[Determination of the effect of a new anti-anginal drug, isosorbide dinitrate tape (TY0081), by Holter electrocardiography].
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Biomedical subjects
Publications and source records attributed to J Ando.
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The effects of the benzodiazepine derivatives flurazepam and diazepam on K+- and Ca2+ -induced contracture were examined in isolated taenia coli and longitudinal muscle of the guinea-pig. Flurazepam and diazepam inhibited the tonic component more than the phasic component of the K+ -induced contracture of taenia coli. In longitudinal muscle, both flurazepam and diazepam inhibited the Ca2+ -induced contracture dose-dependently. These findings suggest that the observed effects of flurazepam and diazepam may have been due to inhibition of the transmembrane influx of Ca2+.
This study was undertaken to assess the conditions necessary to cause the "coronary steal" phenomenon in human subjects. We studied 42 patients (36 males, 6 females, ages 27--70 years) with known or suspected coronary artery diseases using continuous monitoring of the changes in blood pressure and electrocardiogram, thallium-201 myocardial imaging and selective coronary arteriography. Dipyridamole in a dose of 0.4 mg/Kg was given as an intravenous infusion for 4 min and thallium-201 was injected at the 4th minute after completion of the dipyridamole infusion. None of the 20 patients without significant coronary artery disease complained of anginal chest pain or showed ischemic S-T segment depression. Dipyridamole images showed no perfusion abnormalities in 17 of the 20 patients. On the other hand, in 4 of the 22 patients with significant coronary artery disease, anginal chest pain accompanied with S-T segment depression occurred after the dipyridamole infusion. Dipyridamole images showed perfusion abnormalities in 18 of the 22 patients. The 4 patients who experienced an anginal attack had 3 vessel disease on the coronary arteriogram and showed regional perfusion defects on scintigrams corresponding to the regions receiving collaterals. Before the onset of pain, the double product (heart rate X systolic arterial pressure) was unchanged significantly but there was a reduction in the systemic blood pressure. The overall data exhibit the following conditions under which attacks of angina pectoris are induced by dipyridamole: 1) the presence of multiple vessel disease, 2) a fall in systemic blood pressure, and 3) regional malperfusion caused by dipyridamole.
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Radionuclide angiocardiography was utilized for the measurement of left ventricular dynamics and the analysis of its segmental wall motion. Left ventricular performance was measured by the first pass method and gated equilibrium method in patients with ischemic heart disease. The left ventricular wall motion was also examined by the analysis of computer-drawn outlines of radioactivity counts of the left ventricular chamber. These measurements were well correlated with those obtained by invasive methods such as contrast cine-ventriculography and thermodilution method in the resting state. The patients with effort angina often showed an almost normal left ventricular performance and wall motion in the resting state without ischemic episodes. However, at the time when anginal attack was provoked with exercise testing, an asynergy and a reduced performance of left ventricle were observed. The extent and localization of this asynergy well corresponded with the defect of myocardial scintigrams determined by 201-Tl stress myocardial imaging. From above findings we conclude that the myocardial ischemia with asynergy is a cause of decreased left ventricular hemodynamics during anginal attack. Although further evaluation is necessary to know limitations and to avoid inaccuracy, these techniques were shown to have a significant usefullness in evaluating ischemic heart disease.
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We report a case of a 44-year-old male with variant angina who developed acute anterior myocardial infarction 2 weeks following demonstration of normal left coronary artery. This experience provides inferential evidence that myocardial ischemia resulting from coronary spasm may progress into myocardial infarction.
A case of aortic regurgitation observed in a thalidomide deformed child is presented. Possibility of thalidomide as an etiologic factor was discussed.
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Using electromyographic techniques, we examined the possibility that idiopathic cardiomyopathy might be a cardiac manifestation of a general myopathy. The EMG studies were done on sixteen normal subjects and seventeen patients with idiopathic cardiomyopathy, including six with hypertrophic obstructive cardiomyopathy (HOCM), six with hypertrophic cardiomyopathy (HCM), and five with congestive cardiomyopathy (CCM). The action potential duration in the brachial biceps were determined exactly by a special recording technique. In the normal subjects, the mean action potential duration was 5.42 +/- 0.12 msec. In the patients with idiopathic cardiomyopathy, the mean action potential duration was 4.43 +/- 0.15 msec, which was significantly shorter than that of the normal subjects; 4.06 +/- 0.30 msec in HOCM, 4.45 +/- 0.20 msec in HCM, and 4.48 +/- 0.13 msec in CCM. These findings suggest that idiopathic cardiomyopathy is only one aspect of a larger disease spectrum, with abnormalities in both voluntary and cardiac muscles.
This study was aimed to evaluate the noninvasive method of radioisotopic angiocardiography for detecting a disproportionate thickning of the interventricular septum relative to the left ventricular free wall in the patient with idiopathic hypertrophic cardiomyopathy. The experimental study was performed to compare the imaged size of myocardial wall obtained my filling up with technetium 99 m labeled sponge in biventricular cavities, with the actually measured thickness of the heart specimen. The resultant correlation between actual and imaged size of the left ventricular wall was excellent (r = 0.95). In the clinical application of this method, a gated cardiac blood pool scan was performed after the intravenous administration of technetium 99 m labeled human serum albumin in a dose of 10 mCi. The cardiac images were obtained in anterior, 30, 35, 40 and 45 degree left anterior oblique projection, and evaluated by visual inspection and semi-quantitatively by tracing the myocardial borders. As a result, the imaged asymmetric septal hypertrophy was evident in all four patients with PMD, with a ratio of septum to left ventricular free wall of 1.35 compared to 0.76 in five patients with left ventricular hypertrophy of known heart disease, and 0.88 in twenty-one miscellaneous cardiac patients without left ventricular hypertrophy. Thus, RI angiocardiography provides a safe, repeatable method for detection and evaluation of Primary Myocardial Disease.
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