Jose Gallastegui

Ventricular tachycardia in a young population without overt heart disease.

Since 1974, 24 young patients presenting with ventricular tachycardia and without clinical evidence of heart disease were evaluated and followed. Sixteen patients (67%) were symptomatic. Clinical episodes of ventricular tachycardia were sustained in 18, incessant in four, and nonsustained in two patients. The rate of tachycardia ranged from 130 to 300 beats/min (mean = 200 beats/min). Subtle abnormalities of cardiac size or function were present at cardiac catheterization in 16 of 23 patients (70%). During electrophysiologic studies, spontaneous ventricular tachycardia was present in six patients. The clinical ventricular tachycardia was inducible by programmed stimulation in 13 of 18 patients. The site of origin of tachycardia based on endocardial mapping in 17 patients was the right ventricle in 14, the ventricular septum in one, and indeterminate in two patients. Seventeen patients were treated based on results of short-term drug testing. During a mean follow-up period of 7.5 years, three patients died suddenly; none of these patients were receiving antiarrhythmic medication at the time of death. We conclude that in a young population without clinical evidence of heart disease, ventricular tachycardia may be the first manifestation of cardiomyopathy, since at least two-thirds of these patients have abnormalities at cardiac catheterization. Without treatment mortality in this population may be as high as 13% over an 8 year period. Presently we recommend treatment of ventricular tachycardia in any symptomatic patient, with therapy guided by electrophysiologic and treadmill testing. In addition, we recommend treatment for any asymptomatic patient with exercise-related tachycardia, since this group appears to be at increased risk for sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)

Determination of left ventricular ejection fraction by visual estimation during real-time two-dimensional echocardiography

It has been shown that the measured reduction in the cross-sectional area of the left ventricle (LV), as viewed in the short axis, closely approximates its ejection fraction (EF). We assessed the reliability of using two-dimensional echocardiography (2DE) to visually estimate the EF during real-time viewing, without the need of digitizers, planimetry, or calculations. Twenty-five adult hospitalized patients with either suspected or known cardiac disease were evaluated prospectively. Each patient also had gated nuclear angiography during the same admission, and 14 had cardiac catheterization with left ventriculography. The EF was determined by 2DE using a visual estimate of the percent area reduction of the LV cavity in the short-axis view at the level of the papillary muscles. All 2 DE studies were read by two or more blinded reviewers, with a value for the EF to the nearest 2.5% determined by consensus. These values correlated closely to the values determined in all 25 patients with gated nuclear angiography (r = 0.927) and the 14 patients who had left ventriculography (r = 0.935). We believe that this method of visually estimating the LVEF will enable echocardiographers to easily use 2 DE for a reliable and instantaneous assessment of ventricular function, without the need of sophisticated analytical equipment.

Hemodynamic and electrophysiological actions of cocaine. Effects of sodium bicarbonate as an antidote in dogs.

BackgroundCocaine abuse has been implicated as a cause of death due to sudden cardiac arrest. Methods and ResultsWe examined the hemodynamic and electrophysiological effects of cocaine administered as a series of 5-mg/kg i.v. boluses coupled with a continuous infusion in anesthetized dogs. Sodium bicarbonate (50 meq i.v.) was administered as a potential antidote in 11 of 15 dogs, and intravenous 5% dextrose was given in the remaining four. In a dose-dependent fashion, cocaine significantly decreased blood pressure, coronary blood flow, and cardiac output; increased PR, QRS, QT, and QTc intervals and sinus cycle length; and increased ventricular effective refractory period and dispersion of ventricular refractoriness. No afterdepolarizations were noted in the monophasic action potential recording. Nonsustained monomorphic ventricular tachycardia occurred spontaneously in two dogs, and sustained ventricular tachycardia could be induced by programmed stimulation at the end of the dosing protocol in five of 11 animals. Sodium bicarbonate promptly decreased cocaine-induced QRS prolongation to nearly that measured at baseline but had no effect on the other electrocardiographic or hemodynamic variables. In one dog, sodium bicarbonate administration was associated with reversion of ventricular tachycardia to sinus rhythm. ConclusionsWe conclude that high-dose cocaine possesses negative inotropic and potent type I electrophysiological effects. Sodium bicarbonate selectively reversed cocaine-induced QRS prolongation and may be a useful treatment of ventricular arrhythmias associated with slowed ventricular conduction in the setting of cocaine overdose.

