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PubMed1986

Haemodynamic effects and kinetics of concomitant intravenous disopyramide and atenolol in patients with ischaemic heart disease.

The haemodynamic effects of concomitant intravenous administration of disopyramide (Norpace) and atenolol (Tenormin) were studied in a cross-over trial in 7 patients with ischaemic heart disease. Following 150 mg disopyramide i.v. the cardiac index (CI) and stroke volume index (SVI) decreased by 14% and 26%, respectively and the heart rate (HR) and preejection period index (PEPI) increased by 13% and 19%, respectively. A decrease in CI of 14% and HR of 21%, respectively were noted after intravenous administration of 7.5 mg atenolol; PEPI increased by 10% whereas SVI remained unchanged. The cardiac Index (CI) fell by 33% following the administration of both drugs. The effect on CI of the two drugs was additive. The effect of disopyramide and atenolol on HR, SVI and PEPI was not significantly modified by coadministration of the other drug. No change in blood pressure was observed after disopyramide or atenolol. A correlation (rho) of 0.540 and 0.387 was observed between the change in PEPI and the log free and total serum concentrations of disopyramide, respectively. Combined intravenous use of the two drugs in patients with incipient or overt heart failure is not recommended, unless it is due to the arrhythmia to be treated.

Aged↗
PubMed1986

The impact of neglecting nonlinear plasma-protein binding on disopyramide bioavailability studies.

Disopyramide has nonlinear protein binding and thus the relationship between the extent of its bioavailability and AUC, the area under the plasma concentration-time curve, is nonlinear and absorption rate-dependent. The unbound species follows linear pharmacokinetics. A solution of disopyramide, the innovator's product, and two generic formulations were found to be statistically indistinguishable in their bioavailability of disopyramide, whether comparison was based upon AUC or area under the plasma unbound concentration-time curve (AUCu). The AUC and AUCu gave similar results because of truly similar bioavailability, coupled with sufficiently similar release rates, among the four preparations chosen for study. The concentration dependence of disopyramide protein binding and the time course of unbound plasma concentrations were fit by models which then allowed prediction of AUC under various biopharmaceutical scenarios. Nonlinear binding of disopyramide to plasma proteins renders AUC an insensitive parameter for the discrimination of products with different extents of bioavailability; immediate-release products allowing bioavailabilities of 75 or 125% relative to the solution can generate AUCs 86 and 112%, respectively, of that from the solution. Nonlinear binding, furthermore, leads to a tendency for AUC to overestimate the bioavailability of slower release products in single-dose studies; if AUC were the index of bioavailability, products permitting the same bioavailability as the solution but releasing over 12 hr could appear to allow 114% relative bioavailability. Moreover, in some situations the bias arising from the insensitivity of AUC to product differences can be reinforced by the dependence of AUC on release rate; an apparent relative bioavailability of 80% can be achieved by a 12-hr release product allowing a true relative bioavailability of a mere 58%. While multiple-dose studies appear largely to avoid the tendency to overestimate low bioavailability in slow-release products, in these studies AUC appears to be even more insensitive in resolving discrepancies between products. Assay technology now available makes AUCu a feasible and more reliable index of bioavailability than AUC when plasma protein binding of drugs is nonlinear.

Administration, Oral↗
PubMed1981

[The effect of disopyramide of left ventricular function: an echocardiographic study of the extent and time course (author's transl)].

Seven healthy volunteers were evaluated for changes in left ventricular function after a therapeutic intravenous dose of Disopyramide (2 mg/kg, maximum 150 mg given over 5 min) and, subsequently, under oral maintenance therapy (200 mg every 6 h for 3 days). Parameters of left ventricular function were determined by Echocardiography. Measurements were taken before injection, 5--25 min after intravenous Disopyramide in intervals of 5 min and 120 min after the last oral dose of the drug. Peak changes occurred 5 min after termination of injection and included increases in mean arterial pressure (10%), heart rate (22%) and endsystolic ventricular diameter (30%) and decreases in percentage (43%) and mean velocity (36%) of diameter shortening, decreases of systolic thickness and percentage of thickening of left posterior wall (27 and 43% respectively) and of interventricular septum (15 and 22% respectively) as well as a decrease of the relative thickness of left ventricular wall (40%) and of left posterior (36%) and septal (39%) amplitude. After 20 min changes in all parameters were significantly less than 5 min after injection but still significantly greater than under oral maintenance therapy. After 25 min measurements differed from those under oral Disopyramide only slightly. At both times, however, all parameters were significantly different from control values. Thus, Disopyramide given intravenously and orally in therapeutic dosage is a potent myocardial depressant in man. As the acute negative inotropic effect of intravenous Disopyramide might be of clinical importance in patients with decreased myocardial function a slow injection over 15--20 min and a dose reduction is recommended in these cases.

