1979 Volume 46 Issue 1 Pages 8-24
Changes in left ventricular function during the attacks induced by exercise and by rapid atrial pacing were studied in patients of angina pectoris of effort.
1. Exercise-induced angina : A supine type bicycle ergometer was used to induce the attack in 13 cases. Exercise was discontinued when the signs of myocardial hypoxia (ischemic ST depression and/or anginal pain) appeared. There was no significant difference in the hemodynamic parameters, such as heart rate (HR), systolic blood pressure and double product, in exercise-induced angina between with and without left heart catheterization.
Then the hemodynamic parameters obtained by left heart catheterization at the time of induction of myocardial anoxia were compared with those before exercise. There was the signi-ficant increase in HR, mean blood pressure (BPm), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), cardiac index (CI), left ventricular work (LVW), tension-time index (TTI), LV max dp/dt and Vmax, except left ventricular stroke work index (LVSWI).
There was no difference in these parameters between the attacks with and without pain, ex-cept LVEDP, which was higher in attacks without pain, and Vmax, which was larger in attacks with pain.
2. Pacing-induced angina: Rapid atrial pacing was used to produce ischemic ST depression and/or anginal pain 9 times in 8 patients.
There was the significant increase in TTI, LV max dp/dt and Vmax and the decrease in CI, LVW and LVSWI as compared with before pacing. LVEDP was normal or only slightly elevated at the time of induction of myocardial ischemia, but rose significantly soon after cessation of pacing. The latter value did not show a significant difference from that observed on exercise.
3. Comparison between exercise-induced and pacing-induced angina : BPm, CI, TTI and Vmax were significantly higher in exercise-induced angina than pacing-induced angina. LVEDP was also significantly higher in exercise-induced angina than in pacing-induced angina at the time of occurrence of myocardial anoxia, but after cessation of pacing there was no difference. HR, in contrast, was significantly higher when angina was provoked by atrial pacing.
The fact that this elevation was accompanied with increase of LV max dp/dt and Vmax suggests that it might be resulted from the decreased left ventricular diastolic compliance rather than left ventricular failure.
4. Intravenous propranolol : Administration of 2 to 4 mg suppressed significantly not only HR, BPm and TTI at rest, but also the increase of HR, LVSP, TTI, LV max dp/dt and Vmax on exercise. This indicates that the effects of propranolol on angina pectoris of effort can be ascribed the suppression of the increase of myocardial oxygen consumption on exercise.
