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S J Rials

Publications and source records attributed to S J Rials.

At least 37 records · Page 2Linked to original sources
PubMed1997

The top ten fallacies of nonsustained ventricular tachycardia.

Nonsustained ventricular tachycardia (NSVT) continues to remain a subject of controversy. This is true despite a wealth of epidemiologic and basic/clinical laboratory findings that have accumulated during the past 2 decades. However, these data not only generate the impetus to conduct further research, but also provide compelling arguments against continued adherence to time honored precepts about NSVT that evolved since the inception of the "PVC Hypothesis," although never substantiated by rigorous scientific inquiry. This paper discusses the "top ten" fallacies of NSVT and details the data that support abandonment of them.

Anti-Arrhythmia Agents↗
PubMed1996

Atrial fibrillation, anticoagulation, and stroke.

There is a demonstrated statistical association between atrial fibrillation, rheumatic valvular disease, and embolic stroke. This article assesses the results of 6 major clinical trials (AFASAK, BAATAF, SPINAF, SPAF [parts I and II], CAFA and EAFTA--see text for trial names). Multivariate analysis revealed 4 independent clinical features that identified patients with atrial fibrillation at an increased risk for stroke: hypertension, increasing age, previous transient ischemic attack, and diabetes mellitus. Without anticoagulation therapy, patients with any of these risk factors had a 4% annual risk of stroke. Patients with cardiac disorders such as congestive heart failure and coronary artery disease have a stroke rate 3 times higher than patients without any risk factors; patients with atrial fibrillation but no concomitant risk factors or structural heart disease seemed to have little concomitant risk for stroke. Meta-analysis revealed a 64% reduction of risk for stroke in patients treated with warfarin, as compared with placebo. The value of warfarin therapy in patients > 75 years old is less clear because of a high risk of hemorrhagic complications.

Aged↗
PubMed1996

Effect of an intravenous angiotensin-converting enzyme inhibitor on the electrophysiologic features of normal and hypertrophied feline ventricles.

Left ventricular hypertrophy is associated with an increased risk of ventricular arrhythmia and multiple electrophysiologic abnormalities that normalize with regression of hypertrophy. For patients who have hypertension, treatment with angiotensin-converting enzyme (ACE) inhibitors produces regression of hypertrophy and a reduction in ventricular arrhythmia. It is unclear whether the reduction in ventricular arrhythmia associated with ACE inhibitor therapy is due to regression of hypertrophy alone, a direct antiarrhythmic effect of ACE inhibition, or both. We performed electrophysiologic studies in normal cats and cats with fixed left ventricular hypertrophy before and after acute intravenous administration of trandolopril. Trandolopril produced a small, consistent prolongation of monophasic action potential duration in normal and hypertrophied ventricles although this prolongation did not reach statistical significance. Trandolopril had no significant effect on effective refractory period, inducibility of arrhythmia, or ventricular fibrillation threshold in normal or hypertrophied ventricles. These data suggest that the reduction in arrhythmia associated with ACE inhibitors is not caused by a direct electrophysiologic effect but is more likely caused by regression of hypertrophy.

Action Potentials↗
PubMed1996

Monomorphic right ventricular tachycardia in a patient with mitral valve prolapse.

A patient with mitral valve prolapse and symptomatic ventricular ectopy underwent an electrophysiological study during which a sustained monomorphic ventricular tachycardia with a left bundle branch block/right axis deviation morphology was induced. This morphology was replicated by pace mapping at the right ventricular outflow tract. To the best of our knowledge, this finding has not been previously described and suggests that the association between ventricular arrhythmias and mitral valve prolapse may not necessarily be causal.

Adult↗
PubMed1995

Gender differences in device therapy for malignant ventricular arrhythmias.

BACKGROUND: Several recent reports have suggested a gender bias in the treatment of cardiovascular disease. It is not clear whether this is true in the treatment of malignant ventricular arrhythmias. OBJECTIVES: To perform a retrospective chart review of 130 patients evaluated for malignant ventricular arrhythmias between July 1990 and June 1992. To compare baseline cardiovascular and clinical parameters and treatment modalities, including cardioverter-defibrillator implantation rates, between women and men. RESULTS: There was no significant difference in the percentage of women and men who were advised to have cardioverter-defibrillator implantation (61% vs 53%) or who underwent cardioverter-defibrillator implantation (46% vs 52%). Women had a lower incidence of coronary artery disease than men (61% vs 85%, P < .01), a lower incidence of myocardial infarction (46% vs 75%, P < .01), and a higher mean left ventricular ejection fraction (38% vs 32%, P = .02). Of patients with indications for cardioverter-defibrillator implantation, significantly more women refused a device than men (19% vs 2%, P = .01), and significantly more women were considered medically ineligible for cardioverter-defibrillator implantation despite having less severe heart disease as a group (12% vs 0%, P = .04). This resulted in significantly fewer women receiving a defibrillator than men with similar indications (18 of 26 women vs 47 of 48 men, P < .01). Of patients who received defibrillators, significantly more women received investigational devices (50%) than men (21%) (P < .05) (35% of women and 19% of men with indication for cardioverter-defibrillator implantation). In-hospital mortality was low in both groups (women, 0%; men, 4%). The 30-month mortality in patients with indications for device intervention was similar in both groups (women, 21%; men, 19%). CONCLUSIONS: No evidence of difference was found between women and men in the rates of recommendation for, or implantation of, implantable cardioverter-defibrillators. Women refused device implantation more often than men, and they may be considered medically ineligible for device implantation more than men. This combination results in fewer women with medical indications for cardioverter-defibrillator implantation receiving defibrillators than men. This difference does not appear to be associated with increased short-term mortality.

