Journal articles: 'Coronary vasculature'

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TAYLOR, R. "Smoking and the coronary vasculature." Journal of Molecular and Cellular Cardiology 18 (1986): 23. http://dx.doi.org/10.1016/s0022-2828(86)80553-3.

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Kapuria, Subir, Tyler Yoshida, and Ching-Ling Lien. "Coronary Vasculature in Cardiac Development and Regeneration." Journal of Cardiovascular Development and Disease 5, no. 4 (December 17, 2018): 59. http://dx.doi.org/10.3390/jcdd5040059.

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Functional coronary circulation is essential for a healthy heart in warm-blooded vertebrates, and coronary diseases can have a fatal consequence. Despite the growing interest, the knowledge about the coronary vessel development and the roles of new coronary vessel formation during heart regeneration is still limited. It is demonstrated that early revascularization is required for efficient heart regeneration. In this comprehensive review, we first describe the coronary vessel formation from an evolutionary perspective. We further discuss the cell origins of coronary endothelial cells and perivascular cells and summarize the critical signaling pathways regulating coronary vessel development. Lastly, we focus on the current knowledge about the molecular mechanisms regulating heart regeneration in zebrafish, a genetically tractable vertebrate model with a regenerative adult heart and well-developed coronary system.

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Kassab, Ghassan S. "The Coronary Vasculature and its Reconstruction." Annals of Biomedical Engineering 28, no. 8 (August 2000): 903–15. http://dx.doi.org/10.1114/1.1308494.

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Lin, Kai, and James C. Carr. "MR Imaging of the Coronary Vasculature." Radiologic Clinics of North America 53, no. 2 (March 2015): 345–53. http://dx.doi.org/10.1016/j.rcl.2014.11.003.

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Roux, Sebastien, Jean-Paul Clozel, Walter Fischli, and Herbert Kuhn. "Isoproterenol Impairs the Rat Coronary Vasculature." Journal of Cardiovascular Pharmacology 19, no. 4 (April 1992): 525–31. http://dx.doi.org/10.1097/00005344-199204000-00008.

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Fushimi, Etsuko, Takashi Saito, Yasutsugu Kudo, Tohru Abe, Yutaka Kimura, Kazuhito Takahashi, and Mamoru Miura. "Endothelial injury in reperfused coronary vasculature." Journal of Molecular and Cellular Cardiology 24 (May 1992): 163. http://dx.doi.org/10.1016/0022-2828(92)90514-z.

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de Beer, Vincent J., Shawn B. Bender, Yannick J. Taverne, Fen Gao, Dirk J. Duncker, M. Harold Laughlin, and Daphne Merkus. "Exercise limits the production of endothelin in the coronary vasculature." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 5 (May 2011): H1950—H1959. http://dx.doi.org/10.1152/ajpheart.00954.2010.

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We previously demonstrated that endothelin (ET)-mediated coronary vasoconstriction wanes with increasing exercise intensity via a nitric oxide- and prostacyclin-dependent mechanism (Ref. 23). Therefore, we hypothesized that the waning of ET coronary vasoconstriction during exercise is the result of decreased production of ET and/or decreased ET receptor sensitivity. We investigated coronary ET receptor sensitivity using intravenous infusion of ET and coronary ET production using intravenous infusion of the ET precursor Big ET, at rest and during continuous treadmill exercise at 3 km/h in 16 chronically instrumented swine. In the systemic vasculature, Big ET and ET induced similar changes in hemodynamic parameters at rest and during continuous exercise at 3 km/h, indicating that exercise does not alter ET production or receptor sensitivity in the systemic vasculature. In the coronary vasculature, infusion of ET resulted in similar dose-dependent decreases in coronary blood flow and coronary venous oxygen tension and saturation at rest and during exercise. In contrast, administration of Big ET resulted in dose-dependent decreases in coronary blood flow, as well as coronary venous oxygen tension and saturation at rest. These effects of Big ET were significantly reduced during exercise. Altogether, our data indicate that continuous exercise at 3 km/h attenuates ET-mediated coronary vasoconstriction through reduced production of ET from Big ET rather than through reduced ET sensitivity of the coronary vasculature. The decreased ET production during exercise likely contributes to metabolic coronary vasodilation.

