Calibrated low frequency acceleration vibrocardiography (A-VCG) was studied in normal individuals and in patients with coronary heart disease. Experimental studies in anesthetized dogs were also made to look for the hemodynamic determinants of the main waves in the A-VCG, and transmission characteristics of the chest wall over the range of the frequency of the A-VCG. The results were as follows:
(1) The S wave of low frequency acceleration vibrocardiography (A-VCG) coincided with the upward slope of the aortic flow rate curve, but showed a reverse phase, and its trough coincided with the vertex of the first derivative of aortic flow rate.
(2) The amplitude of the S wave was correlated with the peak value of aortic flow rate, the peak value of the first derivative of aortic flow rate and the peak value of the first derivative of aortic pressure, but was not correlated with aortic pressure, stroke volume and the peak value of the first derivative of left ventricular pressure.
(3) In the patients with myocardial infarction, there was a significant increase in A wave amplitude, decrease in S wave amplitude and increased A/S ratio compared with those of normal individuals.
(4) In the patients with angina pectoris, there was a significant increase in A/S ratio compared with that of normal individuals with the age of between 30 and 39.
(5) In normal individuals, there was tendency for A wave amplitude to increase, S wave amplitude to decrease and A/S ratio to increase with age.
(6) During exercise and inhalation of amyl nitrite, increase in S wave amplitude was smaller in the patients with angina pectoris than in normals.
(7) These results suggest that the S wave amplitude in A-VCG reflects contractility of the left ventricle, and that the A/S ratio and changes in S wave amplitude during various conditions offer useful means for detecting latent impairment of the functional reserve of left ventricle.
(8) The wave form and phase of direct A-VCG from the ventricular wall and those from the chest wall were similar, and the S wave amplitude was about 6dB greater in direct A-VCG.

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The clinical findings and the necropsy reports of 5 cases with aortitis syndrome are described. All cases had extensive type of chronic arteritis (aortitis syndrome). The fact that in some cases of aortitis syndrome the lesions of the aorta and its main arteries could extend to the peripheral arteries was noted. The pathological changes of the wall of vasa vasorum were found to correspond to those of the medial and adventitial area of the aorta and pulmonary artery in distribution. The marked similarity between the aortic and pulmonary arterial lesions suggest the common pathogenesis for both lesions.

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Pathological examinations of the heart and coronary arteries were performed in 418 consecutive autopsy cases at a geriatric hospital. Myocardial infarctions or large myocardial scarrings were observed in 91 cases, while cardiac hypertrophy was present in 161 cases.
Large myocardial lesions were present in 20 of 21 cases with obvious occlusion in any one of the coronary arteries. Among the cases without coronary occlusion, the incidence of large myocardial lesions was high in those with significant coronary stenosis, especially when at least 2 main branches of the arteries were severely stenosed. Although myocardial lesions were more frequent in the cases with severe hypertension than in those with normal blood pressure or moderate hypertension, there was no significant differences in the incidence of large myocardial lesions within the groups with the same severity of coronary stenosis regardless of blood pressure.
Cardiac hypertrophy was frequently observed in the cases with severe hypertension or large myocardial lesions. On the other hand, cardiac hypertrophy was rather infrequent among the cases with severe coronary sclerosis when neither associated with hypertension nor large myocardial lesions. The correlation between the severity of coronary stenosis and cardiac hypertrophy was not obvious when the cases with large myocardial lesions were excluded.

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Fatty acids attached to β-position of phosphatidylcholine (PC) and phosphatidylethanolamine (PEA) in the intima, media and atherosclerotic plaque of human arterial wall were splitted by phospholipase A and fatty acid compositions at α- and β-position of PC and PEA were measured. From these data, their molecular distributions were calculated. Results were as follows: (1) The heterogeneity of fatty acid moiety in α- and β-positions of PC and PEA in the intima, media and atherosclerotic plaque was present. (2) Major molecules of PC were dipalmitoyl-PC, 1-palmito-2-oleoyl-PC and 1-palmito-2-linoleyl-PC in the intima, dipalmitoyl-PC and 1-palmito-2-oleoyl-PC in the atherosclerotic plaque and 1-palmito-2-oleoylPC, 1-stearo-2-oleoyl-PC, 1-palmito-2-linoleyl-PC and dipalmitoyl-PC in the media. (3) Major molecules of PEA were 1-stearo-2-palmitoyl-PEA in the intima, 1-stearo-2-palmitoyl-PEA and dipalmitoyl-PEA in the atherosclerotic plaque and 1-stearo-2-arachidonyl-PEA in the media. (4) Disaturated PC and PEA were found comparatively rich in the atherosclerotic plaque.

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Thirty-four out-patients with electrocardiographic evidence of ischemic heart disease were divided into 2 groups, each group comprising of patients closely matched as to variables of sex, age, severity of symptoms and ECG findings. One group received pyridinolcarbamate, 1, 500mg. in 3 divided doses, while the other group received placebo. The response to the therapy in each group was evaluated on the basis of (a) physical work capacity (PWC) (b) nitroglycerine requirement and (c) electrocardiogram. The group that received pyridinolcarbamate showed a statistically significant (p<0.025) favorable response in the 3 parameters evaluated (PWC, nitroglycerine requirement and ECG) compared to the placebo group. The possible mechanism of action of the agent is discussed.

