Effects of quinidine and amiodarone on blood pressure during rapid ventricular pacing in coronary artery disease.

T he hemodynamic response to ventricular tachycardia is an important determinant of prognosis.’ Many factors determine the hemodynamic response to ventricular tachycardia, including (1) the rate of the ventricular tachycardia,2*3 (2) systolic and diastolic ventricular function,4J and (3) the neurohumoral response to the arrhythmia.6v7 Antiarrhythmic drugs such as quinidine and amiodarone may either improve hemodynamics during ventricular tachycardia by slowing the rate of the tachycardia, or may impair the hemodynamic response to ventricular tachycardia by decreasing ventricular contractility, blunting the neurohumoral response to the tachycardia, or by causing vasodilation.8-14 No prior studies have evaluated the effect of antiarrhythmic drugs on the hemodynamic response to ventricular tachycardia independent of their effects on the rate of the tachycardia. The objective of this study was to determine the relative effects of quinidine and amiodarone on the blood pressure (BP) response to rapid ventricular pacing in humans. Previous studies have demonstrated that the BP response during ventricular tachycardia and during ventricular pacing are similar.2 Therefore, in this study ventricular pacing was used to assess the effects of antiarrhythmic drugs on the BP response independent of heart rate. The subjects of this study were 9patients (8 men and I woman, mean age 6.2 f 7 years) who had inducible sustained monomorphic ventricular tachycardia during electrophysiologic testing and who underwent electropharmacologic testing with both quinidine and amiodarone. The indication for electrophysiologic testing was aborted sudden death in 2patients, syncope in 6patients, and nonsustained ventricular tachycardia in I patient. Each patient had coronary artery disease and a history of a prior myocardial infarction. The mean left ventricular ejection fraction was 0.33 f 0.11. Each of the 9 patients was clinically stable at the time of their initial electraphysiology test and throughout theperiodof evaluation. No patient had angina1 symptoms, a history of a myocardial infarction within the prior 3 months, or congestive heart failure requiring adjustment of their medical regimen. Six patients were being treated with digoxin, 5 with diuretics, 4 with an angiotensin-converting enzyme inhibitor, and I patient with a calcium antagonist. The dose of calcium antagonists and angiotensinconverting enzyme inhibitors was kept constant throughout the period of evaluation. The dose of digoxin was reduced by 50% at the time of initiation of quinidine and amiodarone therapy. Electrophysiologv tests were performed in the fasting state >5 half-lives after discontinuation of all antiar-