DIURETICS IN POSTINFARCTION HEART-FAILURE

Severe left ventricular failure, as evidenced by radiographic pulmonar y edema or raised left ventricular filling pressure, accompanying acut e myocardial infarction, carries a high mortality risk. In this situat ion, the intravenous loop-diuretic furosemide induces a rapid reductio n in the raised left ventricular filling pressure due to an immediate and substantial increase in systemic venous compliance accompanied by increasing diuresis. This diuretic-induced venodilatation is probably due to the release of prostaglandins. The transient systemic arterial constriction and small increase in systemic blood pressure that follow s intravenous furosemide probably results from the release of renin an d subsequent activation of angiotensin. These diuretic induced hemodyn amic changes are accompanied by restoration of the vasodilator reflex, which enables the heart to accommodate an acute volume load. Orally a dministered loop diuretics achieve slower, but similar, directional he modynamic changes. There is no information on hemodynamic or neuroendo crine dose-response effects of loop diuretics, and there is no informa tion pertaining to the use of other diuretic groups in this situation. The hemodynamic changes induced by furosemide summate with the change s induced by other anti-heart-failure drugs. In this subset of patient s with acute myocardial infarction and severe heart failure, the influ ence of the diuretics on morbidity incidence and mortality risk remain s to be measured.