The role of ischemia and ventricular asynergy in the genesis of exercise-induced ST elevation.

Sixty-five patients with ST elevation were retrospectively studied in order to evaluate the clinical significance and underlying mechanisms of ST-segment elevation during exercise. Of these, 50 patients had previous myocardial infarction (Group I) and 15 patients did not (Group II). Exercise thallium-201 imaging was performed on 30 patients, resting gated blood pool imaging was performed on 33 patients, and 23 underwent cardiac catheterization for clinical indications. When the two groups were compared, patients in Group I had more frequent multivessel disease (9/13 vs. 3/10, p less than 0.05), anterior infarctions (33/50 vs. 4/10, p less than 0.02), while Group II patients had more frequent single-vessel disease (7/10 vs. 4/13, p less than 0.05). For Group I patients, the most common reason for termination of exercise was fatigue and/or dyspnea (35/50 vs. 0/15, p less than 0.05), with an irreversible defect noted in both stress and delayed views on thallium imaging (20/24 vs. 1/6, p less than 0.05). In Group II, the most common reason for termination was angina (15/15 vs. 2/50, p less than 0.001), with reversible thallium defects noted more frequently (4/6 vs. 3/24, p less than 0.01). Thus, we conclude that in patients with Q waves, left ventricular dysfunction rather than ischemia is the mechanism for ST elevation. In these patients angina is rare, but fatigue, dyspnea, multivessel disease, and fixed thallium defects are common. In patients with non-Q-wave exertional ST elevation, ischemia is the rule, manifested by frequent chest pain and reversible thallium defects.