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PubMed1999

Dispersion of filtered P wave duration by P wave signal-averaged ECG mapping system: its usefulness for determining efficacy of disopyramide on paroxysmal atrial fibrillation.

INTRODUCTION: Although it is desirable to know drug efficacy before initiating antiarrhythmic therapy, there have been no methods for this evaluation. P wave signal-averaged ECG (P-SAECG) is useful to detect subtle changes in disturbance of atrial conduction. The purpose of this present study was to test whether P-SAECG mapping system would give any information on the efficacy of disopyramide on the prevention of paroxysmal atrial fibrillation (PAF). METHODS AND RESULTS: P-SAECG was performed before disopyramide treatment, at 3 hours after a single dose of oral disopyramide (200 mg), and after 4 weeks of disopyramide treatment (300 mg/day). After measuring the filtered P wave duration by the vector magnitude and mapping methods, we calculated filtered P wave duration dispersion, difference between the maximal and minimal filtered P wave duration within 16 chest leads at these three time points. Filtered P wave duration and filtered P wave duration dispersion before treatment were longer in 32 patients with symptomatic PAF than in 31 healthy volunteers. Disopyramide was effective for suppression of PAF in 17 patients and ineffective in 15 patients after 4 weeks of treatment. Filtered P wave duration was similarly prolonged at 3 hours in the two groups, whereas filtered P wave duration dispersion at 3 hours after the disopyramide administration behaved differently; it decreased in all of the effective group and increased in all of the ineffective group. The effective patients were prospectively followed with the same treatment for 6 months. In 16 (94%) of these 17 effective patients, no PAF was documented and they remained to be asymptomatic. CONCLUSIONS: Thus, measuring filtered P wave duration dispersion with the P-SAECG mapping method after a single administration may predict the long-term efficacy of disopyramide in patients with PAF.

Administration, Oral↗
PubMed1984

Oral disopyramide after admission to hospital with suspected acute myocardial infarction. U. K. Rythmodan Multicentre Study Group.

A multi-centre double-blind randomized study is reported in which the effect on mortality of oral disopyramide (300 mg loading dose, then 100 mg qds) was compared with placebo in 1985 patients entering hospital with suspected acute myocardial infarction. Treatment was commenced with 24 hr of onset of symptoms (mean time to first dose 9 hr) and continued until discharge from hospital or 14 days, whichever came first. Nine-hundred and ninety-five patients were allocated to disopyramide and 990 to placebo. The overall mortality, calculated on an intention-to-treat basis, was 7.2% for the disopyramide and 5.6% for the placebo patients. Among those patients with proven infarction mortality was 9.5% of 687 on disopyramide and 7.4% of 716 on placebo. These differences are not statistically significant. Patients with cardiac failure or hypotension at entry did not fare worse on disopyramide, but those with a conduction defect did. Reinfarction was not significantly influenced by disopyramide. The prophylactic use of disopyramide in patients with suspected acute myocardial infarction does not reduce mortality or the incidence of early reinfarction.

Clinical Trials as Topic↗
PubMed1979

Adverse hemodynamic effects of intravenous disopyramide compared with quinidine in conscious dogs.

Disopyramide resembles quinidine electrophysiologically, but its effect on left ventricular function has not been clarified. Twelve awake dogs were instrumented for measurement of cardiac output, left ventricular pressure and its maximal first derivative (dP/dt max), and left atrial and aortic pressures. Disopyramide or quinidine at identical, clinically relevant doses (1 and 5 mg/kg i.v.) was infused over 5 minutes at each level. Peak changes after disopyramide 1 mg/kg included increases in heart rate (34%), mean aortic pressure (24%) and systemic vascular resistance (33%), and decreases in stroke volume (16%) and dP/dt max (19%). With disopyramide at 5 mg/kg these changes were of greater magnitude (e.g., dP/dt -- 36%). Quinidine at both doses caused no changes except a 13% decrease in vascular resistance at 5 mg/kg. Heart rate with disopyramide increased after propranolol (1 mg/kg i.v.), was unchanged after atropine (0.1 mg/kg i.v.), and slowed after propranolol and atropine. Phenoxybenzamine (2 mg/kg i.v.) did not prevent the rise in systemic vascular resistance produced by disopyramide. Thus, disopyramide in clinical dosages exerts opposing direct and indirect effects on cardiac pacemakers and, unlike quinidine, is a potent myocardial depressant and vasoconstrictor in the conscious dog.

