The localized, extremely low-flow condition that was observed in the dome of aneurysms with aspect ratios of more than 1.6 is a common flow characteristic in the geometry of ruptured aneurysms, so great care should be taken for patients with unruptured intracranial aneurysms with aspect ratios of more than 1.6.

We analyzed optical coherence tomographic (OCT) characteristics of different types of coronary thrombi that had been confirmed at postmortem histologic examination. We examined 108 coronary arterial segments of 40 consecutive human cadavers. OCT images of red and white thrombi were obtained and the intensity property of these thrombi was analyzed. Red and white thrombi were found in 16 (17%) and 19 (18%) of the 108 arterial segments, respectively. Red thrombi were identified as high-backscattering protrusions inside the lumen of the artery, with signal-free shadowing in the OCT image. White thrombi were identified as low-backscattering projections in the OCT image. There were no significant differences in peak intensity of OCT signal between red and white thrombi (130+/-18 vs 145+/-34, p=0.12). However, the 1/2 attenuation width of the signal intensity curve, which was defined as the distance from peak intensity to its 1/2 intensity, was significantly different between red and white thrombi (324+/-50 vs 183+/- 42 microm, p<0.0001). A cut-off value of 250 microm in the 1/2 width of signal intensity attenuation can differentiate white from red thrombi with a sensitivity of 90% and specificity of 88%. We present the first detailed description of the characteristics of different types of coronary thrombi in OCT images. Optical coherence tomography may allow us not only to estimate plaque morphology but also to distinguish red from white thrombi.

Background-Recent studies in vitro have demonstrated that endothelium-derived hydrogen peroxide (H 2 O 2 ) is an endothelium-derived hyperpolarizing factor (EDHF) in animals and humans. The aim of this study was to evaluate our hypothesis that endothelium-derived H 2 O 2 is an EDHF in vivo and plays an important role in coronary autoregulation. Methods and Results-To test this hypothesis, we evaluated vasodilator responses of canine (nϭ41) subepicardial small coronary arteries (Ն100 m) and arterioles (Ͻ100 m) with an intravital microscope in response to acetylcholine and to a stepwise reduction in coronary perfusion pressure (from 100 to 30 mm Hg) before and after inhibition of NO synthesis with N G -monomethyl-L-arginine (L-NMMA). After L-NMMA, the coronary vasodilator responses were attenuated primarily in small arteries, whereas combined infusion of L-NMMA plus catalase (an enzyme that selectively dismutates H 2 O 2 into water and oxygen) or tetraethylammonium (TEA, an inhibitor of large-conductance K Ca channels) attenuated the vasodilator responses of coronary arteries of both sizes. Residual arteriolar dilation after L-NMMA plus catalase or TEA was largely attenuated by 8-sulfophenyltheophylline, an adenosine receptor inhibitor. Conclusions-These results suggest that H 2 O 2 is an endogenous EDHF in vivo and plays an important role in coronary autoregulation in cooperation with NO and adenosine.

We clearly demonstrated 3D geometric deformity of the mitral leaflets and annulus in ischemic MR using novel software for creating images by 3D echocardiography. This technique will be helpful in making a proper decision for the surgical strategy in each patient.

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

Background-The phase difference of coronary arterial and venous flows indicates the importance of intramyocardial capacitance vessels in storing diastolic flow and in discharging volume in systole. However, the anatomic and functional characteristics of the capacitance vessels are unclear. We aimed to clarify those characteristics with their transmural difference by 3D visualization of transmural microvessels under diastole and systole. Methods and Results-We performed complete intracoronary filling of a contrast medium into Langendorff's Wistar rat hearts under (1) St Thomas-perfused diastolic arrest (D-mode) and (2) BaCl 2 -induced systolic arrest (S-mode). Precise transmural 3D architectures of capillaries and of pre-and post-capillary microvessels (ie, microvessels larger than capillaries) were visualized clearly with a confocal laser scanning microscope and x-ray microcomputed tomography (microCT), respectively. Vascular volume fraction (VF) and systolic-induced VF reduction rate from D-to S-mode were analyzed. The net capillary VF in D-mode (20.4Ϯ0.9%) was 10 times that of larger microvessels and was reduced in S-mode by 32% without capillary collapse. Systolic-induced VF reduction rate was smaller in capillaries than in larger microvessels (48%; PϽ0.05). The larger microvessel VF in D-mode (2.2Ϯ0.2%) was reduced in S-mode, accompanied by complicated 3D deformation. Conclusions-Capillaries were relatively resistant to the systolic extravascular compression compared with pre-and post-capillary microvessels, conveniently beneficial for the myocardial oxygen delivery throughout a cardiac cycle. Nevertheless, a larger change in the absolute volume of capillaries may function as effective capacitance. On one hand, the pre-and post-capillary microvessels showed a larger phasic change in resistance, which may function to maintain the capillary patency during systole. (Circulation. 2002;105:621-626.)