Electrophysiologic drug testing in symptomatic ventricular arrhythmias after repair of tetralogy of fallot

Nine patients with symptomatic ventricular arrhythmias were evaluated a mean interval of 16 years after surgical repair of tetralogy of Fallot. The clinical arrhythmia was sustained ventricular tachycardia (VT) in 4 patients (group I) and premature ventricular contractions in 5 (group II). All patients underwent cardiac catheterization and electrophysiologic studies. Ventricular tachycardia was induced at electrophysiologic study in all patients in group I and in 3 patients in group II. Six patients with inducible sustained monomorphic VT underwent chronic drug testing based on electrophysiologic study. A mean of 3.3 drugs per patient was tested. Patients with right ventricular systolic hypertension did not respond to any drug tested, and underwent surgery. Five patients received drug treatment based on the results of electrophysiologic study. During a mean follow-up period of 2.2 years, no patient in either group had recurrent episodes of VT or syncope. In the postoperative patient with tetralogy of Fallot with symptomatic ventricular arrhythmias, it is concluded that electrophysiologic study is useful in reproducing clinical episodes of VT and in selecting effective antiarrhythmic medication; a small number of patients with ventricular premature complexes alone will have inducible sustained VT during electrophysiologic study; prognosis of these patients may be improved by treatment that results in prevention of VT induction; and in patients with right ventricular hypertension, VT is likely to be refractory to drug treatment.

Cardiac involvement in the Kearns-Sayre syndrome

Abstract Kearns-Sayre (K-S) syndrome is a multisystemic disorder initially described as chronic progressive external ophthalmoplegia associated with pigmentary degeneration of the retina (retinitis pigmentosa) and complete heart block. 1 Apparently, this entity is caused by mitochondrial abnormalities that affect neuromuscular and cardiac conduction systems. 2 The sequence in which this disorder affects the different organs varies, but usually cardiac involvement and atrioventricular (AV] block develop late.2 We report the clinical and pathologic findings of the heart and its conduction system in 2 patients with K-S syndrome.

Amiodarone for sustained ventricular tachycardia: efficacy, safety, and factors influencing long-term outcome.

Abstract The reported long-term efficacy and safety of amiodarone varies considerably. Further, the role of electrophys ologic drug testing of amiodarone therapy is controversial. In this study, 71 patients with drug-refractory, recurrent sustained ventricular tachycardia were treated with amiodarone and were followed over 20 ± 17 months. Amiodarone had to be discontinued prior to discharge in 6 of the 71 patients because of suspected proarrhythmic actions or side effects. Of the remaining 65 patients started on long-term amiodarone, 21 (32%) had recurrence of ventricular tachycardia and 13 (20%) died suddenly. Of the 21 patients with recurrence of ventricular tachycardia while receiving amiodarone, 15 remained on amiodarone, with or without a therapy modification; the remaining six required drug discontinuation. By actuarial analysis, 57 ± 6% of patients will be able to continue amiodarone, with or without a therapy modification for 2 years and 36 ± 7% will have successful long-term therapy without a recurrence of VT or intolerable side effects for 2 years. Of 63 patients with control electrophysiologic studies, 36 had repeat programmed stimulation after 3 weeks of amiodarone therapy. By chi square and logistic regression analyses, the mode of induction of ventricular tachycardia with amiodarone was useful in predicting long-term outcome. Patients with a more easily induced ventricular tachycardia after amiodarone (compared to control studies) were at higher risk of ventricular tachycardia recurrence or sudden death, whereas patients with a ventricular tachycardia that was more difficult to induce tended to have successful long-term therapy. In summary, a subset of patients with drug-refractory ventricular tachycardia can be successfully treated with amiodarone although therapy modifications are often required. The mode of ventricular tachycardia induction with amiodarone therapy may be helpful in predicting which patients are more likely to have successful long-term therapy and which patients may require therapy modification or other treatments. Repeat electrophysiologic studies after several weeks of amiodarone therapy can be useful in guiding therapy decisions in patients with recurrent ventricular tachycardia.

