Near-maximal treadmill exercise testing was performed on 26 normal individuals (NL) and 78 patients with coronary artery disease (CAD) using a modified Bruce's protocol. Exercise-induced changes in orthogonal P wave measurements were made automatically, using an averaging technique, immediately before and 30sec after treadmill exercise to assess their diagnostic significance in evaluation of left ventricular (LV) function in CAD patients. The maximal inferior and posterior components of the P wave and the maximal P-vector magnitude in the frontal and left sagittal planes showed a statistically significant increase after treadmill exercise both in NL and CAD patients. These changes were considered to be physiological responses of the P wave to dynamic exercise. The percent changes of the maximal horizontal P-vector magnitude (%Hmax) were significantly higher after treadmill exercise in CAD patients than in NL. In patients with effort angina pectoris and without a previous myocardial infarction, the %Hmax showed a highly significant negative correlation with the percent changes of the LV ejection fraction (r=0.66, p<0.01), measured by exercise RI angiography. These results suggest that the exercise-induced increase in %Hmax reflects transient impairment of LV function during exercise. It was concluded that a %Hmax of more than 120% provided a useful, noninvasive index for assessing LV function in treadmill exercise testing.

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Left ventricular performance was studied by measuring systolic time intervals (STIs) in 15 adult cases of chronic severe anemia (CSA) before and after transfusion of 350 and 700ml of whole blood at a moderately rapid rate of 5ml/min. Cases with systemic disease and congestive heart failure were excluded. STIs before blood transfusion (BT) showed wide variations, but these were within normal limits in 80% of the cases. Following BT, left ventricular ejection time (LVET) increased significantly (p<0.001) without much change in the pre-ejection phase (PEP). There was no significant change in the PEP/LVET ratio after BT.
It is concluded that transfusion of 700ml of whole blood at a rate of 5ml/min to patients with CSA is devoid of any risk, so far as myocardial contractile function is concerned.

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Hemodynamic changes in the supine resting position were investigated in 70 male subjects, consisting of 15 healthy volunteers with normotension (blood pressure of 113±7/70±5mmHg, M±SD), 25 patients with borderline essential hypertension (143±12/90±6mmHg) and 30 patients with established essential hypertension (166±13/108±6mmHg). The supine position reduced blood pressure, heart rate, stroke volume and cardiac output (p<0.001), but increased total peripheral vascular resistance (p<0.001). The decrease in systolic blood pressure (p<0.01), stroke volume (p<0.05) and cardiac output (p<0.05), and the increase in total peripheral vascular resistance (p<0.01) were significantly greater in the borderline and established essential hypertensive groups than in the normotensive group. The results demonstrated that the decrease in blood pressure was due to a reduction in both heart rate and stroke volume, and that the decrease in stroke volume and increase in total peripheral vascular resistance seen in the supine position were greater in the hypertensive groups than in the normotensive group. These hyperresponses may contribute to the development and persistence of high blood pressure in patients with essential hypertension.

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Six of 66 patients with hypertrophic cardiomyopathy had an embolic event during an average observation period of 3.73 years. Five of these had probable cerebral embolism, while 1 patient had a femoral artery embolism. The calculated incidence of systemic embolism was 2.4% per patient year. All embolic events occurred in the patients with atrial fibrillation. In comparison to patients without systemic embolism with or without atrial fibrillation, the cardiothoracic ratio was greater, the cardiac index was lower and the left atrial dimension tended to be greater in those patients with systemic embolism.

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The clinical significance of beta-thromboglobulin (β-TG) and platelet factor 4 (PF-4) levels were evaluated in 26 patients with atrial fibrillation (af) complicated by valvular heart disease (VHD), 73 patients with of but without valvular heart disease and 57 normal subjects. The β-TG level was significantly higher in af patients without VHD than in normal subjects (49.4±35.8ng/ml vs 31.2±14.0ng/ml, p<0.01) and in af patients with VHD than in normals (64.1±52.8ng/ml vs 31.2±14.0ng/ml, p<0.01). Af patients with or without VHD tended to show high levels of PF4 compared with normals (af patients without VHD: 34.1±45.5ng/ml, af patients with VHD: 18.6±27.2ng/ml, normals: 11.6±8.2ng/ml). There was no correlation between β-TG levels and age in af patients without VHD or in normals. There was also no correlation between β-TG levels and heart rate in af patients without VHD.
The activation of platelets was suggested in patients with atrial fibrillation on the basis of increased levels of platelet releasing substances, especially in those with VHD. The high levels of β-TG and PF4 in patients with atrial fibrillation may be one explanation for the high incidence of thromboembolism in these patients, indicating the necessity of antiplatelet therapy.

