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1 unohistochemistry in the EC lining the human coronary vessel.
2 curring at cathodal tissue surfaces or large coronary vessels.
3 ssociated with revascularization of occluded coronary vessels.
4 issue boundary and create cardiomyocytes and coronary vessels.
5 MDCT allow for noninvasive assessment of the coronary vessels.
6 the carotid bifurcation, and in the proximal coronary vessels.
7 d a high-fat diet combined with injury to 22 coronary vessels.
8 e method to identify plaque apoptosis in the coronary vessels.
9 ls (BMCs) to differentiate into myocytes and coronary vessels.
10 images were interpreted for tracer uptake in coronary vessels.
11 yocytes and absent in interstitial cells and coronary vessels.
12 rct caused by obstruction of major and minor coronary vessels.
13 opmental mechanisms underlying generation of coronary vessels.
14 olocalized with endothelial cells from small coronary vessels.
15 rst seen in the endothelial cells from small coronary vessels.
16 ed amyloid deposition in the intramyocardial coronary vessels.
17 er balloon angioplasty of stenoses of native coronary vessels.
18 al amounts of class II MHC antigens to human coronary vessels.
19 e, ejection fraction, and number of diseased coronary vessels.
20 hallenging and often limited by the adjacent coronary vessels.
21 cells (EPDCs) contribute to the formation of coronary vessels.
22 smooth muscle (SM) cells, which support the coronary vessels.
23 cells that are required for the formation of coronary vessels.
24 er number of newly formed cardiomyocytes and coronary vessels.
25 vulnerability of both culprit and nonculprit coronary vessels.
26 art with immunocompatible cardiomyocytes and coronary vessels.
27 ive VPCs were identified within the walls of coronary vessels.
28 and smooth muscle cells within them to form coronary vessels.
29 ion of stromal-derived factor 1 from hypoxic coronary vessels.
30 lls capable of generating cardiomyocytes and coronary vessels.
31 scle lineages including smooth muscle of the coronary vessels.
32 irement for Tgfbr3 during development of the coronary vessels.
33 um composed of integrated cardiomyocytes and coronary vessels.
34 Histology was performed on 55 stents in 35 coronary vessels (32 native arteries and 3 vein grafts)
35 nonsmokers, P=0.02) and fatty streaks in the coronary vessels (8.27 percent vs. 2.89 percent, P=0.04)
37 causes embryonic death by E18.5 with reduced coronary vessel and fibrous matrix penetration into myoc
41 c cells (HCs), which are located proximal to coronary vessels and encased by extracellular matrix (EC
44 ved cells (EPDCs) contribute to formation of coronary vessels and fibrous matrix of the mature heart.
45 ed clinically to form functionally competent coronary vessels and improve CBF in patients with ischem
46 relationship between the number of diseased coronary vessels and mean calcium score, i.e. the mean c
49 istinct sites (either in the target or other coronary vessels) and further classified as procedural,
50 ssion, cardiovascular risk factors, multiple coronary vessel, and left main stem disease were more fr
53 tudies also show that the atria, epicardium, coronary vessels, and the majority of outflow tract smoo
60 ound that a substantial portion of postnatal coronary vessels arise de novo in the neonatal mouse hea
62 ysis in mice and cardiac organ culture, that coronary vessels arise from angiogenic sprouts of the si
64 Fog2MC adult hearts displayed a paucity of coronary vessels, associated with myocardial hypoxia, in
65 pable of obtaining cross-sectional images of coronary vessels at a resolution of approximately 10 mic
67 tification method in subjects and individual coronary vessels by using t tests and analysis of varian
68 ing may permit robust discrimination between coronary vessels causing ischemia versus not causing isc
69 , as HH agonists have been shown to increase coronary vessel density and improve coronary function af
71 V-derived) and ventral (endocardial-derived) coronary vessels developed in response to different grow
73 ta4 (Tbeta4) as essential for all aspects of coronary vessel development in mice, and demonstrate tha
76 demonstrate a requirement for Tgfbr3 during coronary vessel development that is essential for embryo
78 for embryonic viability, heart development, coronary vessel development, and adult myocardial functi
79 regeneration likely recapitulates embryonic coronary vessel development, which involves the activati
87 imilar in morphology, conduit and resistance coronary vessels differ importantly in size, function an
90 dose-response relationship to the number of coronary vessels exhibiting obstructive CAD, with increa
91 le starts to envelop the myocardium and that coronary vessels form by ingrowth of these migratory pre
93 chemokine signaling has an essential role in coronary vessel formation by directing migration of endo
94 s important roles in epicardial function and coronary vessel formation during heart regeneration in z
96 e ability of grafted cells to participate in coronary vessel formation was monitored by staining with
97 al EMT is required for myocardial growth and coronary vessel formation, and it generates cardiac fibr
103 dent region, preserves endothelium-dependent coronary vessel function, and upregulates markers of ang
104 However, the mechanism of interventions in coronary vessel geometry over time is less well characte
105 view or >/=50% in 2 orthogonal views in all coronary vessels >/=2.5 mm diameter) within 12 months.
