of the 23 patients, sustained ventricular arrhythmia was inducible on oral therapy with comparable plasma procainamide levels (intravenous = 6.3 +/- 2.1 micrograms/ml, oral = 7.5 +/- 2.1 micrograms/ml). The other eight patients (35%) had concordant responses to repeat testing with comparable intravenous (mean 9.0 +/- 3.3 micrograms/ml) and oral (8.8 +/- 3.1 micrograms/ml) plasma procainamide levels. In the additional 15 patients (Group II) sustained ventricular tachyarrhythmia remained inducible on intravenous procainamide therapy and the patients were retested on oral therapy with similar plasma concentration (p = 0.05). In seven patients (47%) sustained ventricular tachyarrhythmia was noninducible on treatment with oral procainamide (mean plasma level 7.6 +/- 2.7 micrograms/ml) after failure of intravenous procainamide (mean plasma level 10.3 +/- 2.3 micrograms/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Time to first shock and clinical outcome in patients receiving an automatic implantable cardioverter-defibrillator.

The relation between time to first shock and clinical outcome was studied in 60 patients who received an automatic implantable cardioverter-defibrillator (AICD) from August 1983 through May 1988. The mean (+/- SD) patient age was 64 +/- 10 years, 82% were men and the mean ejection fraction was 33 +/- 13%. During follow-up, 38 patients (63%) had one or more shocks; there were no differences in age, gender distribution or ejection fraction at entry between the shock and no shock groups. Among 51 patients with coronary artery disease, 31 (61%) had one or more shocks, whereas all seven patients with cardiomyopathy had one or more shocks (p less than 0.05). Neither of the two patients with idiopathic ventricular fibrillation had shocks. Of the 13 deaths, 12 occurred during post-hospital follow-up and 1 during the index hospitalization. Of the four sudden post-hospital deaths, only one was due to tachyarrhythmia in the absence of acute myocardial infarction. All four sudden deaths and five of eight post-hospital nonsudden deaths occurred in patients who had had one or more appropriate shocks during follow-up. Eight of the nine first appropriate shocks among patients who subsequently died occurred within the first 3 months of follow-up, but the actual deaths were delayed to a mean of 14.1 +/- 13.9 months (p less than 0.05). The mean time to all deaths was 14.8 +/- 13.1 months. The ejection fraction was significantly lower among patients who died than among patients who survived (25 +/- 7% versus 35 +/- 14%, p less than 0.02), but it did not distinguish risk of first shocks.(ABSTRACT TRUNCATED AT 250 WORDS)

Dynamics of, and alternating Wenckebach periods during, 4:1 and 6:1 atrioventricular block.

In summary, the irregular dynamics of progression of 4:1 AV block in atrial flutter, presumably different from those observed in similar degrees of rate-dependent block, most likely reflected the complex electrophysiologic mechanisms operating during the highest degrees of AV nodal block. Occurrence of previously undescribed arrhythmias, namely Wenckebach periods during 4:1 and 6:1 block, tends to support the multilevel block hypothesis.

Dynamics of the uncorrected QT interval during vagal-induced lengthening of RR intervals.

Analysis of 21 episodes of vagal-induced atrioventricular block showed that the uncorrected QT intervals at the end of the corresponding RR pauses were not prolonged, in reference to the pre-block QT intervals, with pauses shorter than 1,280 ms. Subsequently, they gradually lengthened as the RR pauses progressively increased to 13,710 ms. This dynamic behavior of the QT interval in subjects without structural heart disease could have resulted from a complex interaction between the cumulative effects of previous cycle lengths (memory effect?) and the autonomic nervous system.

Frequency of sudden cardiac death and profiles of risk.

The epidemiology of ventricular tachycardia/fibrillation (VT/VF) and sudden cardiac death (SCD) must be explored from multiple aspects, each of which contributes insights into the problem and no one of which exerts exclusive dominance for preventive or therapeutic strategies. These include: (1) population dynamics, using conventional epidemiologic approaches; (2) risk as a function of time from an index event; (3) conditioning risk factors, based on the presence of underlying disease states; (4) transient risk factors that are dynamic and trigger a potentially fatal event at a specific point in time; and (5) "response risk," which refers to individual susceptibility (possibly determined genetically) to the adverse effects of longitudinal and/or dynamic risk factors. Major inroads into profiling individual or population risk of SCD will require better understanding of each of these epidemiologic-clinical-physiologic interactions. The disciplines range from epidemiology, through clinical medicine, to membrane channel physiology, genetic determinants, and molecular biology.

Cycling of inducibility of paroxysmal supraventricular tachycardia in women and its implications for timing of electrophysiologic procedures.