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To determine whether dipyridamole infusion can be used as an alternative method to physical exercise, 87 lead body surface mapping was performed to compare the distribution patterns of ST-segment depression after 0.568mg/kg/4min dipyridamole infusion (D) and after submaximal treadmill exercise (T) in 21 patients with coronary artery disease. Significant ST-segment depression (_??_0.05mV) was observed in 19 patients after D and in 18 after T. After D and T, each patient showed a similar distribution pattern of ST-segment depression. There were no significant differences in the number of leads which showed ST-segment depression (nST: D, 15.6±11.1 vs T, 15.2±10.8) and in the maximal value of ST-segment depression (STmax: D, -0.24±0.16 vs T, -0.20±0.13mV). Good correlations were observed in nST (r=0.84) and in STmax (r=0.87) between D and T. The increase in mean pressure-rate product after T was 89%, while the increase after D was only 22%. Our results suggest that this pharmacologic test to induce myocardial ischemia may be useful in the evaluation of coronary artery disease in patients who are physically unable to perform adequate exercise.

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Changes in hemodynamic parameters following "shaking" in 4, 12, 24 and 48 week old spontaneously hypertensive rats (SHR) and Wistar rats of the Kyoto strain (WKY) were analyzed. Mean arterial pressure (MAP) and cardiac output (CO) were measured in the following two conditions: (A) at rest, and (B) after shaking (these parameters were measured following a 3-sec rest after 5-sec of shaking). Both sets of data were compared in each age group between SHR and WKY. Heart rates (HR) in all age groups of SHR and WKY were significantly increased after shaking compared with those at rest. MAP in 4 week old SHR, but not in 4 week old WKY, was increased compared with that at rest. In 48 week old SHR and WKY, MAP after shaking was not increased compared with that at rest. This increased MAP induced by stress (shaking) in young SHR may be related to a causative factor in hypertension. CO in SHR did not indicate changes in shaking reaction as a result of increasing aging. Heart work index (HWI) after shaking in all age groups of SHR, including the prehypertensive stage, was significantly increased compared with that at rest; this was not the case in WKY. The intermittently increased heart work seen in response to stress may contribute to the early development of left ventricular hypertrophy in young SHR.

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When captopril was injected intravenously in urethane anesthetized rats, a hypotensive effect accompanied by bradycardia was obtained, while an intravenous (i. v.) injection of prostaglandin I₂ (PGI₂), which induced hypotension of the same magnitude as the hypotensive effect obtained with captopril, caused a marked tachycardia. Simultaneously, sympathetic nerve activity recorded from abdominal sympathetic nerves was unchanged following injection of captopril, while it was significantly increased during hypotension induced by PGI₂. The bradycardia, but not the hypotensive effects induced by captopril was abolished by i. v. pretreatment with atropine. Intracisternal injection of a small dose of captopril inhibited reflex tachycardia during hypotension induced by PGI₂ and prolonged the hypotensive effect, while intravenous administration of this dose did not inhibit the reflex tachycardia induced by PGI₂. In spontaneously hypertensive rats (SHR), the hypotensive effect of captopril was increased partly, however, the accompanying bradycardia was significantly reduced. These findings suggest that captopril inhibits the baroreflex and centrally activates the cardiac vagal nerve. Moreover in SHR, the effect of captopril on cardiac vagal activity was disturbed.

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Recently, a number of cases of Takayasu's disease having dilative or aneurysmal lesions have been reported. Such lesions have come to be considered important manifestations of Takayasu's disease. A case, whose right common carotid artery perforated spontaneously and became a pseudoaneurysm, without any other stenotic lesion is presented with a review of the literature. Surgical treatment was performed successfully.

