EFFECTS OF AMIODARONE ON ERECT AND SUPINE EXERCISE HEMODYNAMICS AND EXERCISE CAPACITY IN PATIENTS WITH HYPERTROPHIC CARDIOMYOPATHY

Hypertrophic cardiomyopathy (HCM) is a primary heart muscle disease associated with a high incidence of sudden death. Amiodarone is of benefit in those patients with a high risk profile for sudden death. Amiodarone has also been reported to improve symptoms dramatically in some patients with HCM but to cause functional deterioration in others. In the acute phase of oral amiodarone therapy there are few discernable changes in cardiovascular haemodynamics and the mechanisms of any beneficial effects on symptoms remain unclear. To determine the effect of amiodarone on exercise responses we measured haemodynamic indices in 10 patients during maximal supine- and symptom-limited erect treadmill exercise before and 6 weeks after amiodarone therapy. Following amiodarone therapy there was a significant reduction in resting and peak heart rate during erect exercise (76±13 vs 97±19b.min-1; P=0.001 and 114±26 vs 146±21 b. min-1; P=0.001 respectively). Despite increases in peak pulmonary and systemic artery pressures with amiodarone therapy there was no difference in the peak left ventricular filling pressure or maximum cardiac output achieved. Similarly, during supine exercise the resting and peak heart rates were less following the 6 weeks amiodarone therapy. Comparison of supine and erect exercise haemodynamic indices demonstrated higher peak LVfilling and higher peak systolic and pulmonary artery pressures during supine than during erect exercise (29 ± 10 vs 25 ± 12; P < 0.04; 151 ± 42 vs 126 ± 48; P = 0.01 and 66 ± 27 vs 62±21; P = 0.08 respectively). Despite the higher pre- and after-loads during supine exercise the magnitude of the increase in cardiac output was similar irrespective of the position in which exercise was performed. These results confirm the clinical impression that amiodarone causes little or no change in cardiovascular haemodynamics during chronic therapy and does not adversely affect functional capacity in patients with HCM. © 1992 The European Society of Cardiology.