The correlation between the treadmill exercise test results and the hemodynamic data of 152 patients with previous myocardial infraction were investigated. The patients were classified into 4 groups as follows: h1 left ventricular end-diastolic pressure (LVEDP) &les; 12 mmHg and cardiac index (Cl) &ges;3.0 L/min/m² ; H2 LVEDP > 12 mmHg and Cl &ges; 3.0 L/min/m² ; H3 LVEDP &les; 12 mmHg and Cl < 3.0 L/min/m² ; and H4 LVEDP > 12 mmHg and Cl < 3.0 L/min/m². the duration of the exercise was significantly shortened for group H4 than group h1 (p < 0.01). The maximal ST segment elevation (mSTe) was significantly increased for group h3 and group H4, versus group H1 (p < 0.01) versus group 1. the incidence of exercise-induced premature ventricular contractions (PVCs) was significantly increased in group H3 and group H4, versus group H1 (p < 0.059. There were no significant differences in the maximal heart rate, double product, and ST segment depression among the 4 groups. Our data indicate that the groups with impaired left ventricular functions tend to decrease the duration of the exercise and to increase ST segment elevation and PVC frequencies during exercise.

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To determine left ventricular (LV) systolic and diastolic properties in patients with familial amyloid polyneuropathy (FAP), we analyzed simultaneous recordings of the electrocardiogram, phonocardiogram, carotid arterial pulse, and apex cardiogram in 14 patients and 21 normal subjects. LV systolic and diastolic time intervals were measured. Correlations between the intervals and neurologic disabilities, duration of illness, and age were examined. We found that in patients with FAP, 1) LV relaxation was impaired, especialy in early diastole, whereas systolic function was generally preserved, 2) abnormal LV relaxation could be seen before the development of both clinically identifiable heart disease and the abnormalities in systolic function, 3) indexes of LV systolic function and relaxation decreased in parallel with the progress of the disease, duration of illness, and age, and 4) electromechanical delay was markedly increased.

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Administration of sodium bicarbonate during cardiopulmonary resuscitation (CPR) is controversial, and our aim was to elucidate whether or not its administration is beneficial by analyzing the acid-base status and the level of carbon dioxide in central venous blood during CPR, and their changes following administration of sodium bicarbonate. Six patients were studied. They has all been admitted to the intensive care unit (ICU), had already had pulmonary arterial or central venous catheters inserted, and had acute episodes of circulatory collapse during their stay in the ICU. The following phenomena were observed; 1) hypercapnia and acidosis of central venous blood were prominent during both cardiogenic shock and CPR, although arterial hypocapnia was maintained by hyperventilation; 2) administration of sodium bicarbonate during cardiogenic shock and CPR induced exacerbation of hypercapnia and acidosis of central venous blood; 3) when arterial hypercapnia was present due to disturbed ventilation, administration of sodium bicarbonate exacerbated hypercapnia and acidosis of both arterial and central venous blood; 4) administration of sodium bicarbonate did not induce hypercapnia of central venous blood in a septic shock patient in whom the septic hyperdynamic state was prevalent in spite of low systemic perfusion pressure. It was concluded that hypercapnia and acidosis of the central venous blood and tissue were exacerbated by administration of sodium bicarbonate during CPR, and that such an effect might be dependent on the severity of the decrease in tissue perfusion.

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To assess the participation of cardiovascular eicosanoids (prostaglandins and thromboxanes) system in the initiation of genetic hypertension, we examined eicosanoids metabolism in the heart, aortic wall and kidney in prehypertensive and hypertensive rat models for spontaneous hypertension (SHR). Vascoconstrictor thromboxane A₂ (TXA₂) generation in the aortic wall was significantly enhanced by 49% in the prehypertensive and by 18% in the hypertensive SHR when compared to the respective normotensive Wistar-Kyoto rats. Cardiac TXA₂ content was significantly increased as well by 14% in the prehypertensive and by 30% in the hypertensive SHR. Moreover, vascular vasodepressor eicosanoids generation was decreased by 10% for PGI₂ and by 29% for PGD₂ in the prehypertensive SHR although the alterations were eliminated in the hypertensive SHR. In contrast to the cardiovascular eicosanoids system, there was no difference in renocortical TXA₂ content in either young or adult SHR while vasodepressor prostaglandins contents were decreased by 29% for PGE₂ and by 33% for PGD₂ in SHR when they were in the prehyertensive stage. Thus, in the prehypertensive stage of SHR when they were in the prehyertenisve stage. Thus, in the prehypertensive stage of SHR, the cardiovascular eicosanoids system exhibited enhanced vasoconstrictor TXA₂ and decreased vasodepressor prostaglandins, thereby producing a vasoconstrictor state. These data indicate that the alterations in the cardiovascular eicosanoids system partially contribute to the initiation of hypertension in SHR.