Adult↗
PubMed1983

Pharmacokinetics of disopyramide in patients with chronic renal failure.

The pharmacokinetics study of a single oral dose of 200 mg of disopyramide was performed in 22 normal control subjects and 33 patients with chronic renal failure (CRF). The latter were subdivided into 3 groups of 11 patients each as a function of the gravity of renal insufficiency. With the exception of maximum concentration (C max), which was only slightly modified, and of the apparent distribution volume which remained unchanged, all the other pharmacokinetic blood parameters (t max, concentration at 24th hour, elimination constant (ke h-1), elimination half-life, area under the curve and plasma clearance) were significantly modified in the CRF group; in particular, the elimination half-life was significantly increased (for 22 cases of CRF with mean plasma creatinine greater than 250 microM at 16.3 hours compared to 8.0 hours in controls). The urinary elimination of disopyramide was studied in 14 renal insufficiency patients and in 6 controls. The decreased rate of urinary excretion of disopyramide and its monodealkylated derivative (NMD), during the first 24 hours, was directly related to the severity of renal insufficiency. The ratio of urinary NMD/(disopyramide + NMD) was unchanged in CRF patients as compared to the controls. The results suggest that the dosage of disopyramide should be decreased when plasma creatinine values are greater than 250 microM, and creatinine clearance is less than 30 ml/min. The dose for a 70 kg subject would be 100 mg, administered every 12 hours.

Adolescent↗
PubMed1999

Impact of plasmapheresis on disopyramide elimination.

The impact of plasmapheresis on the disposition of disopyramide was investigated in a 16-year-old female with systemic lupus erythematosus. Determination of total disopyramide plasma concentrations immediately prior to and following a 4-h plasmapheresis treatment revealed a significant reduction (i.e., 1.77 to 0.7 mg/l or approximately 60%). However, reassessment of the total serum concentration after 1.5 h (i.e., post equilibrium) revealed a rebounding of the value to 1.64 mg/l. Associated with this reduction in total serum levels was a decrease in the protein-bound fraction of disopyramide from 69.5% (pre treatment) to 48.6% (post treatment) that corresponded to a commensurate reduction in the concentration of alpha1-acid glycoprotein (i.e., 119 mg/dl pre treatment to 48.9 mg/dl post treatment). Despite these alterations in disopyramide concentrations, the procedure removed only 2.7% of the disopyramide dose and was not associated with the appearance of a cardiac dysrhythmia.

Adolescent↗
PubMed1979

Electrophysiological effects of disopyramide phosphate during experimental myocardial ischemia.

In order to correlate the antiarrhythmic and electrophysiological effects of disopyramide phosphate during acute myocardial ischemia, we performed experiments in 17 mongrel dogs. Refractory periods obtained by the extrastimulus method and conduction times recorded from local electrograms were determined in potentially ischemic and nonischemic areas prior to, after left anterior descending coronary occlusion, and following intravenous administration of disopyramide phosphate 3 mg./Kg. Control refractory periods were similar in both nonischemic and ischemic areas. Following coronary ligation, a disparity of refractoriness of 28 msec. was induced between these two areas. After disopyramide administration, this disparity was reduced from 28 msec. to 5 msec. (p less than 0.001) after 5 to 15 minutes, and to 15 msec. (p less than 0.01) after 15 to 30 minutes. Coronary ligation prolonged conduction times by 8 msec. (p less than 0.005) in ischemic areas and disopyramide further prolonged conduction in these areas by an additional 9 msec. (p less than 0.001). A minimal and transient prolongation of conduction was present in nonischemic areas. We conclude that the differential effects exerted by disopyramide phosphate in ischemic areas may explain its suppressant action of arrhythmias of ventricular origin.

Animals↗
PubMed1993

Acute dose-response effects of intravenous disopyramide in hypertrophic obstructive cardiomyopathy.

