Protection of Jeopardized Ischemic Myocardium by Reduction of Ventricular Afterload

To determine whether reduction of ventricular afterload protects ischemic myocardium, we studied 38 patients with acute myocardial infarction. Serial serum creatine phosphokinase values were used to estimate ischemic myocardial injury (i.e., "infarct size"). In addition, "infarct size" was predicted by nonlinear least-squares approximation from creatine phosphokinase changes during the first seven hours after admission. In 10 hypertensive and 14 normotensive patients "infarct size" as actually observed and as predicted was virtually identical. Another group of 14 patients, hypertensive on admission, were given trimethaphan to lower blood pressure, decrease ventricular afterload, and presumably diminish myocardial oxygen requirements. In these patients, observed "infarct size" was 24 per cent less than that predicted (p<0.01). Mortality within one month was less in the treated than in untreated patients matched for predicted "infarct size." The results suggest that reduction of ventricular afterload in hypertensive patients with acute myocardial infarction protects ischemic myocardium. (N Engl J Med 291:481–486, 1974)