Serum lipid levels of 10, 977 normal Japanese subjects in 1980 were determined by a joint study of 14 institutions, specializing in lipid research, located in 9 districts of Japan. The data obtained were compared with those in 1960 and 1970. Total cholesterol (TC) levels in 1980 increased with age except for the 1st decade and reached maximum (205 mg/dl) at the 7th decade. The mean value in any age was higher than that of 20 years age and reached maximum (130 mg/dl) at the 7th decade. The mean values of subjects over the 5th decade were higher than those of 10 years ago by 10-20 mg/dl. In contrast with TC and TG, HDL-cholesterol levels were highest at the 1st decade and declined gradually with age. TC and TG levels of younger age (1 st to 3rd decade) were equal to or even higher than those of Americans in 1972 -76. It was concluded that serum lipid levels of Japanese have increased in the past 20 years and approached to the levels of Europeans and Americans.

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Echocardiograms were obtained from 48 Japanese children with ventricular septal defect (16 having aortic cusp prolapse, Group I, and 32 without it, Group II). In the case of right coronary cusp prolapse, the right coronary sinus protrudes anteriorly into the right ventricular outflow tract, and thus, the anteroposterior diameter of the aortic root increases. In the case of non-coronary cusp prolapse, the non-coronary sinus bulges posteriorly into the right ventricle, and thus, the aortic root increases in size. For evaluating the degree of these prolapses quantitatively, we measured the aortic root diameter echocardiographically and expressed them as a percent of a normal one. In Group I the aortic root diameter was 131 ± 9% (mean ± SD) and in Group II it was 105 ± 7%, and the difference between the 2 groups was statistically significant (p < 0.001). In Group I 14 of the 16 patients had a value greater than 120% of normal suggests the presence of aortic cusp prolapse. Systolic semiclosure of the aortic valve was found in 8 patients of Group I (50.0%) and in 2 of Group II (8.7%). Coarse systolic fluttering of the pulmonary valve with an amplitude of greater than 3 mm was detected in 6 of Group I (40.0%) and in 3 of Group II (10.0%). Therebore, semiclosure of the aortic valve and fluttering of the pulmonary valve are considered to be also useful for evaluating aortic cusp prolapse qualitatively.

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Serial sections of the atrioventricular (AV) conduction system were microscopically studied in 12 autopsied hearts : four with complete type common AV orifice (CAVO), two with atrial septal defect of the ostium primum type (ASD-I^°), two with ventricular septal defect of the persistent common AV canal type (VSD-C) and four without heart disease. the anatomic findings were semiquantitatively compared with the normal control using Feldt's method and correlated to the mean frontal QRS axis on ECG. The cases of CAVO or VSD-C with left axis devation invariably showed similar patterns regarding the location and course of the AV conduction system (1) posterior displacement of the AV node, (2) relatively short distance between the AV node and the beginning of the left bundle branch (LBB), and (3) postero-inferior displacement of the bundle of His and the LBB. The postero-inferior displacement of the LBB seemed to be responsible for left axis deviation. The cases of ASD-I^° showed some additional findings : (1) impaired contiguity between the AV node and the bundle of His might have caused the occasional advanced AV block in one case, and (2) the posterior radiation of the LBB traversed down through the branch-free muscle bundle, which was assumed to be related to the right axis deviation in the other case. These findings suggest that the disposition of the AV conduction system in CAVO and in its related anomalies were basically the same whatever the type of defect, and this was considered to be correlated to the established ECG pattern.

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The coordinates of the ramifying points of the left coronary artery were measured using biplane coronary cineangiograms in 19 patients who were later diagnosed as normal. The spatial distances (segment length) between any tow of these points were calculated and one cardiac cycle was plotted frame by frame in order to investigate shortening and relaxation characteristics of the segments. In most instances, the segments evidenced shortenings during systole and prolongations during diastole. The extent of shortening, as a percentage of maximum length ranged from 7.8 to 18.0%. The segments measured at the apex started shortening 77 msec than those at the base, in other words, 90.3 ± 6.2 msec before the R wave peak on the electrocardiograms. This indicates that the initial shortening at the apex contributes to the build up of left ventricular pressure. While at the base, since it begins to shorten after the completion of the build up in left ventricular pressure, it contributes more to the ejection of blood from the left ventricle. On the other hand, there is little systolic shortening at the atrioventricular groove and in some instances there is systolic expansion, suggesting that in comparison to the other portions of the left ventricle it is assigned an entirely different role.