To evaluate the acute hemodynamic effects of intravenous disopyramide in hypertrophic obstructive cardiomyopathy (HOCM), 25 patients (12 men, 13 women) with an average age of 40 years (range 18 to 70 years) were evaluated while undergoing cardiac catheterization-angiography. Biplane left ventricular angiography was performed with standard intracardiac-systemic hemodynamics, including resting and provoked (after ventricular premature beat) left ventricular outflow tract gradients, by using simultaneous LV and aortic pressures as disopyramide was being administered (total dose 100 mg, bolus 10 mg every 3 minutes). Average baseline thermodilution cardiac output equalled 4.5 +/- 1.2 L/min, with all 25 subjects demonstrating systolic anterior motion of the mitral apparatus (mild, 3 [12%]; moderate, 8 [32%]; severe, 14 [64%]). Although heart rate originally slowed during disopyramide administration, average heart rate increased during the final stages (before, 78 +/- 15 vs after, 82 +/- 13 beats/min; p < 0.05). Systemic aortic pressures increased during intravenous disopyramide (before, 107 +/- 21/71 +/- 19 mm Hg vs after, 120 +/- 28/81 +/- 13 mm Hg; p < 0.05), with a decline in LV end-diastolic pressure (before, 19 +/- 7 vs after, 16 +/- 6 mm Hg; p < 0.01). Maximum LV systolic pressures decreased (before, 193 +/- 32 vs after, 146 +/- 29 mm Hg; p < 0.01), with a substantial reduction in resting LV outflow tract gradients (before, 86 +/- 34 vs after, 27 +/- 20 mm Hg; p < 0.001) in conjunction with less inducible obstruction (before, 124 +/- 33 vs after, 64 +/- 33 mm Hg; p < 0.001). Only minor electrocardiographic changes were seen during disopyramide infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1975

Electrophysiologic effects of the antiarrhythmic agent disopyramide phosphate.

The electrophysiologic effects of the antiarrhythmic agent disopyramide phosphate given intravenously were studied in 10 patients with cardiac disease. Studies included determinations of sinus recovery time and refractoriness of the atria, the atrioventricular (A-V) node and the His-Purkinje system. Measurements were performed at rest and 15 and 30 minutes after administration of disopyramide. Serum drug levels were measured at these times. Sinus recovery time was shortened at both 15 and 30 minutes, with an average decrease of 39.5 and 146.2 msec, respectively (P less than 0.01). Atrial refractoriness was not altered significantly, but tended to be reduced; the mean effective refractory period was 289.5 msec before administration of disopyramide and 259 and 270 msec 15 and 30 minutes, respectively, after administration. The functional refractory period of the atrioventricular (A-V) node was definitely prolonged in seven patients 15 minutes after administration of disopyramide. The relative refractory period of the His-Purkinje System was not altered. Although this study does not elucidate the mechanism by which disopyramide acheives its antiarrhythmic effects, animal work has shown that it is similar to that of quinidine. In the doses used the drug does not seem to cause first, second or third degree A-V block or fascicular or bundle branch block; it did not increase the severity of first degree A-V block in the three patients with this disturbance. The drug may be particularly useful when arrhythmias are associated with slow sinus rates.

Adult↗
PubMed1984

Effects on ventricular function of disopyramide, procainamide and quinidine as determined by radionuclide angiography.

To evaluate the effects of the 3 commonly used antiarrhythmic agents--disopyramide, procainamide and quinidine--on left ventricular (LV) function, these 3 agents were administered in random sequence after control radionuclide angiography performed at rest and during exercise in 17 patients. Drug dosages were tailored to achieve therapeutic blood levels 5 minutes before and 2 to 3 hours after drug administration. The mean dose of disopyramide was 141 +/- 26 mg every 6 hours, procainamide, 441 +/- 100 mg every 4 hours, and quinidine, 401 +/- 101 mg of the gluconate preparation every 6 hours. The patients received the appropriate dosage for 7 or more days before repeat radionuclide angiography was performed. The ejection fraction at rest was: control 60 +/- 13%, disopyramide 55 +/- 11%, procainamide 58 +/- 11%, and quinidine 59 +/- 12%. The exercise ejection fraction was: control 61 +/- 14%, disopyramide 58 +/- 13%, procainamide 58 +/- 12% and quinidine 61 +/- 13%. In neither case, at rest nor during exercise was there any significant difference observed between any of the agents or between any individual agent and control. However, at rest 8 subjects had a 5% or more decrease from the control value with disopyramide, 5 had a 5% or more decrease with procainamide and 6 had a 5% or more decrease with quinidine, whereas during exercise the decreases were 8, 6 and 5%, respectively. These values were not statistically different but suggest that caution should be taken in administering all 3 agents, particularly to patients with impaired LV function, because individual sensitivity to a given agent may precipitate a significant decline in LV function.