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Effects of ouabain (10^-12M to 10^-5M) on the simultaneously recorded transmembrane action potential and contraction; and (Na⁺-K⁺)-activated membrane ATPase of human papillary muscles were investigated. Ouabain in the concentration of 10^-12M did not affect the transmembrane potential, contraction and (Na⁺-K⁺)-ATPase activity. Ouabain in the concentrations of 10^-11 to 10^-7M produced a concentration dependent inhibition of (Na⁺-K⁺)-APTase associated with shortening of action potential duration and increase in contraction. Ouabain (10^-7M) produced a time dependent inhibition of the (Na⁺-K⁺)-ATPase associated with the shortening of action potential duration and increase in contraction. Ouabain in the concentration of 10^-5M produced an initial marked increase in contraction which was shortly followed by a decrease in contraction and an increase in tone. The muscles developed contracture within 15 to 20min. This concentration of ouabain inhibited the (Na⁺-K⁺)-ATPase completely. These results suggest that there is a relation between the inhibition of the (Na⁺-K⁺)-ATPase and shortening of action potential duration associated with an increase in contraction. Human papillary muscles seem to be very sensitive to the effect of ouabain.

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We studied the changes in the membrane ATPase from hypertrophied rabbit myocardium, and demonstrated a correlation between heart failure and ionic transport mechanism.
In 17 animals cardiac hypertrophy was produced by constriction of the ascending aorta. A modification of the method of Tashima was used for preparation of membrane vesicles from the myocardium of the left ventricle. This preparation was carried out 10 days after the operation. Mgand Na-K-ATPases of the membrane ATPases were measured separately by their different responses to ouabain and cations.
(1) Ventricular weight and heart weight were significantly greater in the experimental group than in the control group. However, the myocardial water content was almost constant in these groups.
(2) The specific activity of Na-K-ATPase in myocardial vesicles was relatively high compared with skeletal muscle and corresponded to about one fourth of its total ATPase activity. This Na-K-ATPase activity was inversely correlated with the left ventricular weight (p<0.02). The difference in Na-K-ATPase activity between heart failure cases and controls was significant at the 5% level. On the other hand, no significant difference in Mg-ATPase activity between the failure and the control group was demonstrated.
These results supported the fact that, during the development of heart failure, the myocardium lost potassium. From these findings, it was postulated that the heart in failure would be characterized by a diminished ability to manipulate active ion transport in response to hemodynamic stress due to the decrease in Na-K-ATPase activity.

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The authors have studied the participation of the sinus node in the occurrence of atrial fibrillation.
In the experiments on dog hearts in situ, an electrical stimulation given to the right atrium easily induced atrial fibrillation in the presence of the normal sinus node.
When the sinus node was injured, atrial fibrillation was very much reduced in frequency of occurrence and duration.
Also in the case of aconitine induced atrial fibrillation, the occurrence of fibrillation was very late when the sinus node had been injured.
Application of aconitine on preparations of the rabbit's right atrium including the sinus node easily induced fibrillation, but by application of aconitine on preparation of right and left atrial common muscle devoid of spontaneous activity fibrillatory contraction has never been observed.
Recently, we have made the studies on aconitine-fibrillation of the right atrium of the rabbit with 2 microelectrodes by means of the isolation technique.
In them, aconitinc was administered to the common muscle chamber in which the solution had been separated from the sinus node chamber with glycerin-soaked cotton. An ectopic pacemaker was produced after aconitine administration. Then the sinus node became a latent pacemaker. As the ectopic impulses increased in frequency, the action potential of the sinus node was a little more reduced in duration than that of the pectinate muscle, showed a marked decrease, and could not synchronize with that of the pectinate muscle, then changed into the fibrillatory potential. Subsequently, the fibrillation occurred to the common muscle.
Authors further demonstrated a clinical case report. The patient was 23 years old male, whose cardiac rhythm alternated to atrial fibrillation with A-V nodal rhythm. We have observed successively ECG alternation by the system of long term recording. It was found that the sinus rhythm apparently appeared every time before the onset of atrial fibrillation.
From the results mentioned above, it oas considered that the sinus node dominantly participates in the occurrence and the duration of atrial fibrillation.

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Blood flow velocity was recorded by using Doppler transcutaneous flowmeter and Doppler catheter flowmeter in an 18-year-old woman with Takayasu's arteritis. Although no right radial artery pulse was felt by palpation, significant decrease and slow rise of the peak blood flow velocity, and inconspicuous dicrotic notch was observed and recorded from the right radial artery by using the transcutaneous Doppler flowmeter, and this was a significant change as compared with the contralateral blood vessel. Significant decrease of phasic peak aortic flow velocity was also observed in the stenotic area of the abdominal aorta by using Doppler catheter flowmeter. To our knowledge, this is the first case of Takayasu's arteritis which in measurements of blood flow velocity has been obtained in various circulatory beds.

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