[Coronary flow and myocardial metabolism during ischemic attack. Effort angina vs vasospastic angina].
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Biomedical subjects
Publications and source records attributed to M Mishima.
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The dose-response relation of contrast medium-induced hyperemic response in coronary blood flow (contrast hyperemia) was investigated to determine the optimal dose of contrast medium (CM, Urografin-76) for the assessment of coronary flow reserve in man. The great cardiac venous flow (GCVF) was determined with the continuous thermodilution method during the contrast hyperemia induced by the intracoronary injection of CM of three different doses, ie, 2, 4, and 6 ml/60 kg of body weight, into left coronary artery. Submaximal coronary vasodilation could be obtained by intracoronary injection of 4 ml of CM with minimal changes in systemic hemodynamics. The contrast hyperemia with this dose of CM was reproducible and also closely correlated with that obtained during pacing-induced angina. Thus, we conclude that the contrast hyperemic technique with intracoronary injection of 4 ml of Urografin-76 could be a reliable method to assess the coronary flow reserve.
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We used a pulsed Doppler technique to examine the flow velocity pattern in the right ventricular outflow tract in 33 adults. In the patients with normal pulmonary artery pressure (mean pressure less than 20 mm Hg, 16 patients), ejection flow reached a peak level at midsystole (137 +/- 24 msec, mean +/- SD), producing a domelike contour of the flow velocity pattern during systole. In contrast, the flow velocity pattern in patients with pulmonary hypertension (mean pressure greater than or equal to 20 mm Hg, 17 patients) was demonstrated to accelerate rapidly and to reach a peak level sooner (97 +/- 20 msec, p less than .01); in 10 of the pulmonary hypertensive patients a secondary slower rise in flow velocity was observed during a deceleration, resulting in the midsystolic notching. The time to peak flow (acceleration time, AcT) and right ventricular ejection time (RVET) were measured from the flow velocity pattern. Either AcT or AcT/RVET decreased with increase in mean pulmonary artery pressure, and a very high correlation (r = -.90) was found between AcT/RVET and log10 (mean pulmonary artery pressure). The use of this technique permitted the noninvasive estimation of the pulmonary artery pressure.
The acute effects of intravenous trapidil on hemodynamics, coronary circulation and myocardial metabolism were evaluated in 19 patients (Group I: 10 patients of chest pain syndrome; Group II: 9 patients of coronary heart disease). The heart rate increased (p less than 0.05) and aortic pressure decreased (p less than 0.01) during a 6-min study period. Pulmonary arterial end-diastolic pressure decreased slightly in both groups and cardiac output increased prominently in Group II. Myocardial oxygen consumption did not change significantly 3 and 6 min after trapidil injection. Coronary sinus flow increased slightly (statistically not significant) despite a decrease in aortic pressure, and thus, coronary vascular resistance decreased significantly in both groups. Coronary A-V O2 difference decreased 3 min after trapidil injection and no significant change in the lactate extraction ratio was observed. The diameter of the left main coronary artery increased by about 6% after an administration of trapidil. These results suggest that trapidil has the beneficial effect of coronary vasodilation and it increases cardiac output, despite a decrease in the preload, without a significant increase in myocardial oxygen consumption. The latter may be due to an afterload reduction effect of this drug.
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Regurgitant flows in valvular diseases were evaluated by a pulsed Doppler flowmeter combined with an electronic beam sector scanning echocardiograph. The apparatus which was newly developed by us allowed the simultaneous demonstration of a sample site on a two-dimensional echocardiogram with flow measurement. Doppler signals of regurgitant flow were recorded as uni-directional or bi-directional wide frequency band signals. The locations, where regurgitant flow signals were detected, were depicted on the corresponding two-dimensional echocardiogram. This procedure was referred to as "a flow mapping technique" for non-invasive visualization of the distribution of regurgitant flow. In 12 patients with mitral regurgitation due to mitral valve prolapse detected by the pulsed Doppler technique, the regurgitant flow was distributed to the opposite side of the prolapsing mitral leaflet. The transmission of the regurgitant murmur was well consistent with the direction of the regurgitant flow. In 14 patients with aortic regurgitation, the distribution of aortic regurgitant flow visualized by the flow mapping technique closely coincided with that obtained by cineaortography. Based on the distribution of the regurgitation, the severity of the regurgitation could be precisely evaluated by the Doppler technique. Regurgitant flow signals were detected in the right atrium in all 13 patients with tricuspid regurgitation diagnosed by right ventriculography. We found 4 patients who did not show Carvallo's sign but in whom were detected regurgitant flow signals by the Doppler technique. In all of them, tricuspid regurgitation was proven at surgery. These results indicate that the Doppler technique presented here has an obvious clinical advantage in detecting and evaluating regurgitant flow in valvular diseases.
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