Salutary effect of disopyramide on left ventricular diastolic function in hypertrophic obstructive cardiomyopathy
H Matsubara,
S Nakatani,
S Nagata,
F Ishikura,
Y Katagiri,
T Ohe,
and
K Miyatake
Department of Medicine, National Cardiovascular Center, Suita, Osaka, Japan.
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.
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