Liaqat Zaman

Long-term survival after prehospital cardiac arrest: Analysis of outcome during an 8 year study

We analyzed long-term follow-up data accumulated during an 8 year study of survivors of prehospital cardiac arrest. All patients included in this study were primary entrants via community-based rescue systems; patients who were tertiary referrals (survivors of cardiac arrest from other hospitals) were not included in this analysis. In the group of 61 patients entering our study between 1975 and 1980, with a follow-up to 1983, there have been a total of 24 deaths (39%). Sixteen of the 24 deaths were the result of recurrent cardiac arrest; eight were nonsudden cardiac deaths or noncardiac deaths. The mean duration from entry to death in the nonsurvivors was 27.5 +/- 19.7 months, and the time from the index event to last follow-up in the long-term survivors was 59.9 +/- 19.4 months. Life table analysis demonstrated a 10% rate of recurrence of cardiac arrest in the first year, with a 5% per year rate in each of the subsequent 3 years. Left ventricular ejection fractions at entry were not significantly different between survivors (mean = 45.3 +/- 13.6%) and nonsurvivors (mean = 37.6 +/- 12.6%), and the severity of ejection fraction abnormality at entry did not correlate with time to death in the nonsurvivors. However, ejection fraction was significantly lower in patients who died from causes other than recurrent cardiac arrest than in those who died of cardiac arrest (24.5 +/- 9.1% vs 42.7 +/- 9.2%; p less than .002).(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)

Cardiac arrest in an adolescent with atrial fibrillation and hypertrophic cardiomyopathy

A 15 year old youth, who presented with out-of-hospital cardiac arrest due to documented ventricular fibrillation, was found to have nonobstructive hypertrophic cardiomyopathy. Electrophysiologic study demonstrated inducible sustained atrial fibrillation with a rapid ventricular response. This rhythm, associated with hypotension and evidence of myocardial ischemia, spontaneously degenerated into ventricular fibrillation. No ventricular arrhythmias were inducible by programmed ventricular stimulation. Therapy with metoprolol and verapamil slowed the ventricular rate during atrial fibrillation and maintained hemodynamic stability, both during follow-up electrophysiologic study and during a subsequent spontaneous episode.

Electrophysiologic effects of diltiazem hydrochloride on supraventricular tachycardia

The effects of intravenous diltiazem hydrochloride (0.25 mg/kg body weight) were studied in eight patients with nine episodes of supraventricular tachycardia. Five episodes of tachycardia were due to atrioventricular (A-V) nodal reentry (group A), two were due to retrograde utilization of a concealed A-V accessory pathway (group B) and two were episodes of atrial fibrillation (group C). Intravenous administration of diltiazem slowed the ventricular rate in eight of nine episodes of tachycardias. Supraventricular tachycardia was terminated within 2 minutes after intravenous diltiazem in four of five patients in group A, and one of two in group B. Cycle length alternation was observed before termination of the arrhythmia in two patients from group A. In group C the ventricular response slowed but also became regular during atrial fibrillation. Although diltiazem depressed both anterograde and retrograde conduction as assessed by programmed stimulation, tachycardia termination or slowing or alternation of cycle length all occurred because of the effects of diltiazem predominantly on anterograde A-V nodal properties during supraventricular tachycardia. Although no statistical conclusions can be made from this limited study, it appears that diltiazem has significant depressant electrophysiologic effects on both anterograde and retrograde A-V nodal function as assessed by programmed stimulation during sinus rhythm. Further electrophysiologic studies are needed before determining the clinical efficacy of this agent for treatment or prophylaxis of recurrent supraventricular tachycardias.

Entrainment of atrioventricular nodal reentrant tachycardias during overdrive pacing from high right atrium and coronary sinus: With special reference to atrioventricular dissociation and 2:1 retrograde block during tachycardias

Entrainment was attempted during electrophysiologic evaluation of 8 patients with atrioventricular (AV) nodal reentrant tachycardia. Entrainment could be performed while pacing from the high right atrium in 35 of 35 episodes, from proximal coronary sinus in 9 of 21 episodes and from distal coronary sinus in 10 of 20 episodes. The minimal rates required were 8 to 40 beats/min faster than those of the tachycardias. That the atria (as defined in electrophysiologic studies) were not a necessary component of the reentry circuit was suggested by the occurrence, during tachycardia, of short episodes of AV dissociation and of 1 episode of 2:1 retrograde block. For the tachycardia to be interrupted, the pacing rate usually had to be slightly faster than that required to entrain, as well as sufficiently rapid to produce anterograde block of an atrial impulse in the slow AV nodal pathway. Moreover, termination of tachycardia apparently was a function of the pacing site. In some episodes, either because of a proximity effect or because of a preferential input into the upper common pathway, coronary sinus pacing terminated the tachycardia at slower rates or with fewer stimuli than high right atrial pacing. Thus, patients with drug-resistant AV nodal reentrant tachycardias may benefit from recently introduced pacing techniques for termination of tachycardia through entrainment.

Annihilation, entrainment and modulation of ventricular parasystolic rhythms.

