Left ventricular hemodynamics in exercise-induced angina pectoris.

SUMMARY The sequence of events characterizing the onset and course of exercise-induced angina pectoris was studied in 10 patients with ischemic heart disease during cardiac catheterization. Exercise produced a precipitous rise in left ventricular end-diastolic pressure prior to the onset of angina and electrocardiographic ischemia. A corresponding abnormal increase in pulmonary artery pressure occurred. Cardiac output increased commensurate with the degree of exertion and was accompanied by a slight reduction in stroke volume. Left ventricular work and stroke work paralleled the changes in cardiac output and stroke volume. Determinants of myocardial oxygen consumption, that is, heart rate, left ventricular systolic pressure, and left ventricular first derivative, were monitored continuously and noted to increase by 43%, 20%, and 38%, respectively, prior to angina. Ischemic ST-segment depression corresponded closely in time with angina. Angina and electrocardiographic and hemodynamic abnormalities persisted throughout exercise. Two minutes after exercise, hemodynamic values returned to normal along with a reduction in intensity of angina; ST-segnent abnormalities persisted until 4 minutes after exercise. Pathophysiological mechanisms occurring during angina are described, and differences from typical heart failure are discussed. Additional Indexing Words: Coronary artery disease Exercise INFORMATION gathered directly from the left ventricle during exercise-induced angina pectoris is scant and contradictory. Co-hen and associates' observed a reduction in systolic ejection rate, whereas left ventricular end-diastolic pressure failed to alter significantly from normal resting values. Parker and associates,2 in a larger series, demonstrated marked elevations of left ventricular end-diastolic pressure in all patients with angina precipitated by exercise, while systolic ejection rate, computed by us from their pub-The opinions expressed herein are those of the authors and cannot be construed as reflecting the views of the Navy Department or of the Naval Service at large. 240 lished data, increased. Although both studies abound in other detail, the relationship of mechanical events in the left ventricle to cardiac pain and electrocardiographic alterations was not examined. The present investigation was concemed with the sequence of hemodynamic and elec-trocardiographic changes that characterize the onset and course of angina pectoris. Attention was directed to those measures of left ventricu-lar function considered to be determinants of myocardial oxygen requirement and to those considered to be estimates of contractility.