This study was made to determine whether patients with coronary artery disease have any specific abnormality in their serum lipoprotein pattern which might be a factor in the etiology of the disease. Serum lipoproteins (Lps) of 18 patients with myocardial infarction (group A), 28 patients with other forms of coronary artery disease (group B), and 22 healthy control subjects (group C) were studied using ultracentrifugal and electrophoretic techniques. All subjects were Japanese living in Japan. Acrylamide gel electrophoresis of the patients' sera showed, in addition to bands of α- and β-globulin and pre-β-lipoprotein mobility, one of mobility between that of β and pre-β-mobility, mid-band. It was present in 100% of sera of group A, 93% of group B but only 50% of group C. The midband is a subfraction of the LDL fraction isolated by ultracentrifugation at d 1.006 to 1.063. The midband may be resolved as a single, double or multiple band fraction on acrylamide gel. By ultracentrifugation subfractions of LDL were detected in 16 of 18 patients in group A (89%), 10 of 13 patients in group B (77%) and 3 of 11 in group C (27%), respectively. Of LDL subfractions Sf 10 LDL was most frequent; in 77% of group A's sera, and 89% of group B's, Sf 10 was the sole or major subfraction. Serum HDL, determined ultracentrifugally was significantly lower (p 0.01) in group A and B (179.3 14.3, and 219.1 20.3, mean SE) than in group C persons (319.9 16.7). The above findings indicate that accumulation of Sf 10 LDL and other LDL subfractions may occur in association with a decrease of HDL in atherosclerotic coronary artery disease. It is suggested that those abnormalities may contribute to the genesis of atherosclerotic coronary artery disease.

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The renin-angiotensin-aldosterone system, electrolyte and water balance, body fluid, and neurogenic tone and reactivity of the vasculature were studied in hypertension induced in uninephrectomized rats by repeated injection of renin-rich kidney extract and 1% saline drinking. The control rats were injected with physiological saline. Various measurements were made in conscious rats on the 10th day of the treatment. As compared with the control, plasma renin concentration and serum sodium increased significantly, while plasma aldosterone and renal excretory function did not differ. Blood volume (BV) expressed as per body weight increased significantly, but absolute BV, absolute or body weight-related plasma volume and hematocrit were not significantly different. The hypotensive effect of 1-Sar-8-Ile-angiotensin II was negligible 12 hours after the preceding injection of kidney extract. It was small but significant 1 hour after the injection. Increase in water turn-over and fractional sodium excretion occurred during the development of hypertension. Spironolactone did not significantly modify the developmental course. We observed increased depressor response to hexa-methonium and increased reactivities to noradrenaline and angiotensin II (A II); these response curves relatively resembled those of spontaneously hypertensive rats. Hypertensive vascular changes were seen in the kidney and heart by histology. Thus, it as suggested that a direct vasculat action of A II played a partial role in this hypertensive process while aldosterone played little role. The significance of BV increase and possible contribution of A II's other actions were discussed.

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Hemodynamic response of nifedipine in 11 patients with congestive heart failure was examined. Thirty minutes after sublingual administration of nifedipine, CI and SVI were increased together with a decrease in PAEDP and TSVRI. The increase in CI was proportional to the decrease in TSVRI. Twenty-four hours after continuous administration of nifedipine, however, six of 11 patients did not show the improvement of left ventricular function. These results indicate that sublingual administration of nifedipine is effective in the short-term therapy of the patients with a markedly decreased cardiac output and an increased systemic vascular resistance.

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1) A prolonged A-H interval suggested A-V nodal involvement. 2) A prolonged duration of the His potential suggested moderate His bundle involvement. 3) Complete block distal to H appeared to reflect total disruption of both bundle branches. 4) The lesion at the penetrating portion of the His bundle could be responsible for A-H block. 5) A-H block occurred in a case of cellular infiltration in the A-V node and the His bundle, in which bilateral bundle branch showed severe fibrosis. 6) A combination of right bundle branch block, marked left axis deviation and H-V prolongation suggested trifascicular disease. 7) In case 6, there was a severe pathologic lesion at the origin of the left bundle branch, yet left bundle branch block was not indicated electrocardiographically. This study revealed a close correlation between electrophysiologic and pathologic findings in 4 out of 6 cases.