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Xiao, Ruoxiu, Jian Yang, Mahima Goyal, Yue Liu, and Yongtian Wang. "Automatic Vasculature Identification in Coronary Angiograms by Adaptive Geometrical Tracking." Computational and Mathematical Methods in Medicine 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/796342.

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As the uneven distribution of contrast agents and the perspective projection principle of X-ray, the vasculatures in angiographic image are with low contrast and are generally superposed with other organic tissues; therefore, it is very difficult to identify the vasculature and quantitatively estimate the blood flow directly from angiographic images. In this paper, we propose a fully automatic algorithm named adaptive geometrical vessel tracking (AGVT) for coronary artery identification in X-ray angiograms. Initially, the ridge enhancement (RE) image is obtained utilizing multiscale Hessian information. Then, automatic initialization procedures including seed points detection, and initial directions determination are performed on the RE image. The extracted ridge points can be adjusted to the geometrical centerline points adaptively through diameter estimation. Bifurcations are identified by discriminating connecting relationship of the tracked ridge points. Finally, all the tracked centerlines are merged and smoothed by classifying the connecting components on the vascular structures. Synthetic angiographic images and clinical angiograms are used to evaluate the performance of the proposed algorithm. The proposed algorithm is compared with other two vascular tracking techniques in terms of the efficiency and accuracy, which demonstrate successful applications of the proposed segmentation and extraction scheme in vasculature identification.

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Westerhof, Nico, Christa Boer, Regis R. Lamberts, and Pieter Sipkema. "Cross-Talk Between Cardiac Muscle and Coronary Vasculature." Physiological Reviews 86, no. 4 (October 2006): 1263–308. http://dx.doi.org/10.1152/physrev.00029.2005.

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The cardiac muscle and the coronary vasculature are in close proximity to each other, and a two-way interaction, called cross-talk, exists. Here we focus on the mechanical aspects of cross-talk including the role of the extracellular matrix. Cardiac muscle affects the coronary vasculature. In diastole, the effect of the cardiac muscle on the coronary vasculature depends on the (changes in) muscle length but appears to be small. In systole, coronary artery inflow is impeded, or even reversed, and venous outflow is augmented. These systolic effects are explained by two mechanisms. The waterfall model and the intramyocardial pump model are based on an intramyocardial pressure, assumed to be proportional to ventricular pressure. They explain the global effects of contraction on coronary flow and the effects of contraction in the layers of the heart wall. The varying elastance model, the muscle shortening and thickening model, and the vascular deformation model are based on direct contact between muscles and vessels. They predict global effects as well as differences on flow in layers and flow heterogeneity due to contraction. The relative contributions of these two mechanisms depend on the wall layer (epi- or endocardial) and type of contraction (isovolumic or shortening). Intramyocardial pressure results from (local) muscle contraction and to what extent the interstitial cavity contracts isovolumically. This explains why small arterioles and venules do not collapse in systole. Coronary vasculature affects the cardiac muscle. In diastole, at physiological ventricular volumes, an increase in coronary perfusion pressure increases ventricular stiffness, but the effect is small. In systole, there are two mechanisms by which coronary perfusion affects cardiac contractility. Increased perfusion pressure increases microvascular volume, thereby opening stretch-activated ion channels, resulting in an increased intracellular Ca2+transient, which is followed by an increase in Ca2+sensitivity and higher muscle contractility (Gregg effect). Thickening of the shortening cardiac muscle takes place at the expense of the vascular volume, which causes build-up of intracellular pressure. The intracellular pressure counteracts the tension generated by the contractile apparatus, leading to lower net force. Therefore, cardiac muscle contraction is augmented when vascular emptying is facilitated. During autoregulation, the microvasculature is protected against volume changes, and the Gregg effect is negligible. However, the effect is present in the right ventricle, as well as in pathological conditions with ineffective autoregulation. The beneficial effect of vascular emptying may be reduced in the presence of a stenosis. Thus cardiac contraction affects vascular diameters thereby reducing coronary inflow and enhancing venous outflow. Emptying of the vasculature, however, enhances muscle contraction. The extracellular matrix exerts its effect mainly on cardiac properties rather than on the cross-talk between cardiac muscle and coronary circulation.