The interaction between monocytes and endothelial cells is considered to play a major role in the early stage of atherosclerosis, and the involved endothelial cell micromechanics may provide us with important aspects of atherogenesis. In the present study, we evaluated (i) the endothelial cell-to-cell and cell-to-substrate gaps with the electric cell-substrate impedance sensing system, which can detect the nanometer order changes of cell-to-cell and cell-tosubstrate distances separately, and (ii) the endothelial cell micromechanical properties with an atomic force microscope after application of monocytes to endothelial cells. Application of monocytic THP-1 cells to IL-1␤-stimulated human umbilical vein endothelial cells immediately decreased the electrical resistance of the endothelial cell-to-substrate (increase of the cell-to-substrate gap), whereas the endothelial cell-to-cell resistance (cell-to-cell gap) did not change. The elastic modulus of the endothelial cells decreased after 2-h monocyte application, indicating an increase of endothelial cell deformability. In conclusion, the interaction of the monocytes to the endothelial cells reduced the adhesiveness to the substrate and increased the deformability of endothelial cells. These changes in the adhesiveness and the deformability may facilitate migration of monocytes, a key process of atherogenesis in the later stage.A t the early stage of atherosclerosis, an aggregation of lipid-rich macrophages that were derived from monocytes was observed in the intima (1). Adhesion of monocytes to the arterial endothelial cells and their migration into the arterial intima are the earliest key events in atherogenesis (1). Previous studies demonstrated that leukocytes could migrate throughout the endothelial monolayer via not only paracellular but also transcellular pathways in vivo and in vitro (2-5). The endothelial cell micromechanics that are involved in endothelial cell micromotion and the mechanical properties of endothelial cells may be key factors in these processes. Earlier studies reported the importance of adhesion molecules in the adhesion and migration of monocytes to endothelial cells (6, 7). We previously demonstrated that the adhesion of monocytes to human umbilical vein endothelial cells (HUVEC) induces the decrease in the amount of focal adhesion kinase (p125 FAK ) with reduction of the density of F-actin stress fibers in HUVEC (8). These results suggest that the adhesion of monocytes induces changes of the adhesiveness of endothelial cells to the substrate and the mechanical properties of endothelial cells. However, the accompanying micromechanics and micromotion of endothelial cells were little understood.For the micromotion measurement of the cultured cells, Giaever and Keese (9) developed a morphological biosensor, the electric cell-substrate impedance sensing (ECIS) system. The advantage of this system is that quantitative estimation of cell-to-cell and cell-to-substrate distances can be performed separately and in real time. Atomic force micros...

We have recently demonstrated that endogenous H2O2 plays an important role in coronary autoregulation in vivo. However, the role of H2O2 during coronary ischemia-reperfusion (I/R) injury remains to be examined. In this study, we examined whether endogenous H2O2 also plays a protective role in coronary I/R injury in dogs in vivo. Canine subepicardial small coronary arteries (>or=100 microm) and arterioles (<100 microm) were continuously observed by an intravital microscope during coronary I/R (90/60 min) under cyclooxygenase blockade (n=50). Coronary vascular responses to endothelium-dependent vasodilators (ACh) were examined before and after I/R under the following seven conditions: control, nitric oxide (NO) synthase (NOS) inhibitor NG-monomethyl-L-arginine (L-NMMA), catalase (a decomposer of H2O2), 8-sulfophenyltheophylline (8-SPT, an adenosine receptor blocker), L-NMMA+catalase, L-NMMA+tetraethylammonium (TEA, an inhibitor of large-conductance Ca2+-sensitive potassium channels), and L-NMMA+catalase+8-SPT. Coronary I/R significantly impaired the coronary vasodilatation to ACh in both sized arteries (both P<0.01); L-NMMA reduced the small arterial vasodilatation (both P<0.01), whereas it increased (P<0.05) the ACh-induced coronary arteriolar vasodilatation associated with fluorescent H2O2 production after I/R. Catalase increased the small arterial vasodilatation (P<0.01) associated with fluorescent NO production and increased endothelial NOS expression, whereas it decreased the arteriolar response after I/R (P<0.01). L-NMMA+catalase, L-NMMA+TEA, or L-NMMA+catalase+8-SPT further decreased the coronary vasodilatation in both sized arteries (both, P<0.01). L-NMMA+catalase, L-NMMA+TEA, and L-NMMA+catalase+8-SPT significantly increased myocardial infarct area compared with the other four groups (control, L-NMMA, catalase, and 8-SPT; all, P<0.01). These results indicate that endogenous H2O2, in cooperation with NO, plays an important cardioprotective role in coronary I/R injury in vivo.