Effect of Angiotensin Converting Enzyme Inhibition with Quinaprilat on the Ischaemic and Reperfused Myocardium

Beneficial Effects of Vitamin E Treatment in Acute Myocardial Infarction

“…2). ST-segment changes were the greatest at 1 day post occlusion and then declined gradually during 3 to 21 days; however, the ST-segment in untreated infarcted animals remained significantly elevated 21 days postocclusion compared with pre-occlusion values. Vit E-treated rats showed a similar pattern of ST-segment changes in ECG after coronary occlusion ; however, the ST-segment changes were significantly smaller in the Vit E-treated than in untreated rats at all periods after occlusion (Fig.…”

“…hour after occlusion of the coronary artery and continued for 21 days. In some experiments, rats were killed by decapitation 21 days after inducing myocardial infarction, hearts removed surgically, and the ventricular tissue weighed. The scar tissue and the right ventricle were separated from the viable left ventricle and weighed.…”

“…The activation of these systems may promote the formation of oxyradicals and oxidants, which in turn increase the oxidative stress and thus result in ventricular dysfunction (6)(7)(8)(9)(10)(11)(12)(13)(14). Previous studies have shown that cardiac dysfunction in ischemiareperfusion, different types of cardiomyopathies, and heart failure is associated with increased myocardial oxidative stress and antioxidants such as vi-tamin E (Vit E) have been shown to exert beneficial effects (15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30). Ventricular arrhythmias in patients with ischemic heart disease are a major cause of death, and, in fact, mortality is 22.5% in the first 3 weeks after infarction and reaches 35% within the first year (31).…”

Cardioprotective effect of angiotensin-converting enzyme inhibitors in patients with coronary artery disease

“…The cardiovascular effects of ACE inhibitors against ischemia and reperfusion are complex, documented by experimental studies, and include reduction in infarct size in some but not all studies [27][28][29][30][31][32][33][34][35], an improvement in intracellular biochemical homeostasis [36,37], a beneficial effect on the stunned myocardium [28,33,34] and on reperfusion arrhythmias [38][39][40], and, possibly (but still very controversial) an antioxidant action [36,37,41,42]. All of these effects have been obtained in experimental animal preparations.…”

“…Inhibition of this effect may potentially account for the cardiac protection and reduction in cardiovascular events [36,37]. The importance of this mechanism in humans is still controversial.…”