Schön H R
First Clinic of Internal Medicine, Technical University of Munich, Germany.
J Hypertens Suppl. 1994 Jul;12(4):S95-104.
Angiotensin converting enzyme (ACE) inhibitors decrease preload and afterload and are therefore of potential value in valvular regurgitation. The present study was designed to assess the effects of treatment for 1 year with an ACE inhibitor on myocardial performance.
Twenty-four patients with isolated moderate to severe chronic aortic regurgitation or mitral regurgitation who were free of coronary disease were studied before treatment (control) with the ACE inhibitor quinapril and were then followed for 1 year during quinapril therapy (10-20 mg/day).
After 1 year of ACE inhibition, the regurgitant fraction fell by 27 and 42%, compared with control values, in the aortic and mitral regurgitation groups, respectively (P = 0.0001). The left ventricular end-diastolic volume was reduced from 150 +/- 33 to 128 +/- 30 ml/m2 in the aortic regurgitation group, and from 146 +/- 26 to 109 +/- 24 ml/m2 in the mitral regurgitation group (P = 0.0001 for each). End-systolic volume decreased from 55 +/- 27 to 44 +/- 28 ml/m2 in the aortic regurgitation group (P = 0.005) and from 63 +/- 43 to 47 +/- 29 ml/m2 in the mitral regurgitation group (P = 0.002). The left ventricular ejection fraction increased slightly at rest and during exercise in patients with aortic regurgitation, but showed no change in the mitral regurgitation patients after 1 year of quinapril treatment. Echocardiographic studies showed that after 1 year of therapy there was a decrease of about 10% in the left ventricular end-diastolic and end-systolic diameter in both patient groups. Moreover, the left ventricular mass was reduced by 35% in the aortic regurgitation group (P = 0.0001), and left ventricular hypertrophy, which was present in all patients, was reversed completely. In the mitral regurgitation group, a mass reduction of 15% was observed after 1 year of quinapril treatment, and the septal wall thickness, which indicated borderline hypertrophy, decreased to normal.
These results demonstrate that long-term ACE inhibition in patients with valvular regurgitation reverses left ventricular dilation and reduces left ventricular mass and hypertrophy, thereby improving left ventricular function. Further, they suggest that ACE inhibition may have the potential to delay aortic or mitral valve replacement.
血管紧张素转换酶（ACE）抑制剂可降低前负荷和后负荷，因此在瓣膜反流中具有潜在价值。本研究旨在评估用ACE抑制剂治疗1年对心肌功能的影响。
对24例无冠心病的单纯中度至重度慢性主动脉瓣反流或二尖瓣反流患者在使用ACE抑制剂喹那普利治疗前（对照）进行研究，然后在喹那普利治疗期间（10 - 20毫克/天）随访1年。
ACE抑制治疗1年后，主动脉瓣反流组和二尖瓣反流组的反流分数分别比对照值下降了27%和42%（P = 0.0001）。主动脉瓣反流组的左心室舒张末期容积从150±33降至128±30毫升/平方米，二尖瓣反流组从146±26降至109±24毫升/平方米（每组P = 0.0001）。主动脉瓣反流组的收缩末期容积从55±27降至44±28毫升/平方米（P = 0.005），二尖瓣反流组从63±43降至47±29毫升/平方米（P = 0.002）。主动脉瓣反流患者在静息和运动时左心室射血分数略有增加，但喹那普利治疗1年后二尖瓣反流患者无变化。超声心动图研究显示，治疗1年后两组患者的左心室舒张末期和收缩末期直径均下降约10%。此外，主动脉瓣反流组的左心室质量减少了35%（P = 0.0001），所有患者均存在的左心室肥厚完全逆转。在二尖瓣反流组，喹那普利治疗1年后观察到质量减少15%，提示临界肥厚的室间隔厚度降至正常。
这些结果表明，对瓣膜反流患者进行长期ACE抑制可逆转左心室扩张，减少左心室质量和肥厚，从而改善左心室功能。此外，提示ACE抑制可能有延缓主动脉瓣或二尖瓣置换的潜力。