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Taylor, Adam Michael, Joe McAleer, and Quenton Wessels. "Novel bilateral bifurcation of the coronary vasculature." Anatomy & Cell Biology 54, no. 1 (March 31, 2021): 132–35. http://dx.doi.org/10.5115/acb.20.241.

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Libby, Peter. "Atherosclerosis: Disease Biology Affecting the Coronary Vasculature." American Journal of Cardiology 98, no. 12 (December 2006): S3—S9. http://dx.doi.org/10.1016/j.amjcard.2006.09.020.

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Chen, Hao, Lei Cheng, Jie Ting Zhang, Ming Li, and Hsiao Chang Chan. "Reconstitution of coronary vasculature in ischemic hearts." Cell Biology International 32, no. 3 (March 2008): S13. http://dx.doi.org/10.1016/j.cellbi.2008.01.064.

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13

Tomanek, Robert J. "Formation of the coronary vasculature during development." Angiogenesis 8, no. 3 (November 25, 2005): 273–84. http://dx.doi.org/10.1007/s10456-005-9014-9.

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Tian, Xueying, Tianyuan Hu, Hui Zhang, Lingjuan He, Xiuzhen Huang, Qiaozhen Liu, Wei Yu, et al. "De novo formation of a distinct coronary vascular population in neonatal heart." Science 345, no. 6192 (July 3, 2014): 90–94. http://dx.doi.org/10.1126/science.1251487.

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The postnatal coronary vessels have been viewed as developing through expansion of vessels formed during the fetal period. Using genetic lineage tracing, we found that a substantial portion of postnatal coronary vessels arise de novo in the neonatal mouse heart, rather than expanding from preexisting embryonic vasculature. Our data show that lineage conversion of neonatal endocardial cells during trabecular compaction generates a distinct compartment of the coronary circulation located within the inner half of the ventricular wall. This lineage conversion occurs within a brief period after birth and provides an efficient means of rapidly augmenting the coronary vasculature. This mechanism of postnatal coronary vascular growth provides avenues for understanding and stimulating cardiovascular regeneration following injury and disease.

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Hatcher, Cathy J., Nata Y. S. G. Diman, Min-Su Kim, David Pennisi, Yan Song, Marsha M. Goldstein, Takashi Mikawa, and Craig T. Basson. "A role for Tbx5 in proepicardial cell migration during cardiogenesis." Physiological Genomics 18, no. 2 (July 8, 2004): 129–40. http://dx.doi.org/10.1152/physiolgenomics.00060.2004.

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Transcriptional regulatory cascades during epicardial and coronary vascular development from proepicardial progenitor cells remain to be defined. We have used immunohistochemistry of human embryonic tissues to demonstrate that the TBX5 transcription factor is expressed not only in the myocardium, but also throughout the embryonic epicardium and coronary vasculature. TBX5 is not expressed in other human fetal vascular beds. Furthermore, immunohistochemical analyses of human embryonic tissues reveals that unlike their epicardial counterparts, delaminating epicardial-derived cells do not express TBX5 as they migrate through the subepicardium before undergoing epithelial-mesenchymal transformation required for coronary vasculogenesis. In the chick, Tbx5 is expressed in the embryonic proepicardial organ (PEO), which is composed of the epicardial and coronary vascular progenitor cells. Retrovirus-mediated overexpression of human TBX5 inhibits cell incorporation of infected proepicardial cells into the nascent chick epicardium and coronary vasculature. TBX5 overexpression as well as antisense-mediated knockdown of chick Tbx5 produce a cell-autonomous defect in the PEO that prevents proepicardial cell migration. Thus, both increasing and decreasing Tbx5 dosage impairs development of the proepicardium. Culture of explanted PEOs demonstrates that untreated chick proepicardial cells downregulate Tbx5 expression during cell migration. Therefore, we propose that Tbx5 participates in regulation of proepicardial cell migration, a critical event in the establishment of the epicardium and coronary vasculature.

