Enalapril improves arterial elastic properties in rats with myocardial infarction

Systemic arterial elastic properties, important determinants of left ventri cular function and coronary blood flow, are compromised in myocardial infar ction (MI). The cardiac effect of angiotensin-converting enzyme inhibitors (ACEIs) has been extensively studied, whereas their arterial effect has bee n poorly reported in MI. The aim of this work was to study the effect of pr olonged ACEI enalapril treatment on systemic arterial structure and elastic properties in rats with MI. One week after the induction of an MI, 40 male Wistar rats received either no treatment (n = 20) Or ACEI enalapril (2 mg/ kg; n = 20) for 17 weeks. At the end of the treatment period, blood pressur e. cardiac output, total peripheral resistance, systemic arterial complianc e, characteristic impedance, and left ventricular power were measured in an esthetized rats. Then the rats were killed for infarct-size determination a nd aortic histomorphometric study. Infarct size, heart, and left and right ventricular weights were similar in the ACEI-treated and untreated infarcte d rats. Prolonged ACEI enalapril treatment reduced blood pressure by 17% (p < 0.001), total peripheral resistance by 22% (p < 0.01), and characteristi c impedance by 26% (p < 0.03), and increased systemic arterial compliance b y 35% (p < 0.01), in comparison with untreated infarcted rats. Enalapril re duced aortic media wall thickness by 9% (p < 0.02) and increased elastin co ntent by 22% (p < 0.03) and elastin-to-collagen content ratio by 42% (p < 0 .01). Enalapril did not affect cardiac output and left ventricular power. S mooth muscle cell nuclei number and size and collagen content of aortic wal l were similar in the ACEI-treated and untreated infarcted rats. These resu lts indicate that long-term treatment with ACEI enalapril improves arterial elastic properties through structural modifications of arterial wall in ra ts with MI, This vascular effect may contribute to improve the left ventric ular function and the coronary perfusion of infarcted myocardium, and added to the cardiac effect, may explain the prevention of left ventricular remo deling observed with ACEI in this model.