Following an acute myocardial infarction (AMI) there is immediate deterioration of contractility in the infarcted left ventricular (LV) wall. This can be followed by regional dilation (expansion) as well as global remodeling. We examined 35 consecutive patients--with no history of myocardial ischemia--who were admitted to hospital within 3 hours after initial symptoms and with ST-segment changes on an electrocardiogram consistent with transmural ischemia. Echocardiography was performed at admission, and at 6 hours, 12 hours, 24 hours, 3 days, and 6 days after onset of the AMI. Within 3 hours after onset of symptoms an increase in both end-diastolic volume index (EDVI) and end-systolic volume index (ESVI) was found in both anterior and inferior infarcts when compared with healthy controls (mean +/- SD EDVI: 99 +/- 13 ml/m2 [anterior], 69 +/- 17 ml/m2 [inferior], 51 +/- 15 ml/m2 [controls], p < or = 0.00001; ESVI: 62 +/- 12 ml/m2 [anterior], 38 +/- 11 ml/m2 [inferior], 17 +/- 6 ml/m2 [controls], p < or = 0.00001). At all points in time, volumes were larger in anterior infarcts than in inferior infarcts (p < 0.05). The volumes did not change during the 6 days (p > 0.1). Thus, major LV dilation is present within 3 hours after onset of symptoms of first AMI. The dilation is more pronounced in anterior versus inferior infarcts. From 3 hours until day 6 no further changes in LV volumes occurred.
Exercise testing early post AMI was evaluated as a predictor of reinfarction in patients treated with thrombolytics. AMI patients exercise-tested prior to discharge were included in the study (n = 178). The patients were followed for 2.9 +/- 0.9 years (mean +/- 1 SD) for the development of new cardiac events defined as cardiac death or reinfarction. Cox regression analysis of clinical and exercise test variables showed that there was significant predictive value of treating heart failure with drugs from two or more therapeutic groups (P < 0.001; hazard ratio 9.4 (3.1-28.2) (estimate and 95% confidence interval)), such as those with a previous history of myocardial infarction (P = 0.001; hazard ratio 4.0 (1.7-9.6)) and of significant ST depression (P = 0.029; hazard ratio 2.5 (1.1-5.7)). Significant ST depression could be substituted by the delta ST/delta HR index (P = 0.042; hazard ratio 2.8 (1.2-6.8)). The exercise test had independent but limited prognostic value in AMI patients treated with thrombolytics. The delta ST/delta HR index did not improve the predictive value of the exercise test.