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Kaimovitz, Benjamin, Yoram Lanir, and Ghassan S. Kassab. "A full 3-D reconstruction of the entire porcine coronary vasculature." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 4 (October 2010): H1064—H1076. http://dx.doi.org/10.1152/ajpheart.00151.2010.

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We have previously reconstructed the entire coronary arterial tree of the porcine heart down to the first segment of capillaries. Here, we extend the vascular model through the capillary bed and the entire coronary venous system. The reconstruction was based on comprehensive morphometric data previously measured in the porcine heart. The reconstruction was formulated as a large-scale optimization process, subject to both global constraints relating to the location of the larger veins and to local constraints of measured morphological features. The venous network was partitioned into epicardial, transmural, and perfusion functional subnetworks. The epicardial portion was generated by a simulated annealing search for the optimal coverage of the area perfused by the arterial epicardial vessels. The epicardial subnetwork and coronary arterial capillary network served as boundary conditions for the reconstruction of the in-between transmural and perfusion networks, which were generated to optimize vascular homogeneity. Five sets of full coronary trees, which spanned the entire network down to the capillary level, were reconstructed. The total number of reconstructed venous segments was 17,148,946 ± 1,049,498 ( n = 5), which spanned the coronary sinus ( order −12) to the first segment of the venous capillary ( order 0v). Combined with the reconstructed arterial network, the number of vessel segments for the entire coronary network added up to 27,307,376 ± 1,155,359 ( n = 5). The reconstructed full coronary vascular network agreed with the gross anatomy of coronary networks in terms of structure, location of major vessels, and measured morphometric statistics of native coronary networks. This is the first full model of the entire coronary vasculature, which can serve as a foundation for realistic large-scale coronary flow analysis.

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Liu, Yaofang, Wenlong Wan, Xinyue Zhang, Shaoyu Liu, Yingdi Liu, Hu Liu, Xueying Zeng, Weiguo Wang, and Qing Zhang. "Segmentation and Automatic Identification of Vasculature in Coronary Angiograms." Computational and Mathematical Methods in Medicine 2021 (October 7, 2021): 1–10. http://dx.doi.org/10.1155/2021/2747274.

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Coronary angiography is the “gold standard” for the diagnosis of coronary heart disease, of which vessel segmentation and identification technologies are paid much attention to. However, because of the characteristics of coronary angiograms, such as the complex and variable morphology of coronary artery structure and the noise caused by various factors, there are many difficulties in these studies. To conquer these problems, we design a preprocessing scheme including block-matching and 3D filtering, unsharp masking, contrast-limited adaptive histogram equalization, and multiscale image enhancement to improve the quality of the image and enhance the vascular structure. To achieve vessel segmentation, we use the C-V model to extract the vascular contour. Finally, we propose an improved adaptive tracking algorithm to realize automatic identification of the vascular skeleton. According to our experiments, the vascular structures can be successfully highlighted and the background is restrained by the preprocessing scheme, the continuous contour of the vessel is extracted accurately by the C-V model, and it is verified that the proposed tracking method has higher accuracy and stronger robustness compared with the existing adaptive tracking method.

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Wallace, Arthur W., Mark B. Ratcliffe, Daniel Galindez, and James S. Kong. "L-Arginine Infusion Dilates Coronary Vasculature in Patients Undergoing Coronary Bypass Surgery." Anesthesiology 90, no. 6 (June 1, 1999): 1577–86. http://dx.doi.org/10.1097/00000542-199906000-00013.