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To determine whether bunazosin (α₁-adrenoceptor blocking agent) can alter the hemodynamic profile of chronic heart failure secondary to myocardial infarction, the drug was administered to Wistar rats 4 weeks after coronary ligation, and continued for 4 weeks. In rats without bunazosin treatment, the left ventricular end-diastolic pressure (LVEDP) and the total vascular resistance index (TVRI) increased as a function of infarct size, while the cardiac index (CI) decreased. But in infarcted rats with bunazosin treatment, the mean aortic pressure and TVRI were reduced, the LVEDP was modestly lessened, and the CI was maintained. The greatest increase in CI after the treatment occurred in rats with infarcts of small and moderate size. Thus, long-term therapy with bunazosin improved LV dysfunction, relative to the size of infarction. This study suggests the beneficial effects of bunazosin therapy in patients with chronic heart failure.

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We studied the combined effects of hypoxia and the absence of glucose on postextrasystolic potentiated and resting contractions in papillary muscle of guinea pigs. Postextrasystolic potentiations (PESPs) were evoked following trains of 40 externally applied continuous stimulations. During hypoxia resting (regular) contractions decreased to about 25% of baseline tension at 30°C, whereas postextrasystolic potentiated contractions decreased to about 35% of baseline measurement of postextrasystolic potentiated contraction. In contrast, with reoxygenation, PESPs recovered quickly while resting contractions recovered gradually. Caffeine abolished the potentiation of postextrasystolic contraction not only in normoxia but also in hypoxia. We speculate that calcium release from the sarcoplasmic reticulum (SR) is attributable to PESP for the most part, and that the trans-sarcolemmal calcium influx generally contributes to the steady-state tensions developed by continuous stimulations. In addition, it seems that PESP works in a ischemic heart to compensate for the decreased tension during hypoxia as a potentiation by a premature ventricular contraction. Trans-sarcolemmal calcium influx might be affected more easily than the SR calcium release, by a combination of hypoxia and the absence of glucose, that is, the sarcolemma may be more susceptible to hypoxic injury than the SR.

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To determine whether the renal nerves affect central baroreflex regulation, the aortic depressor nerve (ADN) was stimulated electrically, while blood pressure, heart rate, and splanchnic nerve activity were recorded in renal denervated and sham-operated rats anesthetized with urethane. Tail cuff systolic pressure fell 6 days after renal denervation, but mean blood pressure recorded after anesthetizing with urethane did not differ between renal denervated and sham-operated rats. Urinary sodium excretion was greater in renal denervated than in sham-operated rats. ADN stimulation produced frequency-dependent falls in blood pressure accompanied by inhibitions of sympathetic nerve activity and heart rate. Depressor and sympathetic inhibitory responses to ADN stimulation were significantly smaller in renal denervated than in sham-operated rats. These findings suggest that the renal nerves can regulate baroreflexes centrally.

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There is a clinical dilemma in the treatment of patients with hypothyroidism and coronary artery disease; excess thyroid hormone administration may exacerbate anginal symptoms, and yet inadequate thyroid replacement may induce congestive heart failure. A case of successful coronary artery bypass grafting in a patient with angina pectoris and hypothyroidism is described in this paper. A 55 year-old woman with this complication initially received thyroid replacement therapy under strict monitoring. Forty days after the start of they thyroid replacement therapy, serum levels of thyroid hormone had reached the normal range, and then coronary artery bypass grafting was successfully performed. She recovered without any complications, and is now free from chest pain in spite of thyroid replacement therapy.

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A case of arteriovenous fistula between the internal mammary artery and the pulmonary artery was presented. In a recent review of the literature only 19 cases of this abnormality were described. In most instances, patients had continuous precordial murmur that might be confused with a patent ductus arteriosus. Definitive diagnosis was enabled by selective angiography.

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