EARLY VERSUS LATE CONGESTIVE-HEART-FAILURE AFTER INITIALLY UNCOMPLICATED ANTERIOR WALL ACUTE MYOCARDIAL-INFARCTION

We determined the incidence and clinical noninvasive, and angiographic variables contributing to postdischarge early (less than or equal to 3 months) and late (>3 months) congestive heart failure (CHF) after anterior wall acute myocardial infarction. The patient cohort consisted of 94 consecutive patients <65 years of age who underwent predischarge exercise thallium-201 planar scintigraphy, rest radionuclide angiography, and coronary arteriography. At a mean of 49 months of follow-up, 10 of the 68 medically managed patients developed early CHF, and 10 had late CHF. The 10 patients with early CHF had significantly higher peak creatine kinase values (2,494 vs 1,032 IU/L, p = 0.01), and at discharge, a lower left ventricular (LV) ejection fraction (28 +/- 11% vs 41 +/- 11%, p <0.02), more persistent thallium-201 defects (3.4 +/- 1.2 vs 2.1 +/- 1.2, p <0.02), and fewer stress-induced redistribution defects (1.4 +/- 1.1 vs 0.4 +/- 1.1, p less than or equal to 0.05) than those with late CHF. The early group held less multivessel disease (40% vs 90%, p less than or equal to 0.03). Fifty percent (5 of 10) of patients who developed late CHF did so after a recurrent infarction compared with 10% (1 of 10) in the early CHF group (p <0.07) and 8% in the group without CHF (p <0.003). The 26 patients who underwent bypass surgery within 3 months had an LV election fraction and extent of ischemia and extent of angiographic stenoses comparable to patients with late CHF. None required hospitalization for CHF or had sustained a recurrent infarction. These data suggest that risk variables for developing CHF early after discharge after an uncomplicated anterior infarction are related to infarct size and early LV dysfunction, whereas late-onset CHF is related to extent of coronary artery disease and recurrent ischemic events. Early revascularization in patients with residual ischemia and multivessel disease may reduce incidence of CHF by diminishing risk of future ischemic events.