106 e that subtle variation in the patterning of coronary vessels has significant but uncharacterized eff
109 nts with normal flow at rest and supplied by coronary vessels having </=50% diameter stenosis were st
110 scarred myocardium and generate myocytes and coronary vessels improving the hemodynamics of the infar
114 staining also reveal that there are very few coronary vessels inside the myocardium of mutant hearts.
115 ailed to reconstitute healthy myocardium and coronary vessels integrated structurally and functionall
119 rat and regenerated human cardiomyocytes and coronary vessels, leading to a remarkable restoration of
120 e (FFR)-guided PCI in the treatment of small coronary vessel lesions as compared with an angio-guided
122 ng the 3D volume along the major axis of the coronary vessels may help to overcome such limitations.
123 stolic compression of sections of epicardial coronary vessels (myocardial bridging) with myocardial p
124 mediate and maintain collateral formation in coronary vessel occlusion are yet to be identified.
127 DGFRbeta(-/-) hearts failed to form dominant coronary vessels on the ventral heart surface, had a thi
128 the left main stem, >70% stenosis in a major coronary vessel, or 30% to 70% stenosis with fractional
129 the current view of a common source for the coronary vessels, our findings indicate that the coronar
133 Patients with a greater number of diseased coronary vessels received an IMA more often (one, 78%; t
134 or stable or unstable angina in small native coronary vessels (reference vessel diameter and stent si
135 uggest that correct transmural patterning of coronary vessels requires the correct transmural express
141 current was compared in cells isolated from coronary vessels taken from different points along the v
142 to develop the fine and continuous plexus of coronary vessels that cover the entire ventricle around
143 h muscle and endothelial cell lineage of the coronary vessels, the expression of WT1 and RALDH2 becom
144 ositive EPDCs, and provoked anomalies in the coronary vessels, the ventricular myocardium, and the AV
145 endothelium-derived peptide that constricts coronary vessels through stimulation of the ET-A and ET-
146 of subjects with stenosis of all three major coronary vessels to be distinguished from subjects with
147 etion of KCNJ8 blunted the responsiveness of coronary vessels to cytokine- or metabolic-mediated vaso
150 RI) late gadolinium enhancement (LGE) of the coronary vessel wall can detect and grade coronary allog
156 approach may be useful for the assessment of coronary vessel wall in patients with suspected coronary
160 isotropic resolution identified an increased coronary vessel wall thickness with preservation of lume
165 Restoration of the dilatory capacity of coronary vessels was required to rescue the Kir6.1 knock
166 ctors of >/=70% stenosis in at least 1 major coronary vessel were identified from >200 candidate vari
167 ODS AND A large number of cardiomyocytes and coronary vessels were created in a rather short period o
171 e due to a widespread process throughout the coronary vessels, which may have implications for the ma
175 efficiently differentiate into myocytes and coronary vessels with no detectable differentiation into
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