RELATIONSHIP BETWEEN ISCHEMIC ST SEGMENT DEPRESSION AND LEFT-VENTRICULAR FUNCTION DURING SITTING BICYCLE EXERCISE

Eleven cases with angina of effort and 6 cases with giant negative T wave were subjected to bicycle exercise test in the sitting position to assess the hemodynamic changes as compared with those in 6 control cases. Measurements were made of the mean pulmonary capillary wedge pressure (m-PCP LVEDP) as a parameter of left ventricular function and ST segment depression in the electrocardiogram during exercise every minute. In control group, m-PCP increased 3mmHg (Δm-PCP = 2-4mmHg) on average, observing a constant value of m-PCP during exercise. In all cases of angina, chest pain was elicited during exercise where there was a progressing increase in m-PCP with a significant difference from control group (p<0.05). In 7 cases of angina, the PCP-LVSWI relationship demonstrated impairment of left ventricular function due to myocardial ischemia. In cases of two or three vessel disease, the increase in m-PCP during exercise was coincident with the onset of ST segment depression in the exercise ECG. There was a high-grade correlationship between the increment in m-PCP and the magnitude of ST segment depression (r = 0.87-0.99). A close correlationship also existed between the magnitude of ST segment depression and the rate-pressure product (r = 0.88-0.99). This suggests that the magnitude of ischemic ST segment depression reflects the severity of myocardial ischemia and is also closely related with impaired left ventricular function due to the reduction of contractility and compliance of the heart. The cases of giant negative T wave proved to have a normal pumping function without coronary artery lesions. The increase in m-PCP during exercise was more marked in 5 of 6 these cases than in control group (Δm-PCP = 5-9mmHg), probable because of decreased left ventricular compliance due to atypical hypertrophy. The blood pressure during exercise in this group was significantly higher (p<0.05) than in control group, leading to a part of cause for atypical hypertrophy. © 1979, The Japanese Circulation Society. All rights reserved.