A new method for the quantitative estimation of aortic regurgitation is reported in this paper. A mathematical model of the transport porcess of a radioisotope in a circulatory system with aortic regurgitation is developed and a simulation circuit of the transport process using analog computer is given. On the mathematical model, the regurgitation at the aortic valve is expressed as a back flow from the aorta with a transport delay equivalent to one cardiac cycle. The rate of regurgitant flow, as given by the ratio of regurgitant flow to the total outflow from the left heart, is determined after curve fitting between an actual radiocardiogram and a theoretical one produced by the simulation circuit for a moderate or large regurgitation, in cases where a definite change appears on the radiocardiogram. It is difficult to determine the rate of regurgitant flow for a small regurgitation of less than 30%. As a result of the simulation study of many radiocardiograms with aortic regurgitation, the following is made clear: (1) Rates of regurgitant flow obtained by the simulation are well correlated to those measured by left ventricular angiography; (2) A linear relationship exists between the computed mean left heart volume and the mean left ventricular volume by angiography; (3) In 31 radiocardiograms with isolated aortic regurgitation, the computed mean left heart volume increases linearly in proportion to the regurgitant volume per beat; (4) Pulmonary blood volume shows a slight but significant increase and it does not show any correlation with the grade of regurgitation; (5) Mean right heart volume does not increase and the ratio of mean right heart volume to mean left heart volume is inversely correlated with the rate of regurgitant flow.

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On cases with valvular disease, essential hypertension and coronary heart disease, each of which has a cardiac function estimated Class I and Class II according to the functional classification by NYHA, the reactivity of the sympathetic nerve center to the endogenous or exogenous stimulation, and the responses in the cardiovascular system to the induced sympathetic hyperactivity were studied, and the following results are obtained: (A) Valvular disease l. A sympathicotonic state was shown even during the rest, and the reactivity of the sympathetic nerve center to various stimuli was augmented. 2. The responsiveness of a failing heart to CA was normal or lowered. This leads to an increase in the CA secretion as a homeostatic mechnism. 3. Despite the increase in the CA secretion, cardiac output during the exercise was less greatly increased than that in a control. As to the p-blocker administration, the increase in the CA-secretion by the exercise was augmented but that in cardiac output was suppressed conversely by the β-blocker. These facts will mean that CA plays an important role in the regulatory mechanism in a failing heart, limits having been naturally set to its effects. 4. The suppressing effect of the β-blocker on the tachycardia caused by the exercise was not so great as that in a control, in hypertension, or in coronary heart disease. The changes in stroke volume by the exercise were slight, regardless of being pretreated by the β-blocker or not. In a failing heart, pulse rate plays an important role in maintaining the cardiac output. And it will be understood as a compensatory mechanism to maintain the cardiac output that the increase in heart rate by the exercise is not easily suppressed' by the β-blocker. The heavy suppression of the increase in heart rate may, therefore, possibly induce aggravation of heart failure. (B) Essential hypertension 1. The sympathetic activity during the rest was normal, and the responsiveness of the sympathetic nerve center to various stimuli was slightly but insignificantly higher than that in a control. 2. The reactivity of the peripheral vascular system to the exogenous or endogenous sympathetic stimulation was demonstrated greater than that in coronary heart disease as well as than that in a control. 3. The increase in blood pressure by the exercise was suppressed by the β-blocker not so greatly as that in a control or in the other disease groups. 4. The increase in stroke volume by the exercise was suppressed only slightly by the β-blocker. From above, it indicates that the a-receptors in the peripheral vascular beds are on a hypersensitive state, and, furthermore, the sympathoadrenal system may participate greatly in the pathogenesis of essential hypertension. (C) Coronary heart disease 1. The reactivity of the sympathoadrenal system to endogenous or exogenous stimuli was elevated. 2. Augmented hemodynamic responses to CA were demonstrated, and the oxygen-requirement as well as cardiac work was liable to be increased, and even an amount of NA within a physiological range can also cause a similar diseased state to exercise-induced myocardial ischemia. 3. The response of the cardiovascular system to the exercise was suppressed by the β-blocker. These results suggest that the sympathoadrenal system plays an important role in myocardial ischemia and that the β-blocker is of clinical use in preventing an anginal attack. On cases of valvular disease, essential hyper-tension and coronary heart disease, the reactivity of the sympathetic nerve center, and the corresponding changes in the sympathetic activity, as well as the reactivity of the cardiovascular system, were studied. Each of them in one of the three underlying diseases was demonstrated to differ from those in other underlying diseases. [the rest omitted]

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How much of the variability of cerebrovascular accidents are explainable by meteorologic factors and what meteorologic factors are more influential on cerebrovascular attacks and deaths are explored by various sets of standardized multiple linear regression analyses with the prerequisites of the evaluation of distribution characteristics and correlations of meteorologic factors to be included in the analyses. Meteorologic effect on cerebrovascular accidents is discussed in view of an acute precipitating stress as well as a chronic stress which promotes their intricate developmental mechanisms and is of importance in increasing susceptibility to them.

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In a patient with atrial fibrillation. and digitalis intoxication, a pattern of RBBB with LAH and that of RBBB with LPH were observed in the presence of advanced A-V block. The mechanism of these conduction disturbance is considered on the basis of idioventricular rhythm arising from the posterior and the anterior division of the LBB.

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To asses the cardiocirculatory response to exercise in patients with ischemic heart disease, simultaneous digital plethysmograms and electrocardiograms were taken at rest and after a double Master's two step test. Patients were divided into three groups: Group I, negative Master's test (47 patients). Group II, positive Master's test (32 patients), and Group III, old myocardial infartion (30 patients). Pulse volume decreased In 5 of 47 patients (10.6%) in Group I, in 24 of 32 patients (75.0%) in Group II and in 18 of 30 patients (60.0%) in Group III after exercise, and there was highly significant difference between Group I and Group II (P<0.001) and between Group I and Group III (P<0.001). There was no significant difference between Group 11 and Group III. In fifteen patients whose pulse volume de-creased after excercise, the administration of 0.075 mg of ouabain did not cause any significant changes in heart rate and pulse volume at rest, but after exercise, it decreased heart rate and increased pulse volume significantly (P<0.05). In contrast, In 15 patients whose pulse volume increased after exercise, the administration of ouabain did not cause any significant changes in heart rate and pulse volume both at rest and after exercise. It is concluded that exercise digital plethysmogram is useful in the. evaluation of patients with ischemic heart disease from the hemodynamic standpoint.

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