Adult↗
PubMed1984

Actions of disopyramide on potential reentrant pathways and ventricular tachyarrhythmias in conscious dogs during the late post-myocardial infarction phase.

The effect of intravenous disopyramide (plasma level 3.7 +/- 1.6 micrograms/ml, mean +/- standard deviation) on reentrant ventricular tachyarrhythmias was studied by programmed ventricular stimulation in 11 conscious dogs 3 to 8 days after experimental myocardial infarction. Sustained ventricular tachycardia (VT) was induced in 4 dogs (mean cycle length 173 +/- 14 ms) and nonsustained VT in 7 (8 +/- 4 beats, mean cycle length 136 +/- 18 ms). Disopyramide prevented induction of VT in 1 of 4 dogs with sustained VT and 3 of 7 with nonsustained VT, and increased VT cycle length by more than 30% in 2 dogs with sustained VT and 2 of 7 with nonsustained VT. Disopyramide prolonged refractoriness in the infarct zone, measured by analysis of electrograms from an implanted "composite" electrode, by 38 to 53%, depending on the mode of pacing. These values were significantly greater than the increase produced by disopyramide in ventricular effective refractory period (13 +/- 12%), QRS duration and QT interval. Disopyramide has a selective effect on potential reentry circuits in ischemic myocardium, and prolongs refractoriness in abnormal myocardium to a greater extent than its effect on the normal ventricle.

Animals↗
PubMed1989

New observations on the mechanisms of antiarrhythmic actions of disopyramide on cardiac membranes.

Electrophysiologic effects of disopyramide on cardiac membranes were studied using the microelectrode technique applied to papillary muscles and the suction pipette whole-cell clamp method applied to isolated ventricular myocytes from guinea-pig hearts. In contrast to previous reports, the development and recovery from the Vmax blocks of action potentials by disopyramide and lidocaine were best expressed by 2 exponential functions, not 1, suggesting that there might be 2 different processes for the sodium current block. A near-therapeutic concentration (11 microM) of disopyramide depressed Vmax at frequencies of 0.1 to 2.0 Hz decreased action potential amplitude and shortened plateau phase in ventricular myocytes. Action potential duration was prolonged by the drug in most of the preparations but shortened in some. Disopyramide prolonged the refractory period and increased threshold current for excitation. The drug was also shown to depress both the calcium current and the delayed outward potassium current. These multiple actions of disopyramide may explain its variety of antiarrhythmic properties.

Action Potentials↗
PubMed1990

Usefulness of disopyramide for prevention of upright tilt-induced hypotension-bradycardia.

Susceptibility to transient hypotension-bradycardia of neurally mediated origin has been attributed in part to accentuated afferent neural traffic arising from cardiopulmonary mechanoreceptors, and consequently, may be diminished by agents with anticholinergic and negative inotropic effects, such as disopyramide phosphate. This study assessed electrocardiographic and hemodynamic responses to upright tilt testing (alone or during isoproterenol infusion) before and after disopyramide therapy in 10 patients (age range 16 to 74 years) with recurrent syncopal episodes of neurally mediated origin. Untreated, syncope occurred at less than or equal to 7 minutes of tilt alone (6 patients) or tilt plus isoproterenol at less than or equal to 3 micrograms/min (4 patients) and was associated with hypotension (mean arterial pressure, 40 +/- 16 mm Hg vs baseline 76 +/- 10 mm Hg, p less than 0.001) and inappropriate heart rate slowing (mean heart rate, 59 +/- 39 beats/min vs baseline 88 +/- 18 beats/min, p less than 0.005). After oral disopyramide 150 mg 3 times daily (mean plasma level, 3.0 +/- 0.64 micrograms/ml), all patients tolerated 10 minutes of both tilt and tilt plus isoproterenol (maximum dose, 3 micrograms/min) without symptoms, hypotension (mean arterial pressure; tilt 1 min, 79 +/- 7 mm Hg vs tilt 10 min, 77 +/- 8 mm Hg, difference not significant) or bradycardia (mean heart rate; tilt 1 min, 81 +/- 12 beats/min vs tilt 10 min, 83 +/- 11 beats/min, difference not significant). Furthermore, during subsequent 20 +/- 5 months of disopyramide therapy, all but 1 patient remain asymptomatic. Thus, oral disopyramide may be effective for preventing inducible and spontaneous neurally mediated syncope.

