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Hemodynamic effects of encainide in patients with ventricular arrhythmia and poor ventricular function
Insights
Encainide effectively treats ventricular arrhythmias without negatively impacting cardiac function in patients with reduced left ventricular function. This antiarrhythmic drug demonstrates a favorable hemodynamic profile, even in those with congestive heart failure.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Complex ventricular arrhythmias often coexist with depressed left ventricular (LV) function.
- Patients with these conditions may have failed other antiarrhythmic therapies.
- Congestive heart failure is a common comorbidity in this patient population.
Purpose of the Study:
- To evaluate the hemodynamic effects of encainide in patients with ventricular arrhythmia and impaired LV function.
- To assess encainide's impact on ejection fraction and other hemodynamic parameters.
- To determine encainide's safety in patients with a history of congestive heart failure.
Main Methods:
- Gated cardiac scanning was employed before and after encainide therapy.
- Patients received oral encainide (75-200 mg daily) for 1-2 weeks.
- Hemodynamic variables, including ejection fraction, heart rate, and blood pressure, were monitored.
Main Results:
- Encainide significantly reduced premature ventricular complexes by 80%.
- No significant changes were observed in ejection fraction (average 22% pre-encainide, 25% post-encainide).
- Heart rate, blood pressure, stroke volume, and end-diastolic volume remained unchanged.
Conclusions:
- Encainide is hemodynamically well-tolerated in patients with ventricular arrhythmia and depressed LV function.
- Clinically effective doses of encainide do not worsen cardiac function or congestive heart failure.
- Encainide represents a safe therapeutic option for this patient group.
Abstract:
Gated cardiac scanning was used to evaluate the hemodynamic effects of encainide in 19 patients (1 woman) with complex ventricular arrhythmia and depressed left ventricular (LV) function (ejection fraction less than 45%). Patients were 36 to 80 years old (average 61). All were candidates for long-term encainide therapy after having failed with currently available antiarrhythmics. Sixty-three percent had congestive heart failure before they received encainide. All were evaluated in the hospital before encainide therapy by a gated cardiac scan performed at least 3 days after discontinuing all antiarrhythmic drugs. Patients received oral encainide in doses of 75 to 200 mg. Gated cardiac scans were repeated 1 to 2 weeks later when an 80% reduction in frequency of premature ventricular complexes was observed on a 24-hour Holter recording. No patient had worsening of congestive heart failure during encainide therapy. Encainide did not significantly affect ejection fraction, which averaged 22 +/- 10% before and 25 +/- 14% (SD) after encainide (difference not significant [NS]). Other hemodynamic variables, including heart rate, blood pressure, stroke volume and end-diastolic volume, remained unchanged during encainide therapy. Digoxin blood levels in 10 patients averaged 1.04 +/- 0.43 before and 1.22 +/- 0.47 mg/ml (NS) during encainide therapy. Thus, encainide given orally in clinically effective doses does not appear to have significant hemodynamic effects in patients with ventricular arrhythmia and depressed LV function.