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The purpose of this study was to investigate the diurnal variation and chronotype differences, i.e., in morning-types and evening-types, in post-exercise vagal reactivation. Twelve healthy male college students who were classified as morning-type (6) and evening-type (6), based on responses to a questionnaire, participated in this study. Post-exercise vagal reactivation was assessed as the time constant of the beat-by-beat heart rate decrease for the first 30 sec after exercise (T30) at an intensity lower than the ventilatory threshold. The subjects performed 3-min cycle ergometer exercise at an intensity corresponding to 80 % of the ventilatory threshold after a 1 min warm-up exercise in the morning (7:00 - 8:00) and evening (17:00 - 18:00) to obtain the T30. A significant interaction (chronotype-by-time) effect was found for T30. The morning value of the T30 in evening-type subjects was significantly larger than their evening value and the morning value in morning-type subjects. There was no significant interaction effect for heart rate and oxygen uptake during exercise. These results suggest that diurnal variation in post-exercise vagal reactivation is different between morning-type and evening-type, and post-exercise vagal reactivation in evening-type individuals is sluggish in the morning.

Systolic time intervals (STIs) were measured in 57 patients with progressive muscular dystrophy (PMD) of the Duchenne type, and were correlated with the stages of physical disability. The total electromechanical systole (Q-A2), pre-ejection period (PEP), and left ventricular ejection time (LVET) were corrected for heart rate using the linear regression equations calculated from 91 normal subjects. Each systolic time interval index (STII), i.e. corrected STI, was analyzed. In 15 ambulatory patients (Group P-1), the STIIs did not differ significantly from those in normal controls. In 37 patients who were unable to walk (Group P-2) and 5 patients who were confined to bed (Group P-3), there was a significant increase (p less than 0.001) in the PEP index (PEPI), a decrease (p less than 0.001) in the LVET index (LVETI), and an increase (p less than 0.001) in the PEP/LVET compared with those in controls. The PEPI (p less than 0.001), LVETI (p less than 0.025), and PEP/LVET (p less than 0.001) in Group P-2 differed significantly from those in Group P-1. In Group P-3, the PEPI (p less than 0.005), LVET (p less than 0.001), and PEP/LVET (p less than 0.001) were significantly changed in comparison with those in Group P-2. Remarkable myocardial histopathologic changes suggestive of dystrophy were revealed in autopsies of 3 patients who had been in the severely disabled stage and had shown impaired STIs. It is suggested that cardiac function in patients with moderate to advanced PMD of the Duchenne type is deteriorated in proportion to the disability stages, i.e. the severity of changes in the skeletal muscles.

QA2 interval, preejection period and ejection time were calculated from the data of simultaneously recorded ECG, PCG, and external carotid arterial pulse wave in patients with adrenocortical overfunction, namely, Cushing's syndrome and primary aldosteronism, and in patients with nephrotic syndrome or collagen disease under longterm treatments with large doses of glucocorticoids.PEP/ET ratio, which is considered inversely related to the maximal dp/dt of the left ventricle, was markedly increased in the patients with Cushing's syndrome, and in those who were treated with large doses of glucocorticoids for prolonged periods. The PEP/ET ratio in the patients with primary aldosteronism was also increased but not so marked. These results suggest that longterm use of large doses of glucocorticoids impairs the myocardial contractility.

Echocardiographic evaluation of left ventricular volume change during rapid and atrial filling periods was made in patients with mital stenosis. The significant reduction of rapid filling volume was observed and the rate of rapid filling was approximately the half of normal in mitral stenosis. The rapid filling period showed a good correlation to the mitral valve area measured at operation. After surgical treatment, the rate of rapid filling was significantly increased but was still significantly smaller than normal. It was suggested that the remained structural abnormality of mitral apparatus depressed the inflow through the mitral valve in early diastole despite successful mitral valvotomy. Left ventricular filling during atrial contraction (atrial filling) was augmented twice as much as normal in patients with milder mitral stenosis, compensating the decreased early diastolic filling. In contrast, the atrial filling did not increase in severe mitral stenosis, resulting in the decreased cardiac output. Following mitral commissurotomy, the atrial filling in milder mitral stenosis was reduced but remained significantly larger than normal. There was no change of atrial filling in severe mitral stenosis postoperatively. This fact suggested the existence of impaired contraction of left atrium in cases with severe mitral stenosis. Our results show that the altered left atrial transport function plays an important role in the left ventricular filling in mitral stenosis.

The purpose of this study was to evaluate the acute effects of sublingual nifedipine (10 mg) on left ventricular systolic function (ejection fraction, peak ejection rate, time to peak ejection rate) and diastolic function (peak filling rate, time to peak filling rate, filling fraction during rapid filling) at rest and during exercise using radionuclide angiography in 17 patients with ischemic heart disease. The results of the study were as follows. Diastolic indexes in the patient group were significantly different from the values in the control group at rest and during exercise. Peak filling rate and filling fraction improved significantly after nifedipine administration. These values did not show significant differences from the values in normal subjects which were obtained before nifedipine administration. The peak filling rate during exercise after nifedipine administration increased significantly, although the value was lower than that in the control group. At rest, systolic indexes in the patient group showed abnormal values, although the differences from the control values were not significant. Ejection fraction and peak ejection rate were significantly lower than those in the control group during exercise. After nifedipine administration, peak ejection rate at rest and during exercise, and ejection fraction at rest in the patient group improved significantly. Seven of 17 achieved the same exercise workloads as control conditions without symptoms or ECG changes. These data suggest that nifedipine improved left ventricular systolic and diastolic dysfunction, as well as exercise tolerance in patients with ischemic heart disease.

A case of systemic-pulmonary arteriovenous fistula is described. Chest trauma with multiple bone fractures 9 years prior to this admission was the suspected cause. Three years after the trauma, chest X-rays revealed abnormal vessels in the right lung. Eight years after the trauma, the patient developed congestive heart failure. This has been well controlled with digitalis and occasional diuretics.