We examine whether regional wall motion abnormality (RWMA) could contribute to the slowed relaxation rate of the left ventricle (LV) in patients with coronary artery disease (CADpts). Simultaneous observations were made on the time constant (Tc) of the isovolumic pressure decay and left ventriculography at the control period and after right atrial pacing. Subsequently, the subjects investigated were divided into 3 groups, i.e. normal subjects (Group I, n=8), CADpts with normal wall motion during the control period (Group II n=21), and CADpts with RWMA during the control period (Group III, n=28). The latter two groups were further divided into two subgroups according to the presence (Group IIa and IIIa) or absence (Group IIb and IIIb) of pacing-induced RWMA. We measured Tc by a method of exponential analysis that could estimate the asymptote. During the control period, Tc was significantly prolonged in Group III (82 ± 26 msec) than that in Group I (60 ± 6 msec) and Group II (63 ± 12 msec). Tc was prolonged in proportion to the extent of RWMA during the control period. Immediately after right atrial pacing, Tc was markedly prolonged in Group IIa (from 61 ± 12 to 90 20 msec, p < 0.001) and in Group IIIa (from 73 ± 26 to 95 ± 34 msec, p < 0.001). The post-pacing prolongation of Tc was closely correlated with the extent of post-pacing RWMA. From these results, it is postulated that RWMA may play an important role as a causes of the altered LV relaxation in CADpts.

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Exercise tolerance and heart response were examined by cross-sectional echocardiography before and during exercise tests to assess the effects of aging, training and myocardial ischemia on the cardiac reserve of 40 healthy men, 20 athletes and 25 patients with angina on effort. The cardiac response to exercise can be divided into 4 types according to parameters derived from a short axis section echocardiogram. Type A : The left ventricular end-diastolic volume (LVEDV) increased slightly in the early stage of exercise, and thereafter, the cardiac response was maintained by a gradual increase of myocardial contractility and heart rate. Type B : Initial response to exercise was similar to Type A, but cardiac output was maintained only by an increase of heart rate under additional exercise load. Type C : LVEDV, LVESV (left ventricular end-systolic volume) and contractility remained virtually unchanged throughout the exercise. Type D : The contractility decreased from the early stage of the exercise, and LVEDV and LVESV increased. Most young subjects and all athletes showed Type A response, while in the aged healthy subjects the Type B response was more frequent. Anginal cases tolerating 125-watt load responded as Type B or C, and those tolerating only 75 watts showed Type C or D. All patients in Type D had multi-vessel disease.

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Net sodium (Na) efflux and potassium (K) influx were determined in Na-loaded/K-depleted erythrocytes derived from 37 patients with essential hypertension and 25 age-matched normotensive subjects with no family history of hypertension, together with the measurement of basal red cell sodium and potassium contents. Intraerythrocyte sodium content was significantly higher in the essential hypertensives than in the normotensives (10.9 ± 1.4 vs 10.0 ± 1.2 mmol/L·cells, mean ± SD, p < 0.02), but potassium content was nearly equal between the two groups. Net Na efflux in the hypertensives was significantly reduced compared with that in the normotensives (4.57 ± 0.70 vs 5.18 ± 1.02 mmol/L·cells·hr, p < 0.01), but both net K influx and net Na/K flux ratio were not significantly different between the two groups. Net Na efflux and K influx showed a significant inverse correlation with red cell sodium content (r=-0.64 and r=-0.56, respectively, p <0.001). These results suggest that the reduced net Na efflux with the increase of red cell sodium content may be related to the pathogenesis of essential hypertension. However, it is impossible to determine the genetic marker of essential hypertension by using the net Na/K flux ratio of Japanese subjects, although Garay et al. have reported that this index was abnormally low in the case of Europeans.

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A new beta-blocking agent, atenolol was studied on the supposition that it was a beta-blocker without any action on central nervous system. Atenolol was orally given to 10 patients with essential hypertension once a day and changes in various parameters were observed through 24 hours. As the results, hypotensive effect was accompanied by marked reduction of heart rate, systemic vascular resistance, plasma renin activity and blood aldosterone level over 24 hours. It was a decrease in systemic vascular resistance that showed best correlation with hypotensive effect.

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We analyzed electrocardiograms obtained from 29 Japanese patients with primary aldosteronism (PA) and in 106 patients with essential hypertension (EHT). QRS voltage was higher (p <0.05) and heart rate was slower (p < 0.01) in case of PA. A significant reduction in QRS voltage and a significant increase in heart rate were observed after short-term potassium replacement or after short-term administration of spironolactone, preoperatively, and within 2 to 4 weeks after the removal of aldosteronama. These significant changes in QRS voltage and heart rate were always accompanied by significant increases in the serum potassium concerntration but not always by a reduction in blood pressure. The long-term follow-up of EHT-patients showed a slower reduction in their high QRS voltage, despite effective antihypertensive therapy. Thus hypokalemia, in addition to hypertension, may be relevant to the high QRS voltage in PA. There also appeared to be a relationship between hypokalemia and bradycardia.