Animals↗
PubMed1990

Comparison of cardiovascular effects of pirmenol with those of disopyramide in isolated canine heart preparations cross-circulated with a donor dog.

To assess the cardiovascular profiles of pirmenol, a new antiarrhythmic drug, and to compare them with those of disopyramide, isolated canine sinoatrial node, papillary muscle and atrioventricular node preparations cross-circulated with a donor dog were used. Pirmenol injected intraarterially into the isolated preparations showed negative chronotropic and inotropic effects, which were comparable to those of disopyramide; and it also showed coronary vasodilator and negative dromotropic effects on atrio-His as well as His-ventricular conduction, which were significantly more potent than those of disopyramide. Similarly, pirmenol administered intravenously into the donor dog showed more potent negative dromotropic effects on the PQ interval and QRS width than disopyramide, while in the isolated preparations cross-circulated by the donor dog, pirmenol and disopyramide showed equipotent cardiodepressant effects. In the same preparation, pirmenol decreased coronary blood flow following a transient increase, while disopyramide only decreased coronary blood flow. Since the antiarrhythmic action of class I drugs is considered to result from inhibition of the fast inward current, which generates and propagates action potentials and also induces ventricular automaticity, our results suggest that pirmenol possesses an electrophysiologic effect typical to an efficacious class I agent such as disopyramide.

Action Potentials↗
PubMed1999

Hypoglycemia induced by interaction between clarithromycin and disopyramide.

A 59-year-old man receiving hemodialysis was hospitalized due to severe hypoglycemic attack. The patient had been treated with disopyramide (50 mg/day) because of paroxysmal atrial fibrillation. Hypoglycemia occurred after taking clarithromycin (CAM, 600 mg/day), a macrolide antibiotic. The serum disopyramide concentration reached 8.0 micrograms/ml (23.6 microM) in the presence of CAM, while it was 1.5 micrograms/ml before the addition of CAM. A 75 g oral glucose tolerance test and daily profiles of blood glucose value showed that blood glucose levels were significantly lower in the presence of CAM and disopyramide compared to that in the absence of these drugs. The Turner index in the presence of CAM and disopyramide was significantly higher than that in the absence of these drugs, suggesting that a toxic concentration of disopyramide enhanced insulin secretion, resulting in the induction of hypoglycemic attacks, in which the inhibitory effects of CAM on the hepatic chytochrome P-450 might be involved. QT and QTc intervals were prolonged in the presence of CAM and disopyramide, but torsades de points were not observed in this patient receiving nicorandil (15 mg/day). Thus, it should be taken into account that life-threatening hypoglycemia may result from the interaction between clarithromycin and disopyramide.

Anti-Arrhythmia Agents↗
PubMed1987

Disopyramide. A reappraisal of its pharmacodynamic and pharmacokinetic properties, and therapeutic use in cardiac arrhythmias.

Disopyramide is a widely used class IA antiarrhythmic drug with a pharmacological profile of action similar to that of quinidine and procainamide. Over the past 10 years disopyramide has demonstrated its efficacy in ventricular and atrial arrhythmias. In therapeutic trials, usually involving small numbers of patients, the efficacy of disopyramide was comparable with that of mexiletine, perhexiline, tocainide, propafenone or prajmalium. Recent comparisons with quinidine have confirmed the similar efficacy and better tolerability of disopyramide. The suggestion from initial studies that disopyramide may be less effective than amiodarone or flecainide requires further investigation. In addition, studies have failed to demonstrate that the early administration of disopyramide after acute myocardial infarction decreases important arrhythmias or early mortality. Thus, disopyramide is now well established as an effective antiarrhythmic drug in ventricular and supraventricular arrhythmias although its role in therapy relative to that of recently introduced antiarrhythmic agents is not clear.

Arrhythmias, Cardiac↗
PubMed1991

[Doppler and echocardiographic assessments of effects of disopyramide on non-obstructive hypertrophic cardiomyopathy].