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Net Na⁺ and K⁺ fluxes were measured in Na⁺ -loaded red cells from 19 normotensive control subjects, 22 essential hypertensive patients, and 8 secondary hypertensive patients. The ratio of Na⁺/K⁺ net fluxes was significantly lower in essential hypertensive patients than in normotensive control subjects. However, by the addition of the patients' own plasma, the net Na⁺ efflux rate was significantly increased in essential hypertensive patients, which caused the increment in the ratio of Na⁺/K⁺ net fluxes. This resulted in disappearance of the difference between normotensive and hypertensive subjects in the ratio of cation fluxes. It was possible that the abnormalities of cation transport in red cells from essential hypertensive patients might be compensated for by humoral factors in the plasma.

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Many reports have suggested that cardiac dysfunction with cardiomegaly is more often observed in patients with chronic hemodialysis. Moreover, cardiac dysfunction has been thought as one of the most important factors affecting the prognosis of these patients. In this study, in order to clarify the role of 1-carnitine in the pathogenesis of cardiomegaly, 33 patients with chronic hemodialysis were studied using the multivariate analysis method. Among the factors which may affect cardiac function, the following 10 variables were examined. 1) age, 2) duration of dialysis, 3) plasma carnitine, 4) serum total cholesterol, 5) serum HDL-cholesterol, 6) triglyceride, 7) systolic blood pressure, 8) diastolic blood pressure, 9) left ventricular voltage on a electrocardiogram at rest and 10) hematocrit. The plasma carnitine levels in these patients were markedly reduced and inversely correlated with the cardiothoracic ratio (CTR) on the chest X-ray films (r=0.38, p < 0.05). In principal component analysis, the CTR was closely related to hematocrit and plasma carnitine levels. By multiregression analysis, both hypo-carnitinemia and anemia were independently shown to be important causes of cardiomegaly. Thus, it is suggested that the cardiomegaly in patients with chronic hemodialysis may be improved by supplemental therapy with 1-carnitine, even in cases with severe anemia.

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Molsidomine is a derivative of the sydnonimines and is a long-acting vasodilator that may be effective in the treatment of chronic stable angina pectoris. To evaluate the therapeutic efficacy and drug tolerance, eight men with stable angina pectoris performed a symptom-limited maximal exercise test on a computer-assisted treadmill. After ingesting either placebo or molsidomine administered treadmill. After ingesting either placebo or molsidomine administered in single blind fashion 90 min before the exercise test on the first day of treatment, molsidomine decreased the average systolic blood pressure response from 154 ± 3 (SEM) to 135 ± 4 mmHg (p < 0.01). However it did not significantly change the average heart rate response (117 ± 7 to 124 ± 8 beats/min) and the rate-pressure product (18.1 ± 1.2 × 10³ to 16.8 ± 1.1 × 10³). The average time up to the onset of ischemia at which significant ST-segment deviation (0.1 mV) first appeared was increased from 9.0 ± 1.7 to 12.8 ± 1.2 min (p < 0.001) after molsidomine. At peak exercise after molsidomine, the mean value of ST-segment deviation in V5 or aVF was decreased (p < 0.001). This result was obtained even though the average exercise duration was increased from 11.4 ± 1.7 to 13.6 ± 1.2 min (p < 0.001). The treadmill score according to Hollenberg was also improved from -47 ± 24 to 1 ± 14 after molsidomine administration. After six weeks of continued therapy with molsidomine the favorable effect on exercise tolerance was significantly decreased in terms of exercise duration, the time up to the onset of ischemia, and the treadmill score. The discontinuation of molsidomine treatment after six months' therapy did not deteriorate the exercise tolerance. Thus, molsidomine is effective in treating stable angina pectoris, but appears to possess a drug tolerance on long-term treatment.