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Clinicopathologic correlations of nonbacterial thrombotic endocarditis (NBTE) were studied with special reference to their pathogenetic role in cerebral and myocardial infarction. In 2340 cases of consecutive autopsies of the aged, NBTE was observed in 217 cases or 9.3%. The age distribution of NBTE revealed a gradual increase with advancing age. The underlying diseases of NBTE were malignant neoplasm (51.6%), infection (28.3%) and other diseases (20.1%). The incidence of NBTE in each cancer was high in cancers of the colon (16.2%), pancreas (15.2%), gall bladder or bile duct (14.1%) and lung (13.0%). The vegetations of NBTE were found on the aortic valve in 46.1%, on the mitral valve in 40.6% and on the both valves in 8.3%. The incidence of myocardial infarction and scar was 51.2% in the NBTE group, while it was 38.6% in the non-NBTE control group (p < 0.02). This difference was marked in patients with a small infarction (10.6% vs. 5.3%) and a myocardial scar (30.4% vs. 19.0%). The grade of coronary stenosis was less in the NBTE group than in the control group (p < 0.001), suggesting that the origin of the myocardial ischemic lesion was embolism from NBTE. The incidence of large cerebral infarction was 14.7% in NBTE and 9.2% in the control group, and that of medium sized cerebral infarction was 35.0% and 23.6% respectively. In this latter group, cortical infarction comprised 57.9% in the NBTE group and 26.6% in the control group. In large cerebral infarction, cerebral atherosclerosis was less severe in NBTE than in the control group (p < 0.001), also suggesting an embolic mechanism. Disseminated intravascular coagulations was found in 41.9% of NBTE. The incidence of myocardial and cerebral infarctions showed no difference between the cases with DIC and those without DIC, suggesting that infarctions were derived not from in situ thrombosis but from embolism caused by NBTE.

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Contractile properties of a ventricular wall region have often been analyzed by regional force, shortening, and work. Regional force cannot be measured directly and is often indirectly determined from ventricular pressure and geometry, although regional shortening can be measured directly. Regional work can be calculated from these force and shortening values. We examined whether the calculated regional work, which may be mechanically reasonable, is also reasonable from an energetics viewpoint. We calculated regional contractile power (time rate of work) from the regional force and shortening velocity and integrated it globally over the entire ventricular wall, using some conventional geometric models of the ventricle and assumptions of ventricular wall mechanics. We then compared this globally integrated power with the stroke power of the entire ventricle and assumptions of ventricular wall mechanics. We then compared this globally integrated power with the stroke power of the entire ventricle determined directly from ventricular pressure and volume. Results show that the globally integrated regional power is not always identical with stroke power, depending on the model and assumptions used. Therefore the regional ventricular wall work determined from the regional force and shortening is not always consistent with the law of conservation of energy.

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Glomerular mesangial cells were isolated from explants of normal rat whole glomeruli according to the differential growth capacities of the cultured cells. The cultured mesangial cells comprised almost all of the grown cells on day 31 of the primary culture when the subculture could be performed. They contained abundant cytoplasmic microfilaments and actin. The contractile response to vasoactive hormone of both primarily cultured and subcultured mesangial cells was quantified as a decrease in cell surface area. The maximum decrease in surface area in response to 1 nM of angiotensin II was about 30%. This magnitude of contraction is consistent with that observed in cultured rat vascular smooth muscle cells. The mesangial cells did not phagocytose horse-radish peroxidase or sensitized sheep red blood cells, nor did they have binding capacities for Fc or C3b, while the cells derived from explanted glomerulus and probably of blood-born monocyte origin did. We conclude that the most important function of the glomerular mesangial cell is the control of glomerular blood flow and filtration by contraction.

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Direct cardiodepressant activities of three β-blockers, carteolol, pindolol and propranolol, were estimated using heart-lung preparation of the dog. β-blocking doses of these drugs to inhibit the positive chronotropic effect of isoproterenol by 50% were 2.2 μg for carteolol, 4.0 μg for pindolol and 21 μg for propranolol. Cardiac performance of the preparation was not influenced by up to 1 mg of these three β-blockers. After 10 mg of these drugs, the cardiac function curves were shifted rightward and downward indicating the heart failure. It was doubtful however, that this result indicated the cardiodepressant action of β-blockers, for the preparation showed spontaneous deterioration without β-blocker treatment. The influences of these β-blockers on the compromized heart-lung preparations showed essentially similar results. In conclusion, direct cardiodepressant activity of the β-blocking doses. The implication of the results in clinical use of β-blockers, especially in relation to heart failure, was discussed.

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Although nonspecific pericarditis, myocarditis, valvulitis and coronary arteritis are known as cardiac lesions that accompany rheumatoid arthritis (RA), there have been few reports of the occurrence of clinically severe valvular disease. We report here the case of 69-year-old man with a 25-year history of RA who died of acute left-sided heart failure complicating to aortic steno-insufficiency and angina pectoris. Autopsy findings revealed the coincidence of a congenital bicuspid aortic valve with chronic inflammation, fibrosis and calcification ; eccentric hypertrophy and myocardial fibrosis of the left ventricle ; 75% luminal narrowing of the proximal portion of the coronary artery due to atherosclerosis, and narrowing of the small arteries of the cardiac muscle due to angitis. It is deduced that the coronary artery lesions, aortic valve lesions and myocardial lesions were aggravated by the bicuspid aortic valve, changes with ageing and corticosteroid therapy.

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