As exercise-induced ST depressions are most frequent and marked in lead V5 independent of which single coronary artery is obstructed, some other mechanisms of ST depressions than local ischemia should be searched for. Left ventricular hemodynamics during exercise was studied in two groups of patients with severe effort angina, 19 with and 12 without ST depression after exercise (STAE). During supine exercise until angina, stroke index became significantly lower (37 vs. 52 ml/m2) and left ventricular end-diastolic pressure (LVEDP) significantly higher (40 vs. 30 mmHg) in the STAE group. The best discriminator was the early diastolic pressure (LVeDP) (22 vs. 11 mmHg), which is interpreted as a sign of a more ischemic ventricle in the STAE group. The sum of STAE in all leads is correlated to LVeDP but not to LVEDP during exercise. The link between the significant ischemia in various locations and STAE appearing most frequently and markedly in V5 seems to be some global mechanism as the occurrence of STAE and the height of the R wave were positively correlated in the various leads. As STAE in coronary heart disease shows similar configuration and distribution as in aortic valvular stenosis and digoxin medication of healthy subjects, a possible link could be the compensatory increase in contractility in non-ischemic parts of the ventricle.
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