We assessed the effects and therapeutic implications of disopyramide on left ventricular systolic and diastolic functions in 19 patients with non-obstructive hypertrophic cardiomyopathy by Doppler echocardiography. All patients were in sinus rhythm. Parameters measured were fractional shortening (FS (%)), mean velocity of circumferential fiber shortening (mean Vcf (circ/sec)), ejection fraction (EF (%)), peak left ventricular outflow velocity (peak-LVOT (cm/sec)), peak rapid filling inflow velocity (peak-R (cm/sec)), peak late filling inflow velocity (peak-A (cm/sec)) and peak-A/peak-R ratio (A/R ratio). These values were compared before and after infusion of disopyramide (2 mg/kg). There was no significant difference in heart rate, systolic and diastolic blood pressures before and after infusion of disopyramide. Following the intravenous drip infusion of disopyramide, FS decreased from 38.1 +/- 5.4 to 33.2 +/- 4.9 (p less than 0.05) and the mean Vcf decreased from 1.285 +/- 0.181 to 1.141 +/- 0.188 (NS). EF and peak-LVOT also decreased from 67.7 +/- 6.3 to 61.9 +/- 7.0 (p less than 0.05), and from 107.6 +/- 29.5 to 92.4 +/- 25.2 (p less than 0.01), respectively. The infusion of disopyramide increased the peak-R from 47.3 +/- 18.2 to 55.5 +/- 19.2 (p less than 0.05), and decreased peak-A from 52.0 +/- 13.6 to 40.2 +/- 12.6 (p less than 0.01), resulting in a decrease of A/R ratio from 1.277 +/- 0.537 to 0.818 +/- 0.475 (p less than 0.01). These results suggest that disopyramide improved left ventricular diastolic function, although systolic function decreased slightly. In conclusion, disopyramide can be also used beneficially in non-obstructive hypertrophic cardiomyopathy without arrhythmias.

Adult↗
PubMedDate not supplied

Disopyramide: clinical indications, pharmacokinetics and laboratory assessment.

Disopyramide is an antiarrhythmic drug similar to quinidine and used primarily to treat ventricular ectopic systoles. Unlike quinidine which shows drug-drug interaction with digoxin, disopyramide appears to be free of this problem. Side effects include anticholinergic symptoms, cardiovascular problems, and some gastrointestinal discomfort. Disopyramide is metabolized to N-desisopropyl disopyramide in the liver with approximately 50 percent of the parent drug excreted unchanged. The elimination half-life varies from 4.5 to nine hours, and it can be even longer in cases of renal failure or myocardial infarction. There exists an extremely variable degree of protein binding (10 to 70 percent), which is highly dependent on concentration. The unbound (free) fraction increases with increasing drug concentration, making the interpretation of total disopyramide concentrations very difficult. Since the free drug concentration is more representative of availability to its receptor, and only the free fraction is available for renal excretion, the free drug concentration may represent a better predictor of therapeutic effectiveness. Methods for determining concentrations of disopyramide include gas chromatography, high performance liquid chromatography, homogeneous enzyme immunoassay (EMIT), and fluorescence polarization immunoassay. A method for performing both total and free disopyramide determinations is also described.

Cardiac Complexes, Premature↗
PubMedDate not supplied

Disopyramide-pyridostigmine: report of a beneficial drug interaction.

A previously unrecognized beneficial drug interaction is described. Without affecting the antiarrhythmic properties of disopyramide, a sustained-release form of pyridostigmine (a cholinesterase inhibitor) was shown to prevent completely anticholinergic side effects in a study population (17 patients), whereas side effects occurred in 26 of 89 patients (29%) in a control group (p less than 0.025). Pyridostigmine also diminished or abolished disopyramide-induced anticholinergic side effects in each of 10 patients in whom they were already present. Pyridostigmine allowed an increase in tolerated disopyramide blood levels (4.53 +/- 1.59 micrograms/ml versus 3.85 +/- 1.78 micrograms/ml) and a significant increase in disopyramide dosages (224 +/- 68 mg versus 188 +/- 68 mg every 6 h) (p less than 0.02). No patients suffered side effects from pyridostigmine. These data suggest that pyridostigmine can be used to prevent as well as to treat the anticholinergic side effects of disopyramide. The usefulness of disopyramide has previously been limited by these anticholinergic side effects. Further investigation is in progress to determine what role pyridostigmine can play in making disopyramide therapy available to patients who otherwise could not benefit from its use.

Adult↗
PubMed1987

A review of the effects of disopyramide phosphate on left ventricular function and the peripheral circulation.

