Hemodynamic evaluation of exercise-induced ST-segment depression and elevation in ischemic heart disease Left ventricular cineangiography during exercise.

In order to elucidate the hemodynamic significance of exercise-induced ST-segment shifts in ischemic heart disease, left ventricular cineangiography was carried out in 41 patients at rest and during supine bicycle ergometer exercise. These patients were divided into 2 groups, that is, a normal coronary artery group (6 patients), having neither significant coronary artery stenosis nor exercise-induced ST-segment shifts, and a diseased group (35 patients) having significant coronary artery stenosis (inner-diameter stenosis greater than or equal to 75%). The latter was further divided into 3 subgroups according to exercise-induced ST-segment shifts: ST-unchanged group (17 patients), ST-depression group (11 patients) and ST-elevation group (7 patients). In the normal coronary artery and ST-unchanged groups, exercise produced an increase in left ventricular end-diastolic volume index (LVEDVI), a decrease in left ventricular end-systolic volume index (LVESVI) and increases in stroke index and ejection fraction. In the ST-depression group, the appearance or aggravation of left ventricular wall motion abnormality was induced at the site of coronary artery stenosis by exercise in 9 patients. Both LVEDVI and LVESVI increased, stroke index remained unchanged, and ejection fraction decreased during exercise. In the ST-elevation group, ST-segment elevation was induced in leads with abnormal Q waves. In 2 patients, exercise induced aggravation of wall motion abnormality at the infarctional segment. LVESVI increased, but LVEDVI showed little increase, and stroke index and ejection fraction tended to decrease during exercise. In the ST-depression group, exercise-induced left ventricular pump dysfunction was due to lowered contractility (increased LVESVI) caused by transient myocardial ischemia. In the ST-elevation group, exercise-induced pump dysfunction was mainly due to lowered contractility, and in some of them, the findings suggested that transient myocardial ischemia at or around the region of infarction might be the cause of pump dysfunction. In addition, a poor compensatory effect of the Frank-Starling mechanism seemed to play a role in the onset of such dysfunction in this group.