Developmental Mechanism of Angina Pectoris and Action of Coronary Vasodilators

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Abstract
RPQ index (heart rate X mean blood pressure XQT duration), a implification of Sarnoff''s TTI (tension-time index), was used to study the mechanism of development of angina pectoris and mechanism of action of anti-anginal agents from the clinical-analytical standpoint, using 41 cases of angina pectoris and 12 healthy subjects. RPQ index increased in the exercise test. The increase was more pronounced in cases with positive test than in those with negative test and controls. Similar results were obtained in the anoxia test. Analyzing the time course of occurrence of anginal attack at anoxia test, increase in heart rate and elevation of blood pressure preceded the RS-T depression and the anginal attack. In cases with positive test, increase in heart rate has more pronounced effects on that increase in RPQ index rather than elevation of blood pressure. The augmentation of myocardial O consumption due to increase in heart rate and elevation of blood pressure, especially the former, has been suggested to play an important role in the induction of the anginal attack. The occurrence of more pronounced increases in heart rate and elevation of blood pressure in anginal patients than in healthy subjects might be explained by the liberation of some trigger substance at a very early stage of coronary insufficiency. Inhibition of anginal attack by [beta]-adrenergic blocking agents, such as nethalide and propranolol, supports the assumption that the substance is related to catecholamine. In cases in which nitrate was effective, an inhibition of the increase in heart rate and blood pressure at exercise and anoxia tests was observed, suggesting that the action of the drug is attributed to the inhibition of these changes. In cases in which xanthine was effective, no definite changes were observed in blood pressure or heart rate at exercise and anoxia tests, while in cases in which the drug was ineffective, RPQ index showed a marked increase. This suggests that the coronary vasodilating action might be effective in suppressing angina pectoris in the cases in which myocardial O consumption does not increase very much.