Matsubara H, Nakatani S, Nagata S, Ishikura F, Katagiri Y, Ohe T, Miyatake K
Department of Medicine, National Cardiovascular Center, Suita, Osaka, Japan.
J Am Coll Cardiol. 1995 Sep;26(3):768-75. doi: 10.1016/0735-1097(95)00229-W.
The purpose of this study was to estimate the effect of disopyramide on left ventricular diastolic function in patients with hypertrophic obstructive cardiomyopathy.
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.
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.
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.
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.
本研究旨在评估丙吡胺对肥厚性梗阻性心肌病患者左心室舒张功能的影响。
尽管已有报道称丙吡胺可减轻肥厚性梗阻性心肌病患者的临床症状，但关于其对这些患者舒张功能影响的数据却很少。
对13例肥厚性心肌病患者（6例有左心室流出道梗阻，7例无左心室流出道梗阻）进行了检查。在静脉注射丙吡胺前后，进行了血流动力学和血管造影研究。
在有流出道梗阻的患者中，流出道压力梯度从平均±标准差100±45降至26±33 mmHg（p<0.01）。尽管两组患者的收缩功能均有类似损害，但仅在有流出道梗阻的患者中，左心室压力衰减时间常数（tau）从56±10缩短至44±8 ms（p<0.01），左心室腔硬度常数（kc）从0.049±0.017降至0.038±0.014 m2/ml（p<0.01）。tau的缩短与左心室收缩压的降低相关性最好（r = 0.84，p<0.01）。相比之下，无流出道梗阻的患者tau从52±10延长至64±11 ms（p<0.01），kc无变化。
丙吡胺对肥厚的左心室的主要作用是负性肌力和负性变时性。然而，有流出道梗阻的患者的左心室舒张特性随着流出道压力梯度的降低而改善。丙吡胺治疗肥厚性梗阻性心肌病临床症状的缓解可能部分归因于舒张功能的改善，这似乎是心室后负荷降低的继发结果。
