BRIEF REPORTS Effects of Quinidine and Amiodarone on Blood Pressure During Rapid Ventricular Pacing in Coronary Artery Disease Hugh Calkins, MD, Yu Shyr, MS, Anthony Schork, PhD, Alan Kadish, MD, and Fred Morady, MD T he hemodynamicresponse to ventricular tachycardia is an important determinant of prognosis.’ Many factors determine the hemodynamicresponse to ventricu- lar tachycardia, including (1) the rate of the ventricular tachycardia,2*3 (2) systolic and diastolic ventricular func- tion,4J and (3) the neurohumoral response to the arrhyth- mia.6v7 Antiarrhythmic drugs such as quinidine and amiodarone may either improve hemodynamicsduring ventricular tachycardia by slowing the rate of the tachy- cardia, or may impair the hemodynamicresponse to ven- tricular tachycardia by decreasing ventricular contractili- ty, blunting the neurohumoral response to the tachycar- dia, or by causing vasodilation.8-14 No prior studieshave evaluated the effect of antiarrhythmic drugs on the he- modynamic response to ventricular tachycardia indepen- dent of their effects on the rate of the tachycardia. The objective of this study was to determine the relative ef- fects of quinidine and amiodaroneon the blood pressure (BP) responseto rapid ventricular pacing in humans. Previousstudieshave 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 subjectsof this study were9patients (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 electro- pharmacologic testing with both quinidine and amioda- rone. The indication for electrophysiologic testing was aborted suddendeath 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 meanleft ventricu- lar 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 eval- uation. No patient had angina1 symptoms,a history of a myocardial infarction within the prior 3 months, or con- gestiveheart failure requiring adjustment of their medi- cal regimen. Six patients werebeing treated with digox- in, 5 with diuretics, 4 with an angiotensin-converting enzyme inhibitor, and I patient with a calcium antago- nist. The dose of calcium antagonists and angiotensin- converting enzyme inhibitors waskept constant through- out the period of evaluation. The dose of digoxin was reduced by 50% at the time of initiation of quinidine and amiodarone therapy. Electrophysiologv testswere performed in the fasting state >5 half-lives after discontinuation of all antiar- From the Division of Cardiology, University of Michigan Medical Cen- ter, Bl F245, 1500 East Medical Center Drive, Ann Arbor, Michigan 48109-0022; and the Department of Biostatistics, School of Public Health, Ann Arbor, Michigan. Manuscript received March 9, 1992; revised manuscript received and accepted June 4, 1992. rhythmic drugs and /3 blockers. Each patient gave in- formed consent. Quadripolar electrode catheters were inserted into a femoral vein and positioned at the high right atrium, acrossthe tricuspid valve to record a His bundle electrogram, and at the apex of the right ventri- cle. A 5Fr cannula wasinserted into afemoral artery for BP monitoring. Leads VI, I and III, the intracardiac electrograms,and BP wererecorded at a paper speed of 10 or 25 mm/s using a Siemans-Elema Mingograph 7 recorder. All patients also underwent electrophysiologic test- ing after treatment with quinidine and amiodarone.Fol- low-up testing during quinidine therapy wasperformed 248 hours after initiation of treatment with quinidine gluconate at a dose of 486 to 648 mg 3 times a day. The follow-up electrophysiology test was performed <2 hours before the next scheduleddose. The mean plasma quinidine concentration at the time offollow-up electro- physiologic testing was 3.2 f 1.0 mg/liter (range 2.2 to 4.3 mg/liter). Each patient still had inducible sustained monomorphic ventricular tachycardia during treatment with quinidine and was then treated with amiodarone. Follow-up electrophysiologic testing during amiodarone therapy was performed 9 to 10 days after initiation of treatment with amiodarone at a dose of 1,800mg/day in 3 divided doses. The pacing protocol was performed in each patient after completion of the clinically indicatedportion of the electrophysiology test.Pacing was performed at the right ventricular apex at cycle lengths of 600, 500, 400, 350, 300,280 and 260 ms. Ventricular pacing wasperformed at e.ach cycle length for 30 to 40 secondsor until the patient became presyncopal. The minimal duration of pacing at eachcycle length was20 seconds. Thesequence of cycle lengths at which pacing was performed was randomized. If thepatient’s systolic BP was<40 mm Hg at a given cycle length, pacing at shorter cycle lengths wasnot performed. Between pacing at eachcycle length, the patient was allowed to recover for 25 minutes or until mean BP returned to within 5 mm Hg of the base- line mean BP. No patient developedangina or ischemic ST changesduring pacing. At each pacing cycle length the systolic, diastolic and mean BPS weremeasured after 30 seconds of pacing or at thepoint at which thepatient becamepresyncopal (mini- mum of 20 seconds). BP was determined by averaging the BP response during 4 to 6 beats. Thirty seconds was selected becauseprevious studies have demonstrated that the initial abrupt decrease in BP during rapid ven- tricular pacing isfollowed by an increasein BP. Stabili- zation of the BP is generally achievedwithin 30 seconds of the onset of rapid ventricular pacing.6,7To confirm stabilization of BP within 30 seconds of pacing, BP was compared30 and 40 seconds after onset of pacing in each patient at I or more cycle lengths between 300 and 400 1206 THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 70 NOVEMBER 1, 1992