Annihilation and one-to-one entrainment of modulated parasystolic rhythms in humans has not been previously discussed. In 9 nonmedicated patients, it was possible to measure the intrinsic, parasystolic ectopic cycle length given by the intervals between 2 consecutive parasystolic beats without any interposed nonparasystolic beat. The corresponding values varied between 960 and 2,350 ms (corresponding to rates between 62 and 26 beats/min). In addition, modulation could be determined, because nonparasystolic beats falling during the initial 59% of the cycle prolonged the parasystolic cycle length (by 12 to 37.5%), whereas those that fell later in the cycle shortened it (by 9 to 25%). Plotting this prolongation or shortening as a function of the temporal position of the nonparasystolic beats in the cycle yielded biphasic response curves, of which 7 were symmetric and 2 asymmetric. In 2 patients, episodes of concealed one-to-one entrainment were initiated by late nonparasystolic (sinus) beats and, later on, terminated by early ventricular extrasystoles. In 2 other patients (and in 2 separate occasions) nonparasystolic beats, falling in part of the cycle located in between those of maximal delay and acceleration, produced pacemaker annihilation (cessation of automatic activity for the remaining monitoring time). Parasystolic annihilation and concealed entrainment may be one of the causes that can explain the large, spontaneous, day-to-day variability in the incidence of ectopic ventricular beats reported in Holter recordings. Nevertheless, future prospective studies performing interventions that can change the sinus and ectopic rates are required to corroborate our finding.

Outcome of resuscitation from bradyarrhythmic or asystolic prehospital cardiac arrest

Previous studies of outcome as a function of the initial electrophysiologic mechanisms recorded at the scene of prehospital cardiac arrest have demonstrated that bradyarrhythmias and asystole have the worst prognosis. In this report, our observations in bradyarrhythmic and asystolic arrests occurring from 1980 to 1982 are compared with those from 1975 to 1978. From 1980 to 1982, 61 (27%) of 225 cardiac arrest events meeting entry criteria for the study were bradyarrhythmic or asystolic. Only 2 (8%) of 24 patients with asystole and 1 (20%) of 5 patients with sinus bradycardia survived prehospital intervention. Only 1 of these 29 patients was discharged from the hospital alive. In contrast, 15 (47%) of 32 patients who presented with idioventricular rhythm at initial contact survived prehospital intervention and were hospitalized, and 8 (25%) of these 32 were ultimately discharged alive. When compared with the 1975 to 1978 patients with bradyarrhythmia and asystole, both prehospital survival (8 versus 30%, p less than 0.001) and survival after hospitalization (0 versus 15%, p less than 0.05) significantly improved, but the improvement occurred predominantly in the subgroup with idioventricular rhythm. Survivors within this subgroup tended to have a prompt response to prehospital pharmacologic interventions that were not available to the 1975 to 1978 group. The response was manifested by return to a sinus mechanism or increase in the rate of idioventricular rhythm. In conclusion, outcome has improved for a specific subgroup of victims of prehospital cardiac arrest with bradyarrhythmia or asystole; the improved outcome may relate to field interventions by rescue personnel at the scene of arrest but the mortality rate is still high.

The arrhythmias of dual-chamber cardiac pacemakers and their management.

The field of cardiac pacing has developed exponentially in the past several years. The widespread use of atrioventricular synchronous pacemakers has resulted in the recognition of several types of pacemaker-associated arrhythmias. Certain of these arrhythmias follow asynchronous stimulation of either cardiac chamber; others are the result of the artificial bypass tract created with dual-chamber sensing and pacing. All the arrhythmias, however, are associated with normal pacemaker function.

Magnetic resonance imaging compared with angiography in the evaluation of intermediate-term result of coarctation balloon angioplasty

Between July 1986 and December 1990, 24 consecutive adult patients with native coarctation of the aorta underwent balloon dilatation. Their ages ranged from 15 to 55 (mean 25) years. Dissection of the aorta developed in one patient. The remaining 23 patients were restudied by catheterization and magnetic resonance imaging (MRI) 8 to 60 (mean 21) months after dilatation. Both studies were performed between 1 and 180 (mean 40) days of each other. The diameter of the aorta at the site of previous coarctation was measured on angiogram and MRI by two independent observers. The data were compared by means of linear regression analysis. The gradient across the previous coarctation site ranged from 0 to 20 (mean 7 +/- 7.3) mm Hg. The diameter of the aorta at the site of previous coarctation measured on angiogram was 13.7 +/- 3.7 mm and on MRI it measured 13.5 +/- 3.7 mm, with excellent correlation (r = 0.96, SEE = 0.92, p < 0.001). Two patients had small aneurysms 2 cm in diameter demonstrated by angiography and MRI, and two patients developed restenosis, diagnosed correctly by both cardiac catheterization and MRI. This study demonstrates that MRI provides excellent visualization of the anatomy of the aorta and is a good noninvasive method for follow-up of patients undergoing balloon coarctation angioplasty.

Multiple electrophysiologic manifestations and clinical implications of vagally mediated AV block

Clinical, surface ECG, and intracardiac findings were analyzed in 20 patients with spontaneous conduction disturbances in whom vagally mediated AV block could be induced by carotid sinus pressure during electrophysiologic evaluation. The latter demonstrated that the surface ECG pattern attributed to bradycardia-dependent (phase 4), and paroxysmal block within the His bundle and bundle branches could reflect vagally mediated, bradycardia-associated (rather than bradycardia-dependent), and paroxysmal AV nodal (AH) block. The decision regarding the use of pacemakers was not based on QRS duration or on patterns (or site) of block but on the underlying clinical settings and the correlation of symptoms with maximal ventricular (R-R) pauses. However, more studies are required to extend our findings, especially to other subgroups of patients (or normal individuals) in whom vagally mediated block occurs.