Adult↗
PubMed1979

Effects of disopyramide on SA nodal pacemaker activity and contractility in the isolated blood-perfused atrium of the dog.

The isolated blood-perfused preparations of canine atrium were suspended in a bath and perfused with arterial blood led from the carotid artery of the heparinized donor dog. Disopyramide caused dose-related negative chronotropic and inotropic effects in a dose range of 30-1000 microgram when injected directly into the cannulated sinus node artery of the isolated atrium. The order of potencies for inducing the negative chronotropic effect in isolated atrium preparations was verapamil greater than propranolol greater than lidocaine = quinidine greater than phenytoin greater than or equal to disopyramide greater than procainamide. On the other hand, the order of potencies for inducing the negative inotropic effect was verapamil = propranolol greater than lidocaine greater than or equal to phenytoin greater than disopyramide greater than procainamide greater than or equal to quinidine. When disopyramide (1 mg/kg or 3 mg/kg) was administered i.v. into the jugular vein of the donor dog, the systemic blood pressure of the donor dog was markedly decreased. However, the tension developed and sinus rate of the isolated atrium were only slightly decreased. Disopyramide produced greater suppression at higher frequencies and slightly depressed the calcium chloride-induced positive inotropic effects.

Animals↗
PubMed1995

Effects of disopyramide on the atrial fibrillation threshold in the human atrium.

The effects of disopyramide on the atrial fibrillation threshold (AFT) in the human atrium were investigated. To evaluate atrial vulnerability, the following electrophysiologic parameters were measured before and after the administration of disopyramide (2 mg/kg) in 12 patients with paroxysmal atrial fibrillation: The right atrial effective refractory period (ERP) and percentage maximum atrial fragmentation (%MAF) were measured by atrial premature stimulation based on a cycle length of 500 ms. The inter-atrial conduction time (ACT) was measured by burst pacing (120/min) for 30 s. AFT was measured by applying a high-frequency (50 Hz) stimulation for 1 s given at the right atrial appendage. AFT was defined as the lowest intensity of electrical current that could induce atrial fibrillation lasting for more than 30 s. Disopyramide significantly reduced %MAF, and prolonged ERP and ACT. AFT was measured in all patients and the mean AFT was 3.1 +/- 1.7 mA. After the administration of disopyramide, AFT significantly increased to 6.1 +/- 3.6 mA. There was a positive correlation between ERP and AFT, and a negative correlation between %MAF and AFT. No correlation was detected between ACT and AFT. In conclusion, disopyramide increased AFT in the human atrium.

Adult↗
PubMed1995

Salutary effect of disopyramide on left ventricular diastolic function in hypertrophic obstructive cardiomyopathy.

OBJECTIVES: The purpose of this study was to estimate the effect of disopyramide on left ventricular diastolic function in patients with hypertrophic obstructive cardiomyopathy. BACKGROUND: Although disopyramide has been reported to lessen clinical symptoms in patients with hypertrophic obstructive cardiomyopathy, few data exist regarding its effect on diastolic function in these patients. METHODS: Thirteen patients with hypertrophic cardiomyopathy (six with and seven without left ventricular outflow obstruction) were examined. Before and after intravenous disopyramide, hemodynamic and angiographic studies were performed. RESULTS: In patients with outflow obstruction, pressure gradient at the outflow tract decreased from a mean +/- SD of 100 +/- 45 to 26 +/- 33 mm Hg (p < 0.01). Although systolic function was similarly impaired in both groups, the time constant of left ventricular pressure decay (tau) shortened from 56 +/- 10 to 44 +/- 8 ms (p < 0.01) and the constant of left ventricular chamber stiffness (kc) decreased from 0.049 +/- 0.017 to 0.038 +/- 0.014 m2/ml (p < 0.01) only in patients with outflow obstruction. Shortening in tau correlated best with decrease in left ventricular systolic pressure (r = 0.84, p < 0.01). In contrast, tau was prolonged from 52 +/- 10 to 64 +/- 11 ms (p < 0.01) and kc was unchanged in patients without outflow obstruction. CONCLUSIONS: The primary effects of disopyramide on the hypertrophied left ventricle were negative inotropic and negative lusitropic. However, left ventricular diastolic properties in patients with outflow obstruction were improved with a decrease in outflow pressure gradient. Relief of clinical symptoms in hypertrophic obstructive cardiomyopathy with disopyramide might be due in part to improvement of diastolic function, which appears secondary to the reduction in ventricular afterload.