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Plasma renin activity and aldosterone concentration were measured by radio-immunoassay technique in seven patients with low cardiac output syndrome after open cardiac surgery. Plasma renin activity and aldosterone concentration markedly increased, and plasma renin activity was well correlated with plasma aldosterone concentration. Plasma renin activity and aldosterone concentration, however, had no direct correlation with plasma sodium and potassium concentration or administered doses of inotropic agent, potassium and diuretic. Sodium and potassium balance was closely correlated with plasma aldosterone concentration. In the present study, it was suggested that the secondary hyperaldosteronism following low cardiac output syndrome after open cardiac surgery was mainly induced by the increased release of renin and that it influenced on the balance of sodium and potassium metabolism under such disturbed circulatory circumstances.

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The present study was done to investigate the interrelationships between renal kallikrein-kinin, renal prostaglandin E and renin-angiotensin-aldosterone systems in human and the possibility that renal kallikrein-kinin and renal prostaglandin E may participate in the pathogenesis of essential hypertension by means of measuring urinary excretion of kallikrein and prostaglandin E, plasma renin activity and plasma aldosterone concentration before and after stimulation or inhibition of the renin-angiotensin-aldosterone system and inhibition of renal prostaglandin E generation. Urinary kallikrein excretion was increased after the stimulation of the renin-angiotensin-aldosterone system by low Na diet or the administration of furosemide and upright posture, while it tended to decrease after the inhibition of the renin-angiotensin-aldosterone system by the administration of 1-sarcosine-8-isoleucine angiotensin II under sodium depletion or spironolactone. These data showed that the changes in urinary kallikrein excretion paralelled with those of the renin-angiotensin-aldosterone system following various stimuli, suggesting that renal kallikrein-kinin system may regulate blood pressure by opposing the action of the renin-angiotensin-aldosterone system. Urinary PGE excretion was decreased after sodium depletion and increased after the administration of furosemide in spite of the augmentation of the renin-angiotensin-aldosterone system. The changes in urinary PGE excretion was closely related to those in urinary Na output after various stimuli and a significant positive correlation was found between basal levels of urinary PGE and those of urinary Na, suggesting that renal prostaglandin E may be involved in the regulation of blood pressure by affecting renal sodium handing. The present data showed that basal level of urinary excretion of PGE and kallikrein was lower in essential hypertension than in normal subjects and that the release of renal kallikrein and PGE after furosemide administration was also suppressed in essential hypertension compared with that in normal subjects, suggesting that there exists an impaired defense mechanism against the renin-angiotensin-aldosterone system resulting in sodium retention.

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A case is described wherein Fallot's tetralogy was associated with aortic origin of the right pu pulmonary artery. The left pulmonary artery was the continuation of the pulmonary trunk. Although a number of examples of Fallot's tetralogy associated with aortic origin of the left pulmonary artery are known, combination of Fallot's tetralogy and aortic origin of the right pulmonary artery is rare and has been described in only two cases previously.

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M-mode echocardiography on a fifty-eight year old female with Uhl's anomaly showed several characteristic findings, which were considered to be useful in differentiating Uhl's anomaly from Ebstein's. Those findings were normal tricuspid diastolic closing velocity, the relatively early tricuspid valve opening, easy visualization of the tricuspid valve in usual position and the unusual mid-diastolic pulmonic valve full opening. The premature opening of the pulmonic valve correlated with the right atrial and ventricular mid-diastolic pressure exceeding that of the pulmonary artery.

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We examined the effects of various coronary vasodilator drugs, papaverine, dipyridamole, isosorbide dinitrate, amyl nitrite, nitroglycerin, diltiazem, and nifedipine, on cyclic nucleotides of the coronary artery and left ventricular muscle of anesthetized dogs at maximum coronary blood flow after the administration of each agents. Only papaverine and dipyridamole significantly increased the concentration of c-AMP in the coronary artery. Nitroglycerin and siosorbide dinitrate did not significantly change the concentration of c-AMP but rather increased the concentration of c-GMP. Coronary vasodilator drugs were divided into three groups in association with the relationship of cyclic nucleotides in the coronary artery. Group I, including papaverine, dipyridamole, and amyl nitrite, increased the concentration of c-AMP and the ratio of c-AMP to c-GMP. Group II, including nitroglycerin and isosorbide diltiazem, had no effect on the cyclic nucleotides. Group I drugs also increased the concentration of c-AMP in the left ventricular muscle and so group I drugs may predispose the ischemic heart to develop ventricular arrhythmias. It seems that the most useful coronary vasodilator is no effect on the c-AMP in the ventricular muscle and group II and group III drugs are more useful coronary vasodilator drugs than group I drugs.

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