Aspects of Myocardial Infarction-induced Remodeling relevant to the Development of Heart Failure

Heart failure can be defined as the pathophysiological state in which the pump function of the heart is insufficient to meet the metabolic demands of the body (Guyton, 1986; Ruggie, 1986). Thus, heart failure is a pathophysiological condition (rather than a disease per se), and can occur in the course of a number of cardiovascular diseases. In Western countries, hypertension and coronary artery disease or a combination of both account for the majority of cases of heart failure (McKee & Castelli, 1971; Kannel & Castelli, 1972; Eriksson & Svardsudd, 1989). Cardiomyopathies (of genetic, viral, toxic or idiopathic origin) and congenital heart disease are other important etiological factors (Eriksson & Svardsudd, 1989). In developing countries, acquired abnormalities of heart valves due to the sequelae of streptococcal infection are a common cause of heart failure (Killip, 1985). The incidence of heart failure gradually increases with age, resulting in an incidence rate of 1011000 per year for men, and 8/1000 per year for women (McKee & Castelli, 1971; Kannel & Castelli, 1972; Ho el at., 1993) in the over·65 age group

Chronic aspirin treatment affects collagen deposition in non-infarcted myocardium during remodeling after coronary artery ligation in the rat

Low-dose aspirin (acetylsalicylic acid; ASA), inhibiting platelet thromboxane production in favor of endothelium formation of prostaglandins, is successfully used as primary or secondary prophylaxis against myocardial infarction. Although prognosis may be improved, effects of long-term ASA treatment on wound healing and cardiac remodeling are not well understood. The aim of the present study was to mimic the clinical situation by inducing myocardial infarction in low-dose ASA (25 mg/kg/day, i.p.) pretreated rats, and to determine effects on plasma eicosanoid levels, cardiac hypertrophy and collagen deposition, and left ventricular function during continued ASA treatment. The effects of this dose were verified to selectively inhibit platelet thromboxane production, and lower plasma levels of thromboxane, but did not affect plasma levels of prostacyclin and prostaglandin E2during the acute inflammatory stage following myocardial infarction. As measured by heart dry weight/body weight, cardiac hypertrophy was not affected by ASA treatment. However, interstitial fibrosis in the spared myocardium as well as perivascular fibrosis, associated with infarction-induced cardiac remodeling, were affected by ASA treatment. Replacement fibrosis in the infarct itself, considered as representing wound healing, was not significantly influenced by ASA treatment. Wall thinning following infarction was not aggravated, nor did treatment influence left ventricular cavity diameter in a relaxed state. Results fromin vitroleft ventricular function measurements showed no effects on left ventricular peak velocity of contraction or relaxation after ASA treatment. In conclusion, although low-dose ASA may not be expected to have anti-inflammatory action, it did influence post-infarct cardiac remodeling by affecting interstitial and perivascular fibrosis. ASA treatment did not have effects onin vitroleft ventricular dysfunction