Aged↗
PubMed1995

Effect of left ventricular hypertrophy and its regression on ventricular electrophysiology and vulnerability to inducible arrhythmia in the feline heart.

BACKGROUND: Left ventricular hypertrophy (LVH) is associated with an increased risk of death, susceptibility to ventricular arrhythmia, and multiple electrophysiological abnormalities. The purpose of the present study was to determine whether the susceptibility to arrhythmia and electrical abnormalities persists after regression of hypertrophy in an animal model of LVH. METHODS AND RESULTS: We placed constricting bands on the ascending aorta of cats (n = 9) or performed sham operations (n = 9). Serial cardiac echocardiography was performed to measure left ventricular wall thickness. After LVH had developed in the banded animals, the constricting bands were removed and serial echocardiograms were used to monitor for regression of hypertrophy. Electrophysiological studies were performed in cats that showed regression of LVH (Regress, n = 5), those that showed no change in LV wall thickness (No Regress, n = 4), and in the sham-operated animals (Sham). Cats with persistent LVH had a higher incidence of inducible polymorphic ventricular tachycardia (4 of 4) compared with Regress (1 of 5) or Sham (1 of 9) cats (P < .05) and had lower ventricular fibrillation thresholds (9 +/- 2 mA) than Regress (17 +/- 4 mA) or Sham (16 +/- 3 mA) cats (P < .05). Persistent LVH in the No Regress group was associated with prolongation of epicardial monophasic action potential duration (MAPD) in the left but not the right ventricle. Dispersion of refractoriness was greater in the No Regress group (P < .05 versus Regress or Sham). Regress cats were identical to Sham cats in having a low incidence of inducible polymorphic ventricular arrhythmia, high fibrillation threshold, and MAPD measurements (P = NS versus Sham). CONCLUSIONS: LVH produces multiple electrophysiological abnormalities and increased vulnerability to inducible polymorphic ventricular arrhythmia in this model of LVH. Cats that show regression of hyperthrophy have normal ventricular electrophysiology and have the same low vulnerability to inducible ventricular arrhythmia as Sham animals.

Action Potentials↗
PubMed1995

Parenteral antiarrhythmics for life-threatening ventricular arrhythmias.

The acute management of life-threatening ventricular tachyarrhythmias often includes the use of parenteral antiarrhythmics. There are a number of agents currently available for this purpose. They are used to suppress inducible monomorphic ventricular tachycardia during programmed electrical stimulation, they terminate spontaneous sustained ventricular tachycardia, and prevent ventricular fibrillation in the setting of an acute myocardial infarction. Serious adverse reactions include proarrhythmia, hypotension, severe bradyarrhythmias, and precipitation of congestive heart failure. A comparative evaluation of intravenous antiarrhythmics is difficult due to inherent differences in the choice of agents for study, protocol design, patient population, defined endpoint, and serum drug levels. Likewise, the reported adverse reaction rates vary from 0.4% to 75%. To understand the difficulties in clinical decision-making in this problem area, particularly drug selection, we present here a review of pertinent clinical trials evaluating parenteral drug efficacy and adverse effects.

Anti-Arrhythmia Agents↗
PubMed1993

Evidence for a reexcitability gap in man after treatment with type I antiarrhythmic drugs.

The intention of this study was to determine whether type IA antiarrhythmic drugs cause a disparity between refractoriness and repolarization, and if so, its magnitude. We simultaneously measured monophasic action potential duration (MAPD) and effective refractory period (ERP) at a right ventricular site in 11 patients without overt right ventricular disease. The pacing protocol, which included sinus rhythm and a 600 and 400 msec cycle length of ventricular drive, was performed at baseline and after the intravenous administration of 15 mg/kg of procainamide in nine patients, and of 10 mg/kg of quinidine in two patients. Despite trivial changes in sinus rates, drug therapy caused a 10% to 17% increase in MAPD and ERP that shortened with decreasing drive cycle lengths. At baseline there was a small gap (10 to 13 msec) between MAPD and ERP in sinus rhythm and with a 600 or 400 msec drive. However, the type IA drug caused a significant widening of this gap that was most profound in sinus rhythm (45 msec) and that shortened but was not abolished with a 600 and 400 msec drive (28 and 29 msec, respectively). The disparity was caused in one third of cases by postrepolarization refractoriness. Type I drugs increase the difference between repolarization and refractoriness, and this effect is partially reversed with increases in heart rate. The clinical implications of these findings are discussed.