Adult↗
PubMed1976

Disopyramide: serum level and arrhythmia conversion.

The response of arrhythmias to oral disopyramide in relation to its serum levels has been documented. Disopyramide (100 mg.) was given orally, 6 or 8 hourly, to 16 patients with coronary or hypertensive heart disease who developed acute but stable cardiac arrhythmias (20 episodes) which persisted, despite bed rest and sedation with intravenous diazepam or diamorphine. Blood was taken when arrhythmia conversion was observed and the serum disopyramide levels were estimated by gas chromatography. Over-all control of arrhythmias was achieved in 13 (82 per cent) patients within 24 hours. Disopyramide-serum levels were as follows: effective for atrial arrhythmias, 2.80 to 3.18 mug per milliliter, and 3.27 to 7.48 mug per milliliter for ventricular; mean effective levels for all arrhythmias, 3.69 mug per milliliter; mean ineffective levels, 2.39 mug per milliliter (p less than 0.01). Side effects (prolongation of PR and QTc, fall of diastolic BP, urine retention) were observed with serum levels of 3.61 to 7.48 mug per milliliter (mean, 5.54 mug per milliliter) but they were not troublesome clinically. It is concluded that disopyramide is effective and safe with serum levels ranging from 2.39 to about 3.60 mug per milliliter, and this can be maintained with 100 mg., 8 hourly. The drug, however, should be given with caution to patients with severe myocardial disease or low arterial pressure and in the presence of an abnormal ECG.

Administration, Oral↗
PubMed1985

Electrophysiological effect of disopyramide on rabbit sinus node cells.

The effects of disopyramide on the membrane potentials and currents of rabbit sinus node cells were studied using the conventional microelectrode and voltage clamp methods. Disopyramide (5 and 10 micrograms/m1) produced a negative chronotropic effect, and decreased the maximum rate of depolarization, the overshoot potential and the maximum diastolic potential. The action potential duration at half-amplitude was prolonged, and the slope of diastolic depolarization was reduced. In the voltage clamp experiments, disopyramide (10 and 50 micrograms/m1) reduced the potassium outward current (IK) without changing its kinetics. Disopyramide reduced the slow inward current Isi and increased the recovery time constant of Isi. The hyperpolarization-activated current (Ih) was also decreased by the drug. From these results, it is concluded that disopyramide has a depressant effect on the electrical activity of sinus node cells by mediating depression of IK, Isi and Ih.

Action Potentials↗
PubMed1997

Heart conduction disturbances and cardiovascular collapse after disopyramide and low-dose metoprolol in a patient with hypertrophic obstructive cardiomyopathy.

Disopyramide as an antiarrhythmic can be prescribed to patients with atrial fibrillation and, owing to its negative inotropic effect, to patients with hypertrophic obstructive cardiomyopathy. It is known that in patients with cardiac conduction disturbances and heart failure, disopyramide can adversely affect heart rhythm and conduction and induce cardiovascular collapse. A patient with hypertrophic obstructive cardiomyopathy and paroxysms of atrial fibrillation is described who was treated with disopyramide and also, during the 5 days before admission, with metoprolol. In spite of normal cardiac conduction and function before disopyramide, this treatment was followed by hypotension, bradycardia, and cardiac conduction disturbances. Our case shows the potential for disopyramide, especially when combined with metoprolol, to induce grave adverse effects even in patients with normal cardiac conduction and ventricular function.

Anti-Arrhythmia Agents↗