Holubarsch C, Hasenfuss G, Thierfelder L, Just H
Department of Cardiology, Medizinische Universitätsklinik Freiburg.
Herz. 1991 Sep;16 Spec No 1:298-303.
Vasodilators have been shown to improve hemodynamics of the failing heart as a short-term effect and to decrease mortality as a long-term result. We therefore studied the effect of different vasodilators on myocardial mechanics and energetics in patients with idiopathic dilated cardiomyopathy (IDC) NYHA II to III. In these patients undergoing routine heart catheterization myocardial oxygen consumption was measured using the argon method, and left ventricular pressure and geometry were obtained from left ventricular angiography using a Millar tip microcatheter. All data were analyzed for one single heart beat. The best correlation was found between MVO2/beat and the systolic stress-time integral which considers left ventricular pressure, wall thickness, and geometry. The relation between MVO2/beat and peak systolic wall stress was less relevant. No correlation was found between MVO2/beat and pressure-volume work, dP/dtmax, and mean velocity of circumferential fiber shortening. The intravenous application of nitroprusside and the ACE-inhibitor benazepril decreased both the systolic stress-time integral and the myocardial oxygen consumption in proportion to each other indicating unchanged economy of myocardial contraction. In contrast to other vasodilators, beta 1-agonists and phosphodiesterase inhibitors increase myocardial oxygen consumption independently of changes in the stress-time integral. In conclusion, vasodilators decrease left ventricular pressure and chamber size and thereby proportionally reduce MVO2/beat. The reduction of energy needed for myocardial contraction may partially explain the long-term effects of the ACE-inhibitors and combinations of vasodilators. Pure positive inotropic substances, especially beta 1-agonists, increase myocardial oxygen consumption with minor changes of systolic stress-time integral.(ABSTRACT TRUNCATED AT 250 WORDS)
血管扩张剂已被证明可在短期内改善衰竭心脏的血流动力学,并在长期降低死亡率。因此,我们研究了不同血管扩张剂对纽约心脏协会(NYHA)心功能II至III级的特发性扩张型心肌病(IDC)患者心肌力学和能量代谢的影响。在这些接受常规心脏导管检查的患者中,使用氩气法测量心肌耗氧量,并使用Millar尖端微导管通过左心室血管造影获得左心室压力和几何形状。所有数据均针对单个心跳进行分析。发现每搏心肌耗氧量(MVO2/beat)与考虑左心室压力、壁厚度和几何形状的收缩期应力-时间积分之间具有最佳相关性。MVO2/beat与收缩期峰值壁应力之间的关系不太显著。未发现MVO2/beat与压力-容积功、最大dp/dt、圆周纤维缩短平均速度之间存在相关性。静脉注射硝普钠和血管紧张素转换酶抑制剂苯那普利可使收缩期应力-时间积分和心肌耗氧量成比例降低,表明心肌收缩的经济性未变。与其他血管扩张剂不同,β1激动剂和磷酸二酯酶抑制剂可独立于应力-时间积分的变化增加心肌耗氧量。总之,血管扩张剂可降低左心室压力和腔室大小,从而按比例降低MVO2/beat。心肌收缩所需能量的减少可能部分解释了血管紧张素转换酶抑制剂和血管扩张剂组合的长期效果。单纯的正性肌力物质,尤其是β1激动剂,在收缩期应力-时间积分变化较小的情况下增加心肌耗氧量。(摘要截取自250字)