Interaction of steady-state procainamide with H2-receptor antagonists cimetidine and ranitidine.

Summary This study was designed to compare the effects of equivalent therapeutic doses of two H2 antagonists, cimetidine and ranitidine, on steady-state procainamide pharmacokinetics. Six healthy men were given 500 mg sustained-release procainamide every 6 h, for a total of 13 doses, on three occasions. Subjects were randomly assigned to three treatments by a Latin-square design: cimetidine 1,200 mg/day, ranitidine 300 mg/day, and no H2-receptor antagonist (control) for 4 days. Cimetidine significantly increased the procainamide area under the serum concentration-time curve by 43%, decreased renal clearance by 36%, and decreased the ratio of systemic clearance of procainamide to bioavailability by 28%. Ranitidine did not significantly alter procainamide steady-state pharmacokinetics.

Long-term therapy with disopyramide phosphate: Side effects and effectiveness☆

In this study, the safety and efficacy of long-term therapy with disopyramide phosphate were evaluated in 40 patients with documented, recurrent, symptomatic tachyarrhythmias. Twenty-one (53%) of the patients had organic heart disease, and nine of these patients had compensated congestive heart failure. The tachyarrhythmias which were treated were paroxysmal supraventricular tachycardia (21 patients), paroxysmal atrial fibrillation (six patients), and paroxysmal ventricular tachycardia (13 patients). In each patient there was evidence, from continuous ECG monitoring or electrophysiologic testing, that disopyramide would be effective therapy, and each patient was able to tolerate disopyramide (no side effects or tolerable side effects) during an initial trial period of 1 to 2 weeks. Dosages of disopyramide were 400 to 1600 mg/day (994 +/- 320 mm/day). During long-term therapy, side effects were reported by 28 (70%) of the patients. The side effects were usually anticholinergic, and were usually a continuation of side effects noted during the initial trial period. None of the patients had idiosyncratic reactions to disopyramide. Most of the patients found side effects to be tolerable; however, in seven patients it was necessary to discontinue disopyramide after 1 to 8 (6 +/- 3) months. Actuarial incidence of intolerable side effects was 21 +/- 7% at 12 months. Nine (22%) of the 40 patients had symptomatic recurrences of tachyarrhythmia after 3 to 32 (15 +/- 9) months of therapy. Actuarial incidence of drug ineffectiveness was 32 +/- 10% at 24 months. Disopyramide was both effective and tolerated in 24 (60%) of the patients, who were followed for 2 to 64 (23 +/- 16) months.(ABSTRACT TRUNCATED AT 250 WORDS)

“Late” proarrhythmia due to quinidine

Abstract Late proarrhythmia due to quinidine is obviously not forewarned by the occurrence of early torsades de pointes, and initial in-hospital use and monitoring may not necessarily ensure or predict long-term safety. It is possible that late torsades de pointes, as profiled in this report, explains the increased mortality in patients receiving chronic quinidine therapy observed in previous investigations.

Analysis of antiarrhythmic drug concentrations determined during electrophysiologic drug testing in patients with inducible tachycardias

T he approved type IA antiarrhythmic drugs quinidine, procainamide and disopyramide are widely used in the treatment of cardiac rhythm disturbances and serum concentrations of these drugs are frequently obtained. These drug levels are routinely interpreted in the context of commonly cited “therapeutic ranges” and used to guide therapy decisions and manipulate dosages. The present study was undertaken to evaluate the value of isolated serum concentrations of antiarrhythmic drugs and to analyze the effect of concentration on concordance and discordance of response.