Arrhythmias in women may be affected by phases of the menstrual cycle. This study was designed to determine the prevalence of perimenstrual clustering of spontaneous episodes of paroxysmal supraventricular tachycardia (SVT) in women. It also tested the hypothesis that women with this temporal pattern of events have an altered probability of induction of paroxysmal SVT during electrophysiologic testing at higher estrogen states (midcycle or with estrogen replacement therapy) than at low estrogen states (perimenstrual or without estrogen replacement). A structured history of the relation of spontaneous paroxysmal SVTs to phases of the menstrual cycle was obtained prospectively among 42 women referred during a 3-year period. Patients with cyclical patterns of spontaneous tachycardias, who had had negative electrophysiologic studies at midcycle or while receiving estrogen replacement therapy, had repeat procedures (1) when premenstrual or at the onset of menses, or (2) after stopping estrogen replacement therapy. Seventeen of 42 consecutive female patients (40%) had histories of perimenstrual clustering of arrhythmias. Six women (4 with normal menstrual cycles, 2 on estrogen replacement therapy), who qualified for paired electrophysiologic studies because of a negative initial electrophysiologic study that included provocation with isoproterenol, had inducibility into SVTs during the second study. All 6 had dual atrioventricular (AV) nodal pathway physiology, 4 had AV nodal reentrant tachycardia (AVNRT) induced, 1 had both AVNRT and reciprocating AV tachycardias, and 1 had nonsustained AVNRT and an atrial tachycardia induced. Successful ablation procedures were performed in 5 of the 6 patients. Thus, among women with a history of perimenstrual clustering of paroxysmal SVT and among those receiving estrogen replacement therapy, scheduling of elective electrophysiologic procedures at times of low estrogen levels (premenstrual or off estrogen replacement therapy) may facilitate the probability of a successful procedure.

Reverse alternating Wenckebach periods and other modes of regression of > or = 8:1 to 2:1 atrioventricular block.

The modes of regression of very high degrees of atrioventricular nodal block (> or = 8:1) were studied in patients with atrial flutter and a specific variant of the tachycardia-bradycardia syndrome. The occurrence of reverse alternating Wenckebach periods, previously reported only in 2:1 atrioventricular block, emphasizes the complexities of multilevel block.

Significance of pacing cycle lengths in manifest entrainment of orthodromic circus movement tachycardia by ventricular pacing.

The physiology of entrainment of orthodromic circus movement tachycardia (CMT) was studied using ventricular pacing during 18 episodes of induced CMT in 7 patients with atrioventricular (AV) accessory pathways. The first paced impulse was delivered as late as possible in the tachycardia cycle (mean 88 +/- 5% of the spontaneous cycle length [CL]). Entrainment was demonstrated by the following criteria: 1:1 retrograde conduction via the accessory pathway; capture of atrial, ventricular and His bundle electrograms at the pacing rate; and resumption of tachycardia at its previous rate after cessation of pacing. The number of ventricular paced impulses ranged from 5 to 14 (mean 8 +/- 3), and entrainment occurred in 2 to 7 paced cycles (mean 4 +/- 2). Orthodromic activation of a major part of the reentry circuit (manifest entrainment) was demonstrated during 9 episodes by the occurrence of His bundle electrogram preceding the first CMT QRS at the time anticipated from the last paced beat. In the 9 other episodes, persistent retrograde His bundle activation and AV nodal penetration by each paced impulse caused a delay (mean 79 +/- 25 ms) in activation of the His bundle preceding the first CMT QRS after the last paced beat. The mean pacing CL achieving manifest entrainment was 92 +/- 3% of the tachycardia CL, compared with 84 +/- 3% for retrograde AV nodal penetration (p less than 0.01). In conclusion, manifest entrainment of orthodromic CMT can be demonstrated by ventricular pacing at very long CLs; shorter CLs may cause CMT termination due to retrograde AV nodal penetration.

A shared pathway in atrioventricular nodal reentrant tachycardia and atrial flutter: implications for pathophysiology and therapy.

Atrioventricular (AV) nodal reentrant tachycardia and atrial flutter are considered 2 distinct supraventricular tachycardias. Recent clinical and experimental data suggest that both these tachycardias include an area in the lower right atrial septum in their reentrant pathways. This study was designed to test the hypothesis that there is an association between the mechanisms of AV nodal reentrant tachycardia and atrial flutter because of a shared pathway of reentry. Consecutive patients referred for evaluation and management of supraventricular tachycardia, thought to be due to AV nodal reentry, underwent electrophysiologic testing protocols designed to induce both AV nodal reentrant tachycardia and atrial flutter, if present. Fifteen of 29 patients (52%) had both AV nodal reentrant tachycardia and atrial flutter induced during electrophysiologic testing. Seven of these 15 patients (47%) underwent transcatheter radiofrequency current application (mean power 34 +/- 4 W) against the tricuspid annulus above the coronary sinus. In each patient, neither AV nodal reentrant tachycardia nor atrial flutter could be induced after the procedure. Repeat study after successful ablation (mean 6 days) showed no inducible supraventricular arrhythmia of either type at baseline study or during isoproterenol infusion. Atrial flutter occurs frequently (15 of 29 patients; 52%) in patients with AV nodal reentrant tachycardia, because of a shared pathway in their reentry circuits. Because of this shared pathway, both arrhythmias can be ablated at the same site. These observations promote new insights into the mechanism and therapeutics of supraventricular tachycardias.