In the absence of preexistent myocardial dysfunction, the risk of producing cardiac decompensation in patients being treated with any of the conventional antiarrhythmic agents is low. The availability of disopyramide for clinical use in 1977 produced optimism for an effective antiarrhythmic agent that was free of the well-known immediate and late toxicities of quinidine and procainamide. Unfortunately, shortly after its clinical introduction, reports appeared that raised concern about the negative inotropic actions of disopyramide and the possible role of this drug in precipitating heart failure. In clinical use, the frequency of adverse effects on ventricular function appeared to be out of proportion to disopyramide's greater negative inotropic activity and the contrasting (augmenting) effect on the peripheral vascular resistance compared to that of either quinidine or procainamide, suggesting that the other factors contributed to these observations. Review of the reported literature reveals that certain factors encourage such adverse reactions. These primarily include the routine use of oral and especially intravenous loading dosages of disopyramide in an effort to attain rapid onset of action, the failure to adequately reduce dosages of disopyramide in the setting of compromised renal function, and, most importantly, the use of standard (and even loading) dosages in patients with active heart failure, compromised left ventricular function, or a history of heart failure. The avoidance of loading dosages of disopyramide, adequate reductions of maintenance dosages in the setting of renal insufficiency, gradual dose titration for additional drug action, and omission of patients with decompensated heart failure or significant left ventricular dysfunction should significantly enhance safety in the use of disopyramide.

Anti-Arrhythmia Agents↗
PubMed1988

[Experimental studies of the hemodynamics of disopyramide in comparison with quinidine].

The haemodynamic effects of quinidine and disopyramide i.v. were investigated in 79 rats. Measurements were performed in the intact circulation (LVP, AoP, dp/dtmax). Myocardial function was examined independently of circulatory changes by isovolumetric registrations (peak LVP). Animals with NaCl infusion served as controls. After infusion of 5 mg/kg (10 mg/kg) quinidine, we obtained a reduction (p less than 0.05) in the left ventricular pressure to 81.6 +/- 3.1% (82.6 +/- 3.7%), in the mean aortic pressure to 70.7 +/- 3.4% (79.3 +/- 6.7%), in dp/dtmax to 73.9 +/- 5.6% (72.8 +/- 6.2%), and in the heart rate to 69.7 +/- 7.4% (69.9 +/- 5.4%). Isovolumic pressure maxima after quinidine were not different from the controls (90.7 +/- 2.4% and 93.6 +/- 1.5% respectively vs. 96.1 +/- 1.0%). 1 mg/kg disopyramide caused no significant haemodynamic changes. 2 mg/kg disopyramide led to a slight increase in dp/dtmax (107.2 +/- 5.6%, N.S.), while 4 mg/kg disopyramide had a tendency to reduce the left ventricular pressure (88.5 +/- 6.2%), mean aortic pressure (80.5 +/- 14.8%) and dp/dtmax (75.1 +/- 8.0%). After 4 mg/kg disopyramide, the isovolumic maxima were reduced. Our results indicate that the haemodynamic side effects of class-I antiarrhythmic drugs are different. Quinidine i.v. caused a reduction in pressures and heart rate, but had no influence on the isovolumic pressure maxima. Disopyramide i.v., on the other hand, had no significant haemodynamic effects in clinical doses. After high (not clinically used) doses of disopyramide (4 mg/kg), which also led to high plasma levels, myocardial performance was depressed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

[Comparative study of quinidine and disopyramide in the treatment of stable ventricular extrasystole].

The antiarrhythmic efficiency of quinidine arabogalactan-sulphate (QAGS) and disopyramide were determined in 38 patients showing chronic, stable frequency premature ventricular beats (PVB). The study which was carried out in 4 medical Centers, used a longitudinal cross-over design. After a baseline evaluation which consisted of two 24 hours electrocardiograms, the patients were randomised to one of the two drugs during a period of 6 or 7 days. The drug sequence were followed by a placebo sequence. A 24 hours electrocardiogram was performed at the end of each sequence. The daily doses were equivalent to 660 mg of quinidine base for QAGS and 600 mg for disopyramide. Among the 38 patients who entered in the study, 32 went through each sequence of the test. The average number of PVB was significantly reduced by QAGS and disopyramide (p less than 0.0001). With QAGS 18 patients had more than 65 p. 100 reduction of PVB and 12 of them more than 80 p. 100. With disopyramide, 14 patients had more than 65 p. 100 reduction of PVB and 12 of them more than 80 p. 100. There was no statistical difference in the overall efficiency of the two drugs. Three patients died, one from myocardial reinfarction, one from ventricular fibrillation; in one other case, the cause of the death remained undetermined. QAGS was better tolerated than disopyramide; adverse effects occurred in 6 patients with QAGS and in 10 with disopyramide. The responsibility of disopyramide in the occurrence of two severe ventricular arrhythmia may be questioned.

