Tohmo H, Karanko M, Korpilahti K
Cardiorespiratory Research Unit, University of Turku, Finland.
Eur Heart J. 1994 Apr;15(4):523-7. doi: 10.1093/oxfordjournals.eurheartj.a060537.
In this study, the acute haemodynamic effects of angiotensin converting enzyme (ACE) inhibition with intravenous enalaprilat alone or in combination with preload restoration were determined in patients with severe heart failure complicating acute myocardial infarction. Ten patients with raised pulmonary arterial wedge pressure (PAWP > or = 18 mmHg) were first studied during constant conventional vasodilation with diuretic and inotropic medication, by monitoring central haemodynamics and arterial blood gases. The same variables were measured before enalaprilat infusion, after preload reduction with enalaprilat (1 mg.h-1, rate doubled every 30 min until PAWP decreased > or = 25% or up to total cumulative dose of 10 mg) and after preload restoration with fluid loading (4% albumin given 15 ml.min-1 to restore PAWP to baseline) during continuous low dose enalaprilat infusion. Enalaprilat alone (median dose 0.9 mg) reduced significantly the PAWP (from 25 to 17 mmHg; P = 0.004), the mean arterial pressure (from 87 to 83 mmHg; P = 0.008), the mean pulmonary arterial pressure and the right atrial pressure. The cardiac index, stroke volume index and systemic vascular resistance index remained unchanged. Preload restoration during continuous enalaprilat infusion (median dose of 4% albumin 230 ml, and enalaprilat 0.2 mg) did not further enhance left ventricular function; rather, there was a nearly significant decrease in myocardial perfusion pressure. Arterial oxygenation remained unchanged throughout the study. In conclusion, adding intravenous enalaprilat to conventional therapy makes it possible to relieve pulmonary congestion while maintaining the cardiac function and arterial oxygenation. Preload restoration during continuous ACE inhibition offers no further advantages, and may have adverse effects, since the myocardial perfusion pressure may fall.
在本研究中,我们测定了在急性心肌梗死合并严重心力衰竭患者中,单独静脉注射依那普利拉或联合恢复前负荷时,血管紧张素转换酶(ACE)抑制的急性血流动力学效应。首先,对10例肺动脉楔压升高(PAWP≥18 mmHg)的患者,在使用利尿剂和正性肌力药物进行持续常规血管扩张治疗期间,通过监测中心血流动力学和动脉血气进行研究。在静脉输注依那普利拉前、使用依那普利拉降低前负荷后(1 mg·h⁻¹,每30分钟剂量加倍,直至PAWP降低≥25%或直至累积总剂量达10 mg)以及在持续低剂量依那普利拉输注期间通过补液恢复前负荷后(以15 ml·min⁻¹的速度给予4%白蛋白,使PAWP恢复至基线),测量相同的变量。单独使用依那普利拉(中位剂量0.9 mg)可显著降低PAWP(从25 mmHg降至17 mmHg;P = 0.004)、平均动脉压(从87 mmHg降至83 mmHg;P = 0.008)、平均肺动脉压和右心房压。心脏指数、每搏量指数和全身血管阻力指数保持不变。在持续输注依那普利拉期间恢复前负荷(4%白蛋白中位剂量230 ml,依那普利拉0.2 mg)并未进一步增强左心室功能;相反,心肌灌注压有近乎显著的下降。在整个研究过程中动脉氧合保持不变。总之,在常规治疗中添加静脉注射依那普利拉可在维持心脏功能和动脉氧合的同时缓解肺淤血。在持续ACE抑制期间恢复前负荷没有进一步的益处,且可能产生不利影响,因为心肌灌注压可能会下降。