Objectives: To determine the influence of timing, infarct location and thrombolytic therapy on the electrocardiographic (ECG) response to exercise testing following acute myocardial infarction.
Design: Maximal treadmill exercise testing was performed on postinfarction day 8 and repeated on day 90 as part of a previously reported double-blind, placebo controlled study of recombinant tissue plasminogen activator (rt-PA) in acute myocardial infarction in which left ventricular function was the primary end-point. Patients were systematically evaluated for left ventricular function, myocardial perfusion and coronary anatomy.
Setting: Ten collaborating community and academic hospitals.
Patients: One hundred and fifteen patients, aged 20 to 75 years, with ischemic chest pain 30 mins or longer and ST elevation on ECG. Patients with cardiogenic shock, left bundle branch block, prior aortocoronary bypass surgery, recent percutaneous transluminal coronary angioplasty or standard contraindications to thrombolytic therapy were excluded.
Main results: The analysis is confined to the 70 patients who underwent both exercise tests without intercurrent coronary revascularization. Peak rate-pressure product was greater on day 90 than on day 8 (mean difference +/- SE 2.2 +/- 0.6 x 10(3), P = 0.001), whereas 65% of patients had 1 mm or greater of exercise-induced ST shift on day 8 compared with 47% on day 90 (P = 0.025). Patients following anterior compared with inferior infarction were more likely to have exercise-induced ST elevation (54% versus 21%, P = 0.012) but less likely to have ST depression (29% versus 63%, P = 0.017) on day 8; results were directionally similar on day 90. Treatment with rt-PA, compared with placebo, did not influence exercise performance, the ECG response to exercise or the extent of inducible ischemia on thallium scintigraphy.
Conclusions: Timing and infarct location are important modifiers of the ECG response to exercise testing following myocardial infarction. Thrombolytic therapy in these uncomplicated patients did not influence inducible ischemia.