Pepine C J
Division of Cardiology, University of Florida College of Medicine, Gainesville 32610.
J Hypertens Suppl. 1994 Jul;12(4):S65-71.
To review the evidence on the effects of angiotensin converting enzyme (ACE) inhibitors in coronary artery disease.
In studies of experimental atherosclerosis involving hypertensive and normotensive hyperlipidemic animals, ACE inhibitors have had potent anti-atherogenic effects, reducing the total aortic intimal surface involved and the aortic cholesterol content. In balloon-injured animals, ACE inhibitors have suppressed the myointimal proliferative response in rats and rabbits, but not in higher species such as pigs and baboons, indicating possible species-specific effects. In spontaneously hypertensive rats, ACE inhibitors have modulated alterations in endothelium-related vasodilation, although similar effects have not been observed in human hypertension.
ACE inhibition has not been shown to prevent restenosis after percutaneous transluminal coronary angioplasty. However, cardiac ischemic events have been prevented by ACE inhibition in patients with coronary artery disease and left ventricular dysfunction in a number of studies, including the Studies of Left Ventricular Dysfunction (SOLVD), Survival and Ventricular Enlargement (SAVE) study, Acute Infarction and Ramipril Efficacy (AIRE) study and the Gruppo Italiano per lo Studio della Streptochinesi dell'Infarto Micardico 3 (GISSI-3) trial. Other ongoing studies such as the QUinapril Ischemic Event Trial (QUIET) are assessing ACE inhibitor effects in patients with coronary artery disease and a normal left ventricular function.
ACE inhibitors prevent the development of atherosclerosis in hyperlipidemic animal models. They also prevent the myointimal proliferative response to injury in some animal models, but not in higher animal species or in humans. They can reduce the number of cardiac ischemic events in patients with coronary artery disease and left ventricular dysfunction; their effects in those patients with a normal left ventricular function are now being assessed.
综述血管紧张素转换酶(ACE)抑制剂对冠状动脉疾病影响的相关证据。
在涉及高血压和正常血压高血脂动物的实验性动脉粥样硬化研究中,ACE抑制剂具有强大的抗动脉粥样硬化作用,可减少主动脉内膜总面积和主动脉胆固醇含量。在球囊损伤动物中,ACE抑制剂抑制了大鼠和兔子的肌内膜增殖反应,但在猪和狒狒等高等动物中未观察到这种作用,表明可能存在物种特异性效应。在自发性高血压大鼠中,ACE抑制剂调节了与内皮相关的血管舒张改变,尽管在人类高血压中未观察到类似效应。
ACE抑制尚未显示能预防经皮腔内冠状动脉成形术后的再狭窄。然而,在多项研究中,包括左心室功能不全研究(SOLVD)、生存率和心室扩大研究(SAVE)、急性心肌梗死和雷米普利疗效研究(AIRE)以及意大利心肌梗死研究组3(GISSI - 3)试验,ACE抑制已预防了冠状动脉疾病和左心室功能不全患者的心脏缺血事件。其他正在进行的研究,如喹那普利缺血事件试验(QUIET),正在评估ACE抑制剂对冠状动脉疾病且左心室功能正常患者的影响。
ACE抑制剂可预防高脂血症动物模型中动脉粥样硬化的发展。它们还可在某些动物模型中预防对损伤的肌内膜增殖反应,但在高等动物物种或人类中则不然。它们可减少冠状动脉疾病和左心室功能不全患者的心脏缺血事件数量;目前正在评估其对左心室功能正常患者的影响。