Quantitative assessment of myocardial infarct size from serial determinations of serum creatine phosphokinase activity: significance of previous infarction for the cardiac function and prognosis.

Abstract

In 50 patients with acute myocardial infarction (16 patients with previous infarction and 34 patients without), total creatine phosphokinase (CPK) released which represents infarct size was calculated from the serial change of serum CPK activity by the method of Sobel improved by Norris, and related it to the presence or absence of heart failure, the ejection fraction and one-year-mortality. If the patients with previous myocardial infarction were excluded, mean total CPK released in 10 patients with heart failure (1428 ± 200.4 IU/ml in Group II) was significantly larger (P<0.01) than that in 24 patients without heart failure (735.3 ± 83.6 IU/ml in Group I). However, in patients with previous myocardial infarction there was no significant difference in infarct size between these two groups (Groups I and II) indicating that the complication of heart failure does not directly relate to the size of the recent infarction but in large extent to the presence of prior infarction. The ejection fraction was obtained in 15 patients who had left ventriculography. Both of two patients with prior myocardial infarction in these 15 patients showed smaller ejection fraction than the predicted values myocardial infarction could contribute to impaired cardiac function as well as the recently occured infarction. One-year-mortality in Group II (37.5%) was higher than that of Group I (7.4%). In four patients with prior infarction who died within one year after the onset, mean total CPK released (275.3 IU/ml) was significantly smaller than that in three patients without prior infarction (899.0 IU/ml). These results strongly suggest that the patients with previous myocardial infarction are often complicated with heart failure and have poor prognosis even with comparatively small infarction and also demonstrate the substantially large contribution of the reduced contractility resulting from the previous myocardial infarction to the impaired cardiac function.