Efficacy of intravenous propranolol for suppression of inducibility of ventricular tachyarrhythmias with different electrophysiologic characteristics in coronary artery disease.

The efficacy of intravenous propranolol for suppression of inducibility of sustained ventricular tachyarrhythmias (VT) was studied in 24 patients who had failed greater than or equal to 1 membrane-active antiarrhythmic drug (mean 2.2 +/- 1.2 drugs/patient). The response to propranolol was compared in 13 patients who had only stable monomorphic VTs inducible at baseline and another 11 patients who had greater than or equal to 1 episode of electrically unstable VTs (polymorphic VT, ventricular flutter or ventricular fibrillation) at baseline. Seven patients (29%) became noninducible (responders) and 17 patients (71%) remained inducible to sustained VT (nonresponders) after propranolol. The basal heart rate was faster in responders than in nonresponders (101 +/- 14 vs 86 +/- 11 beats/min, p less than 0.01). The magnitude of heart rate reduction was also greater after propranolol in responders (from 101 +/- 14 to 80 +/- 9 beats/min, p less than 0.001) than in nonresponders (from 86 +/- 11 to 74 +/- 9 beats/min, p less than 0.01) (p less than 0.05 between the groups), despite equal plasma propranolol concentrations (84 +/- 50 vs 88 +/- 43 ng/ml, difference not significant). Seven of 11 patients (64%) who had greater than or equal to 1 episode of unstable VTs inducible at baseline responded to intravenous propranolol, whereas none of the patients with only stable monomorphic VTs became noninducible after beta blockade (p less than 0.001). Responders had shorter cycle length of inducible VTs than nonresponders (225 +/- 38 vs 302 +/- 66 ms, p less than 0.001). Thus, intravenous propranolol appears to be efficacious in suppressing fast, electrically unstable VTs, compared to monomorphic VTs with slower rates.

Mechanisms and dynamics of episodes of progression of 2:1 atrioventricular block in patients with documented two-level conduction disturbances.

Twenty episodes of progression of 2:1 atrioventricular (AV) block were identified during incremental atrial stimulation in 7 patients with documented (2-level) block in the AV node and His-Purkinje system. All occurred at cycle lengths shorter than those at which stable 2:1 HV block had been detected. Thirteen episodes were typical since 2:1 increased to 3:1 AV block when an atrio-His (AH) Wenckebach period was completed with an atrial impulse that otherwise would have been conducted. These episodes occurred with dynamic A(M): V(N) ratios similar to those seen at the AV node. Seven atypical episodes were identified (while AH Wenckebach periods were occurring): (1) 2:1 increasing to 3:1 AV block and then to 4:1 AV block resulting from prolonged refractoriness in the His-Purkinje system subsequently followed by concealed conduction in the latter structure; (2) conversion of 3:2 directly into 3:1 AV block due to block of the next-to-last atrial impulse in the His-Purkinje system with completion of AH Wenckebach period with the following atrial impulse; and (3) 4:2 AV block presumably due to supernormal conduction in a transversely dissociated His-Purkinje system. These episodes occurred with A(M): V(N) ratios, which in other structures would have been indicative of different degrees of AV block. In conclusion, progression of 2:1 AV block during documented 2 level conduction disturbances (1) can be explained by mechanisms different than those currently known, and (2) has rich, but different dynamics from those observed exclusively in the AV node and exclusively in the His-Purkinje system.

A different approach to the analysis of pure ventricular parasystole.

Until recently, it had not been recognized that predictions regarding the number of sinus beats interposed between two consecutive parasystolic beats could be made. In a case of perfect, pure parasystole resulting from unintentional fixed rate ventricular pacing, the following was observed: there were consistently three different values (0,2,3) for the number of interposed sinus beats; only one of these values was odd, and the sum of the two smaller values was one less than the larger value. Our findings, which are in keeping with those obtained in an mathematical model, may be of additional help in the diagnosis of this elusive arrhythmia.

Resection of right atrial lymphoma in a patient with AIDS.

Although cardiac problems are common in acquired immunodeficiency syndrome, there is limited experience with heart surgery in this group of patients. We report a case in which a right atrial lymphoma was resected to alleviate tricuspid valve obstruction in a patient with AIDS. The patient did well for approximately 7 months. At that time, he developed multiple complications of AIDS and deteriorated rapidly; he died 8 months after operation. Cardiac surgery can be successfully performed in AIDS patients. However, the late outcome is compromised by the nature of the underlying viral infection.