Adult↗
PubMedDate not supplied

Intravenous disopyramide in acute myocardial infarction: a haemodynamic and pharmacokinetic study.

We studied the haemodynamic and pharmacokinetic effects of intravenous disopyramide phosphate in 12 patients (average age, 59 years) with proven transmural myocardial infarction, whose symptoms began less than 12 h prior to the study. The aim was to assess the effects of intravenous disopyramide (2 mg/kg given over 5 min) on cardiac index (CI), left ventricular filling pressure (LVFP), heart rate (HR), mean systemic arterial blood pressure (BP), and systemic vascular resistance (SVR) for 60 min after administration of the drug. Both total and free concentrations of disopyramide in the plasma were also measured. A significant elevation (p less than 0.01) of LVFP (estimated indirectly as pulmonary artery end-diastolic pressure) occurred and persisted through the 1-h evaluation period. There was a small but significant (p = 0.02) initial fall in CI and a rise in SVR (p = 0.05). No significant changes occurred in HR or BP. Serum concentrations of disopyramide reached recommended therapeutic concentrations. There was no significant correlation of the changes in cardiac variables from pretreatment values with total serum concentrations, but the free concentration of disopyramide in plasma correlated better with cardiac effect, and the relationships of the free concentration of disopyramide to the changes in LVFP and in SVR from pretreatment values were significant (p less than 0.05). In two patients studied in detail, there was evidence of dose-dependent protein binding of disopyramide.

Aged↗
PubMed1993

Acute effects of conventional oral dose of disopyramide on left atrial and ventricular functions.

Disopyramide, an antiarrhythmic drug, is known to impair cardiac function, but acute cardiac effects of conventional oral dose of disopyramide are not well known. To examine the extent of acute cardiac effects of daily oral dose of disopyramide, we gave 150 mg of disopyramide to thirteen patients with normal or impaired cardiac function, and observed cardiac function on an hourly basis for 3 hours after baseline period. The serum level of disopyramide reached a therapeutic level (2.0-5.0 micrograms/ml) mostly 1 hour after administration. Doppler-echocardiographically determined left ventricular ejection fraction, and the ratio of the peak early filling velocity to the peak atrial filling velocity in left ventricular inflow velocity remained unchanged throughout the experimental period. Other hemodynamic variables, such as blood pressure and heart rate remained unchanged. We conclude that daily oral dose of disopyramide appears to have no significant effects on cardiac function after administration. Disopyramide seems to be safe and may not be necessarily withheld from patients who need it, when hemodynamic variables are to be measured.

Adult↗
PubMed1991

Effects of the enantiomers of disopyramide and its major metabolite on the electrophysiological characteristics of the guinea-pig papillary muscle.

Disopyramide, a Class Ia antiarrhythmic drug, is clinically used as a racemic mixture; R(-)disopyramide and S(+)disopyramide. The major metabolite in man is desisopropyldisopyramide: R(-)desisopropyldisopyramide and S(+)desisopropyldisopyramide. The effects of the four compounds were compared on the electrophysiological characteristics of the guinea-pig papillary muscle using the standard microelectrode technique. At an external K+ concentration of 5.4 mmol/l and a stimulation frequency of 1 Hz, S(+)disopyramide (20 mumols/l) increased action potential duration (APD) by more than 18%, while it was diminished by 6% in the presence of R(-)disopyramide. Resting membrane potential amounted to -87.1 +/- 0.5 mV (n = 14) and -85.6 +/- 1.2 mV (n = 10), respectively. Also a small but significant difference in effect on the maximal rate of depolarization was observed, R(-)disopyramide being more potent, related with a slower recovery of the maximal rate of depolarization. The enantiomers of the metabolite appeared to be three times less potent than those of the parent drug in their effect on the maximal rate of depolarization. The characteristics of the enantiomers of the metabolite correlated with those of the parent drug: also the R(-)enantiomer was more potent in decreasing the maximal rate of depolarization and caused more shortening of the action potential than the S(+)enantiomer. Time constants for onset and recovery of/from rate dependent block of the maximal rate of depolarization were dependent upon the external K+ concentration, both for the enantiomers of the parent drug and those of the metabolite. Onset slowed down while recovery accelerated when external K+ was increased. Time constants were lower for the metabolite. When stimulation interval was shortened, the effect on the maximal rate of depolarisation increased. Only for the metabolite statistical significant stereoselective differences were observed at all stimulation intervals. The effects on the action potential duration were dependent upon stimulation interval; for all enantiomers the action potential duration tended to be relatively (% of control) higher at short stimulation intervals than at large stimulation intervals. The effect on the maximal rate of depolarization was also voltage dependent, but no significant differences were observed between the enantiomers, for the parent drug as well as for the metabolite.