Action Potentials↗
PubMed1993

Electrophysiologic testing in patients who respond acutely to intravenous amiodarone for incessant ventricular tachyarrhythmias.

The outcome of patients who receive intravenous amiodarone for suppression of incessant ventricular tachyarrhythmia has not been studied conclusively. We conducted a prospective study in which all patients who responded acutely to intravenous amiodarone and went on to receive a subsequent oral loading dose were subjected to electrophysiologic testing before hospital discharge to determine whether additional or alternative therapy would be required. Among 18 patients (17 with ischemic heart disease) who entered the protocol, 16 had a clinical response to intravenous amiodarone alone (12 patients) or in combination with another antiarrhythmic drug (4 patients) and survived to study. Of these, 10 had monomorphic ventricular tachycardia (VT) when first seen, five had polymorphous VT or ventricular fibrillation (VF), and three had both. In seven patients sustained monomorphic VT was inducible (group 1), and in nine it was not (group 2). The only clinical factor that distinguished group 1 from group 2 was age (group 1 > group 2). Five patients in group 1 and one in group 2 received an implantable cardioverter defibrillator; one patient in group 1 had a successful endocardial resection. During a mean follow-up period of 11 months, four patients in group 1 have had appropriate implantable cardioverter defibrillator discharges, whereas only one patient in group 2 has had a clinical event (sudden death). We conclude that intravenous amiodarone is a highly effective drug used alone or in combination to suppress spontaneous incessant VT/VF. Predischarge electrophysiologic testing, even in patients who have polymorphous VT, has predictive value over and above the observed clinical response. These preliminary results favor predischarge testing and aggressive device treatment in this cohort.

Administration, Oral↗
PubMed1992

Does programmed stimulation really help in the evaluation of patients with nonsustained ventricular tachycardia? Results of a meta-analysis.

There has been considerable debate regarding the value of programmed electrical stimulation in patients who present with asymptomatic, or minimally symptomatic, nonsustained VT. Unfortunately, there has never been a sufficiently large study of an untreated group of patients to make any sense of the issue. We culled the literature for reports published between 1986 and 1990 that met certain minimum requirements, the most important of which were adequate patient profiling and outcome data. The survey identified 12 studies of 926 patients, mean age 61 years, with a 5:1 male preponderance. Underlying heart disease was coronary in 818 patients, including 665 who had experienced previous but not recent myocardial infarctions. Of these, 302 (33%) had inducible sustained ventricular arrhythmias (monomorphic VTs in 264). Eighty-three percent of these patients were treated with antiarrhythmic drugs compared to only 13% of the noninducible group (p less than 0.0001). Sudden death or a sustained arrhythmic event occurred in 54 (18%) of the 302 patients in the inducible group compared with 46 (7%) of the 624 in the noninducible group (p less than 0.001). The sensitivity, specificity, and positive and negative predictive accuracies of the test were 54%, 70%, 18%, and 93%, respectively. Thus a patient with an inducible sustained arrhythmia who manifests nonsustained VT is two and a half times as likely to have a major arrhythmic event, but a negative result bodes well for the patient. However, widespread application of the technique cannot be recommended until these results are confirmed in a large, prospective study in which antiarrhythmic therapy is controlled.

Cardiac Pacing, Artificial↗
PubMed1992

Effect of gallopamil on electrophysiologic abnormalities and ventricular arrhythmias associated with left ventricular hypertrophy in the feline heart.

Left ventricular hypertrophy increases vulnerability to ventricular fibrillation. To determine whether calcium channel blockade protects against ventricular arrhythmia in left ventricular hypertrophy, we studied the effects of gallopamil, a potent and specific calcium channel antagonist, in 37 cats undergoing aortic banding (group 1, n = 28) or a sham procedure (group 2, n = 9). Each cat underwent serial echocardiography and was studied after the development of left ventricular hypertrophy, defined as an increase of at least 30% in left ventricular posterior wall thickness. After baseline electrophysiologic testing, animals received gallopamil (70 micrograms/kg loading dose followed by 2.5 micrograms/kg/min infusion) (n = 19) or a control infusion of saline solution (n = 18), and testing was repeated. There was no significant difference between groups 1 and 2 in baseline excitability thresholds intraventricular conduction times, ventricular effective refractory periods, or monophasic action potential durations. Thresholds for induction of ventricular fibrillation were lower in group 1 than in group 2, and only in group 1 was ventricular fibrillation inducible during programmed stimulation. This altered vulnerability was associated with a significantly greater dispersion of excitability thresholds, ventricular effective refractory periods, and monophasic action potential durations. Gallopamil did not change baseline measurements except for prolonging sinus cycle length and atrioventricular conduction time.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Arrhythmias in the elderly.

The elderly patient is susceptible to a variety of cardiac rhythm disturbances that may or may not cause symptoms. It is incumbent on the physician who cares for geriatric patients to have a familiarity with the diagnostic criteria for each of these arrhythmias and with the drugs and devices that are used to treat them. This includes the potential adverse effects of therapy and methods to counter them. Even more important is a sense of when to intervene, which is based in part on a knowledge of "normal variation" in the aged.

Aged↗