Halperin J L, Faxon D P, Creager M A, Bass T A, Melidossian C D, Gavras H, Ryan T J
Am J Cardiol. 1982 Nov;50(5):967-72. doi: 10.1016/0002-9149(82)90403-9.
The coronary hemodynamic effects of vasodilator therapy with angiotensin-converting enzyme inhibitors (captopril and teprotide) were studied in 11 patients with ischemic heart disease and severe congestive heart failure (CHF). Over 2 hours, systemic vascular resistance was reduced from 2,408 +/- 240 to 1,715 +/- 170 dynes . s . cm-5 (p less than 0.001), and cardiac output improved 18%, resulting in lower arterial pressure (101 +/- 8 to 86 +/- 5 mm Hg, p less than 0.001) and left ventricular filling pressure (30 +/- 2 to 21 +/- 2 mm Hg, p less than 0.001). Coronary sinus thermodilution blood flow paralleled perfusion pressure but did not significantly vary overall (160 +/- 20 to 133 +/- 12 ml/min, difference not significant [NS]). Coronary vascular resistance was unchanged. Although the left ventricular stroke work index rose slightly (37.7 +/- 8.8 to 41.3 +/- 7.9 g l m/m2, p less than 0.05), there was no change in the coronary arteriovenous oxygen content difference (10.8 +/- 1.0 to 10.4 +/- 1.0 ml/10 ml, NS) or calculated myocardial oxygen consumption (16.4 +/- 1.9 to 13.9 /- 1.6 ml/min, NS). The heart rate-systolic blood pressure product declined significantly during this period (8,824 +/- 703 to 7,087 +/- 514 beats . mm Hg, p less than 0.02); this relief of cardiac effort was a function of the pretreatment plasma renin activity. A derived index of external myocardial efficiency improved 37% (19 +/- 3 to 26 +/- 6, p less than 0.05), reflecting greater left ventricular work without increased oxygen demand. Enhancement of myocardial performance after converting enzyme inhibition appears dependent on reduction of angiotensin-mediated ventricular afterload and preload. The lack of coronary vasomotor effects in patients with advanced ischemic cardiomyopathy may reflect limited coronary vascular reserve. Improvement of heart failure in these patients developed without evidence of myocardial ischemia, since balance was maintained between oxygen supply and demand.
在11例缺血性心脏病合并严重充血性心力衰竭（CHF）患者中，研究了血管紧张素转换酶抑制剂（卡托普利和替普罗肽）血管扩张治疗对冠状动脉血流动力学的影响。在2小时内，全身血管阻力从2408±240降至1715±170达因·秒·厘米⁻⁵（p<0.001），心输出量提高了18%，导致动脉压降低（101±8至86±5mmHg，p<0.001）和左心室充盈压降低（30±2至21±2mmHg，p<0.001）。冠状窦热稀释血流与灌注压平行，但总体上无显著变化（160±20至133±12ml/min，差异无统计学意义[NS]）。冠状动脉血管阻力未改变。虽然左心室每搏功指数略有上升（37.7±8.8至41.3±7.9g·lm/m²，p<0.05），但冠状动脉动静脉氧含量差（10.8±1.0至10.4±1.0ml/10ml，NS）或计算的心肌氧耗量（16.4±1.9至13.9±1.6ml/min，NS）无变化。在此期间，心率-收缩压乘积显著下降（8824±703至7087±514次·mmHg，p<0.02）；这种心脏负荷的减轻是预处理血浆肾素活性的作用。一个推导的心肌外效率指数提高了37%（19±3至26±6，p<0.05），反映出左心室做功增加而氧需求未增加。转换酶抑制后心肌性能的增强似乎依赖于血管紧张素介导的心室后负荷和前负荷的降低。晚期缺血性心肌病患者缺乏冠状动脉血管舒缩效应可能反映了冠状动脉血管储备有限。这些患者心力衰竭的改善在没有心肌缺血证据的情况下出现，因为氧供需之间保持了平衡。