Action Potentials↗
PubMed1979

Suppression of ventricular arrhythmias with intravenous disopyramide and lidocaine: efficacy comparison in a randomized trial.

Twenty-six patients with clinically significant ventricular arrhythmias were randomly assigned to treatment with either intravenous disopyramide or lidocaine; crossover to the other agent was permitted in nine cases of primary drug failure. In addition, disopyramide was administered nonrandomly to seven patients with ventricular arrhythmias not controlled by lidocaine in standard doses. Arrhythmia control (greater than 50 percent reduction of premature ventricular complexes) was achieved in all 22 trials with disopyramide and in 9 of 13 trails with lidocaine in the random study, whereas clinical efficacy (arrhythmia control with absence of side effects) occurred respectively in 15 of 22, and 8 of 13 trials. In all 11 patients (7 nonrandom, 4 random) whose arrhythmia was not controlled with lidocaine the arrhythmia was controlled with disopyramide. Thus, the clinical efficacy of intravenous disopyramide ran parallel to that of lidocaine in patients with ventricular arrhythmias. Furthermore, intravenous disopyramide was an effective alternative agent for patients with arrhythmia not controlled by lidocaine.

Acute Disease↗
PubMed1983

Effects of disopyramide on left ventricular function: assessment by radionuclide cineangiography.

To determine the effects of disopyramide on resting systolic left ventricular (LV) function and LV functional reserve, gated equilibrium radionuclide cineangiography was performed at rest and during maximal symptom-limited supine bicycle exercise in 12 patients after a single 300 mg oral loading dose of disopyramide, and in 22 patients (including the 12 patients just mentioned) after they received disopyramide 150 mg 4 times daily for 5 to 10 days (average 7). The oral loading dose (average serum level 3.6 +/- 1.3 micrograms/ml [standard deviation] produced decreases in ejection fraction in 9 of 12 patients with a decrease in average resting ejection fraction from 40 +/- 15% to 33 +/- 11% (p less than 0.005). However, the lower, sustained dosage of disopyramide was associated with a lower average serum level of 2.5 +/- 0.8 micrograms/ml and with smaller but significant decreases in ejection fraction in 3 of 22 patients during exercise only. At this dosage there was no significant decrease in average ejection fraction for the group at rest or during exercise. Adverse effects of disopyramide on ejection fraction occurred even in patients with previously normal LV function at rest. Hence, disopyramide may be associated with significant decreases in LV systolic function, particularly when given in high, oral "loading" doses. However, sustained therapy with lower dosages as well as lower drug levels is also associated with less depression of LV function.

Adult↗
PubMed1988

Disopyramide in hypertrophic cardiomyopathy. II. Noninvasive assessment after oral administration.

The effects of oral disopyramide 150 mg 4 times a day were compared with propranolol 40 mg 4 times a day and placebo in 10 patients with hypertrophic cardiomyopathy and resting obstruction (7 patients) or latent obstruction (3 patients), in a randomized double-blind crossover design; each drug was given for a period of 4 days. As determined from echocardiographic evaluation of systolic anterior motion of the mitral valve, the subaortic pressure gradient was decreased from 61 +/- 20 mm Hg with placebo to 5 +/- 15 mm Hg with disopyramide (p less than 0.01), and 30 +/- 30 mm Hg with propranolol (p less than 0.01). Disopyramide was more effective than propranolol (p less than 0.01). Disopyramide and propranolol both shortened left ventricular ejection time from 352 +/- 51 ms with placebo to 314 +/- 26 and 322 +/- 41 ms, respectively (p less than 0.01). Preejection period was lengthened from 93 +/- 35 ms with placebo to 119 +/- 25 ms with disopyramide, but was unchanged by propranolol at 98 +/- 23 ms. Disopyramide increased exercise duration versus placebo (10.4 +/- 2 vs 9.6 +/- 2 minutes, respectively (p less than 0.05), whereas propranolol produced no significant change (8.8 +/- 2 minutes).

Administration, Oral↗