One other implication of this study concerns the residual ST integral decrease at 5 min postcessation of exercise. Residual ST decrease was also a finding in our previous study of patients with isolated left anterior descending CAD. The findings of this larger study sample provide additional support for the concept that clinical myocardial ischemia is not a sudden, discontinuous on/off phenomenon, but rather a modification of myocardial metabolism that has an important and continuous temporal spectrum. A related implication is that all CAD patients may have “silent” ischemia; if not during ST segment depression- or fatigue-limited exercise, then during the late postexercise recovery period when angina has disappeared but ischemic ST changes persist.
Previous quantitative exercise BSPM studies in patients with CAD are scarce.’ One study of 100 patients suggested a positive correlation between the number of obstructed coronary arteries and both the severity of exercise ST depression at 80 ms after QRS offset and the anterior torso area over which it occurred. In another study of 27 patients the authors considered the size of the torso area of ST depression, 60 ms after the J point, in the ST difference map to be proportional to the severity of the underlying CAD. However, another study of 25 subjects reported no significant differences in the magnitude of ST integral minima or the spatial extent of ST integral decrease on the torso surface in patients with single-, as compared with multiple-, vessel CAD. Our findings are more in keeping with the former data.