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A coronary artery-to-left ventricular fistula is a rare finding; to the best of our knowledge, a total of only 35 cases have been reported. Only 5 cases of a generalized arterio-systemic fistula with three vessel involvement have been reported in the literature. We describe another case involving all major coronary arteries. A review of the literature is presented and the data of the reported cases are analyzed.
A 55 year old woman was examined because of recurrent chest pain which had persisted for 2 years. On physical examination, the only abnormal finding was a fourth heart sound. Exertional chest pain, a positive exercise stress test, and the results of a lactate extraction study suggested severe myocardial ischemia. Thallium myocardial scintigraphy showed no evidence of a perfusion defect. Cardiac catheterization revealed an irregular left ventricular endocardial pattern (Thebesian veins). Selective coronary angiography showed communicating fistulae of all three major coronary arteries with the left ventricular cavity. We assume that this vascular anomaly causes a coronary steal phenomenon and subsequent myocardial ischemia.

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The present results showed that the irradiation localized to the heart with the dosis of 3000-5000 rad successfully induced lesions such as intimal proliferation and occlusion in coronary arteries in SHRSP with hypertension. This intimal proliferation was enhanced by the deposition of lipid and cholesterol under hyperlipidemic condition. Therefore, hypertension and lipidemia appear to accelerate proliferative and occlusive coronary lesions in SHRSP after irradiation focused on the heart and these rats can be used as model for coronary arterio- or atherosclerosis or myocardial infarction.

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Suppression of dopamine (DA) biosynthesis by carbidopa, a peripheral inhibitor of dopa decarboxylase, induced a decrease in urinary excretion of sodium (Na) and the Na retention in the body, which contributed to accerelate the development of hypertension (HT) in young SHR. Therefore the peripheral dopaminergic mechanism may play an important role in the development and maintenance of HT in SHR.

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Hypertensive diabetic animal models have been developed by injecting streptozotocin (STZ) in neonatal stroke-resistant spontaneously hypertensive rats (SHRSR) and stroke-prone SHR (SHRSP) at the age of 2 days. They showed mild insulin deficiency and mild hyperglycemia at the age of 3 to 4 months, but strain difference in the susceptibility was noted; the incidences of diabetes were higher in SHRSR and SHRSP than in Wistar-Kyoto rats (WKY).

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Angiopathy in optic fundi was observed in all of SHRSP at the age of 13 months after birth. And their death of stroke occurred rather shortly after retinoparhy were complicated in addition to angiopathy. Experimental and clinical studies as of today have not been clearly substantiated corelationship between retinal angiopathy and the development of stroke. In this study, changes in optic fundi were observed in the advanced age, i.e., from 13-18 months. Therefore, in the convience of male and female comparative investigation, an antihypertensive agent was administrated at the age of 13 months. Although vascular affect of such an antihypertensive treatment should be considered, these results suggest that retinopathy should be more focused to in the development of stroke, as well as or in different to angiopathy.

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Effects of antihypertensive treatments on ocular lesions were evaluated in spontaneously hypertensive (SHR) rats with streptozotocin (STZ)-induced diabetes mellitus. STZ treatment induced ocular lesions such as narrowing of retinal arterioles, caliber irregularity, papilledema and cataracta in these rats. Enalapril, ramipril and arotinolol decreased blood pressure (BP) and prevented the progress of ocular lesions. Nisoldipine tended to decrease blood glucose (BG) and prevented the progress of ocular lesions. Therefore, antihypertensive treatments were shown to be effective in preventing the progress of ocular lesions in hypertensive rats with diabetes mellitus. Hypertension, as well as high BG, was suggested to play an important role in inducing ocular lesions.

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SHRSP's were rendered diabetic by injection of either alloxan or streptozotocin and the retina, retinal vessels and choroid were examined histologically.
1. The animals treated with the above substances developed strong urinary reactions for sugar and ketone bodies two days after the injection. They developed also anorexia, loss of weight and polyuria.
2. These diabatic rats demonstrated marked axonal/degeneration in the inner retinal layer, especially in the layer of nerve fibers. The pigment epithelium and the choroid showed no/remarkable changes.These early degenerative changes in the inner retinal layer may be related to the development of retinopathy in later stages.

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