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To examine the angiographic features of vasospastic angina associated with ST segment depression, we attempted to analyze the coronary arteriograms of 12 patients who exhibited ST segment depression during the ergonovine provocative test. Right and left coronary depression during the ergonovine provocative test. Right and left coronary arteriograms were obtained successively within a short period when the ergonovine administration revealed ST segment depression. Eight out of 12 patients showed non-total spastic obstructions in one of the major coronary arteries. Among them, a collateral augmentation was found only in one patient. Two cases exhibited the well-developed collateral channels during non-anginal periods and in one case a collateral blood supply was reduced by the spasm occurred in the donating artery. In another one, the collateral circulation did not change during anginal period. Three out of 4 patients who showed total spastic obstructions demonstrated transiently augmented collateral circulation which was supplied by the non-spastic artery. These findings may indicate that ST segment depression during coronary artery spasm could attribute to a subendocardial ischemia caused by an incomplete occlusion of large coronary artery and transient reduction or augmentation of collateral blood flow.

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Continuous electrocardiographic recordings during anginal attacks in patients with variant angina were reviewed. Twenty-seven attacks in 15 patients were associated with transient T-wave inversion during recovery periods of angina (type A), while in another 69 attacks in 28 patients there was no T-wave inversion (type B). In none of the patients was there an ischemic T-wave inversion during angina-free periods. Both the maximum elevation (0.79 ± 0.57 mV) and duration (5.3 ± 1.2 min) of ST-segment deviation of type A attacks were significantly higher and longer than those of type B (0.44 ± 0.27 mV, 2.8 ± 1.4 min). Ten patients who had both type A and type B attacks one time or the other were selected for further evaluation. In these 10, the duration of ST-segment elevation was significantly longer during type A attacks (5.2 ± 1.2 min, n=18) than during type B attacks (2.7 ± 1.2 min, n=20) but there was no significant difference in the maximum ST-segment elevation. Giant U-wave inversion appeared in 15% of the type A attacks, but never in type B. Therefore, the T-wave abnormality related to ischemic episodes in patients with variant angina seems to be associated with more severe ischemia of longer duration than milder episodes of transient ischemia.

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In order to evaluate the clinical significance of thallium (Tl)-201 myocardial imaging for diagnosing the right ventricular (RV) ischemia, we studied the relationship of right ventricular free wall (RVFW) appearance on myocardial images to coronary arteriographic findings. Patients were divided into 3 groups as follows : 1) normal control (NC) group (19 cases) without angiographically documented coronary artery disease ; 2) non-RCA group (18 cases) with significant coronary artery lesion restricted to the left coronary artery (LCA) ; and 3) RCA group (36 cases) with significant right coronary artery (RCA) stenosis regardless of underlying LCA disease. After the patients had exercised up to 80 - 85 % of the predicted maximal heart rate, immediate and 2-4 hour delayed myocardial images were obtained. As for presence of absence of the RV ischemia on images, the RVFW appearance in 30°and 60° left anterior oblique (LAO) views were assessed carefully. On the immediate images, all patients except one in the NC group an all except 3 in the non-RCA group demonstrated 'continuous visualization' of the RVFW in both views. In the RCA group, 6 showed 'non-visualization' and 11 'defective visualization' of the RVFW in 30° LAO view. In 60° LAO view, 6 presented ' non-visualization' and other 6 'defective visualization' of the RVFW. On the delayed images, although none of the patients in the groups NC and non-RCA demonstrated redistribution phenomenone of the RVFW, 4 patients in the RCA group showed redistribution of Tl-201 into the RVFW. Non-and defective visualization of the RVFW on the immediate images were related to the proximally located RCA lesion, previous history of inferior myocardial infarction and high grade RCA stenosis. Collateral vessels seemed to protect the RVFW against the development of exercise induced ischemia and affect the occurrence of redistribution of Tl-201 into the RVFW. In conclusion, stress Tl-201 myocardial imaging enables us to estimate the myocardial blood flow of the RV and is a useful non-invasive method in the evaluation of RV ischemia.

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