We developed a portable needle-probe videomicroscope with a charge-coupled device (CCD) camera to visualize the subendocardial microcirculation. In 12 open-chest anesthetized pigs, the sheathed needle probe with a doughnut-shaped balloon and a microtube for flushing away the intervening blood was introduced into the left ventricle through an incision in the left atrial appendage via the mitral valve. Images of the subendocardial microcirculation of the beating heart magnified by 200 or 400 on a 15-in. monitor were obtained. The phasic diameter change in subendocardial arterioles during cardiac cycle was from 114±46 ,um (mean+SD) in end diastole to 84±26 ,um in end systole (p<0.001, n=13, ratio of change=24%) and that in venules from 134±60 ,m to 109±45 ,um (p<0.001, n=15, ratio of change=17%). In contrast, the diameter of subepicardial arterioles was almost unchanged (2% decrease, n=5, p<0.01), and the venular diameter increased by 19%1 (n=8, p<0.001) from end diastole to end systole. Partial kinking and/or pinching of vessels was observed in some segments of subendocardial arterioles and venules. The percentage of systolic decrease in the diameter from diastole in the larger (>100 ,um) subendocardial arterioles and venules was greater than smaller (50-100 ,m) vessels (both p<0.05). In conclusion, using a newly developed microscope system, we were able to observe the subendocardial vessels in diastole and systole. The vascular compression by cardiac contraction decreased the diameters of subendocardial arterioles and venules by about 20o, whereas subepicardial arterial diameter changed very little during the cardiac cycle and subepicardial venules increased in diameter during systole. (Circulation Research 1993;72:939-946) KEY WORDS * subendocardial microcirculation heart * needle-probe videomicroscope he phasic flows in the left coronary artery and T vein are unlike those of other organs; the arterial inflow is greatest during diastole, whereas the venous outflow is greatest during systole.1-6 This unique pattern of coronary arterial and venous flow was inferred in 1695 by Scaramucci,7 who is considered the founder of coronary physiology. He hypothesized that the myocardial vessels are squeezed by the contraction of the muscle fibers around them, which

SummaryBackground: Serotonin (5-hydroxytryptamine: 5-HT) reduces the coronary blood flow (CBF) as a product of aggregating platelets. Sarpogrelate, a specific 5HT2-receptor antagonist, has been reported to increase the coronary collateral flow in humans; however, its effect on the microcirculation is still not fully understood.Hypothesis: This study was undertaken to determine whether sarpogrelate might improve the microcirculation in coronary artery disease (CAD).Methods: To investigate the effect of sarpogrelate on the microcirculation in CAD, we measured CBF in 15 patients with CAD but no significant stenosis in the left anterior descending artery (LAD). The patients were randomly allocated to two groups, including those receiving oral administration of 200 mg of sarpogrelate (SPG, 8 patients, age 61 ± 6 years) and those receiving no medication (controls, 7 patients, age 57 ± 8 years). Prior to and 1 h after the administration of sarpogrelate, or in controls at 1-h intervals, the average peak velocity (APV) at baseline and hyperemia was measured by an intracoronary Doppler guidewire. Systemic blood pressure (SBP) and cardiac output (CO) were also measured.Results: In the patients receiving SPG, the medication significantly increased the baseline (18 ± 9 to 19 ± 10 cm/s, p < 0.05) and maximal APV (55 ± 9 to 64 ± 31 cm/s, p < 0.05). However, no significant changes were observed in SBP and CO after the administration of SPG. In the control group, there were no significant differences in baseline and hyperemic APV.

The precise evaluation of left ventricular volume by an ambulatory radionuclide monitoring system combined with a heart rate variability analysis is considered useful for clarifying the pathophysiology of neurally mediated syncope.

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A 67-year-old woman without history of heart disease was admitted with chest oppression. Her electrocardiogram (ECG) at the time of admission showed ST segment elevation in leads V2-V6. Cardiac ultrasound revealed severe hypokinesis in mid to apical portion of anterior wall. Emergent coronary angiography showed normal coronary arteries. Left ventriculography (LVG) revealed akinesis of mid portion of anterior and inferior wall with hyperkinesis of apex and basal portion of anterior and inferior wall. Cardiac ultrasound examination 3 months later revealed improvement in LV contraction without mid-ventricular akisesia. The LVG performed 6 months later showed no focal asynergy. In I-123-beta-metyl-iodophenyl pentadecanoic acid myocardial scintigraphy the discrepancy of uptake between apical and anterior and inferior wall of mid region (more uptake in apex) was reduced. Using I-123-meta-iodobenzyl-guanidine myocardial scintigraphy in acute phase, decreased uptake in the mid portion of anterior and inferior to lateral wall was seen in early and delayed images and that persisted through 6 months. As these findings resembled those of Takotsubo cardiomyopathy other than affected region, it is possible to say that basically they belong to same entity of disease but they are different in their phenotype.