1971 Volume 35 Issue 8 Pages 973-978
In order to evaluate a role of sympatho-adrenomedullary system in the causative mechanism of the anginal attack, the electrocardiographic and hemodynamic changes following the administration of physiological dose of catecholamines were observed in 74 patients with ischemic heart disease, in 51 normal subjects and 16 patients with essential hypertension. Following the administration of 0.2μg/kg/ min. of noradrenaline and 0.1μg/kg/min. of adrenaline the ischemic changes in electrocardiogram evaluated according to Master's criteria were found in 46 out of 64, 58 out of 62 patients, none of 33 and 5 out of 38 normal subjects, none of 10 and 7 out of 14 hypertensive patients, respectively. On the other hand, angiotensin-II (0.015μg/kg/min.) showed positive electrocardiogram in only 6 out of 26 patients. Noradrenaline and adrenaline produced a decrease and a increase of heart rate, respectively, neither of which showed any difference between patients and normal subjects. Noradrenaline increased both systolic and diastolic pressure and adrenaline increased systolic pressure and reduced diastolic pressure. These changes were significantly greater in the patients with ischemic heart disease as compared with those in normal subjects. Moreover, catecholamines and Master's exercise test produced significantly greater increase of cardiac effort index in the patient group. And the patients who showed greater increase of this index was associated with the higher incidence of positive electrocardiogram and the tendency was more remarkable in adrenaline than noradrenaline. Following the infusion of angiotensin-II the ischemic change on electrocardiogram was rarely observed despite of marked elevation of the cardiac effort index. Based on these findings, the importance of the sympatho-adrenomedullary system in the precipitation of anginal attack was discussed.