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Background Nitric oxide-dependent factors (serotonin, activated platelets, acetylcholine) cause vasodilation in normal coronary arteries but vasoconstrict atherosclerotic vessels. This experiment tested the hypothesis that intravenous systemic infusions of L-arginine, a precursor for nitric oxide production, dilate the coronary vascular bed of patients undergoing coronary artery bypass graft surgery. Methods Twenty patients scheduled for coronary artery bypass graft surgery surgery were studied in a prospective, blinded, randomized clinical trial. Saphenous vein graft blood flow was measured with a transit time flow probe, and coronary vascular resistance was calculated. After weaning from bypass, patients were given a venous infusion (placebo or 10% arginine hydrochloride [30 g]) over 15 min. Arterial blood samples for the determination of L-arginine and L-citrulline levels were drawn before, 10 min after starting infusion, and 10 min after end of infusion. Results The placebo group experienced an increase in mean arterial pressure and coronary vascular resistance and a decrease in graft blood flow. Patients in the L-arginine group maintained their baseline values. Mean arterial pressure (L-arginine, 88+/-17 to 92+/-13 mmHg vs. placebo, 80+/-12 to 92+/-9 mmHg, P = 0.021), coronary vascular resistance (L-arginine, 97,000+/-60,000 to 99,600+/-51,000 dynes x s x cm(-5) vs. placebo, 81,000+/-69,000 to 117,000+/-64,000 dynes x s x cm(-5), P = 0.05), and graft blood flow (L-arginine, 55+/-25 to 50+/-19 ml/min vs. placebo, 60+/-34 to 46+/-18, P = 0.05) remained more stable in the L-arginine-treated patients. Conclusions Systemic L-arginine infusion reduced postbypass coronary vasoconstriction. There were no adverse events associated with the drug infusion.

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Tezcan, Mehmet, Omer Yiginer, and Bekir Sitki Cebeci. "Twin hearts: identical anomalous coronary origin, individual vasculature." Anadolu Kardiyoloji Dergisi/The Anatolian Journal of Cardiology 15, no. 4 (April 9, 2015): E11. http://dx.doi.org/10.5152/akd.2015.6064.

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Fuller, Ithiel A., and Mark A. Wood. "Intramural Coronary Vasculature Prevents Transmural Radiofrequency Lesion Formation." Circulation 107, no. 13 (April 8, 2003): 1797–803. http://dx.doi.org/10.1161/01.cir.0000058705.97823.f4.

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Tomanek, R. J. "Formation of the coronary vasculature: a brief review." Cardiovascular Research 31, supp1 (February 1, 1996): E46—E51. http://dx.doi.org/10.1016/s0008-6363(95)00205-7.

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Hatcher, Cathy J., and Craig T. Basson. "Modeling Development of the Epicardium and Coronary Vasculature." Circulation Research 92, no. 5 (March 21, 2003): 477–79. http://dx.doi.org/10.1161/01.res.0000064380.47325.d4.

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23

Kassab, Ghassan S., Daniel H. Lin, and Yuan-Cheng B. Fung. "Consequences of pruning in morphometry of coronary vasculature." Annals of Biomedical Engineering 22, no. 4 (July 1994): 398–403. http://dx.doi.org/10.1007/bf02368246.

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Tomanek, Robert J. "Response of the coronary vasculature to myocardial hypertrophy." Journal of the American College of Cardiology 15, no. 3 (March 1990): 528–33. http://dx.doi.org/10.1016/0735-1097(90)90620-5.

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Zenin, O. K., N. N. Kizilova, and E. N. Filippova. "Studies on the structure of human coronary vasculature." Biophysics 52, no. 5 (October 2007): 499–503. http://dx.doi.org/10.1134/s0006350907050089.

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Bowers, Stephanie L. K., and Troy A. Baudino. "Cardiac Myocyte–Fibroblast Interactions and the Coronary Vasculature." Journal of Cardiovascular Translational Research 5, no. 6 (September 18, 2012): 783–93. http://dx.doi.org/10.1007/s12265-012-9407-2.

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TOMANEK, R. "Formation of the coronary vasculature: a brief review." Cardiovascular Research 31 (February 1996): E46—E51. http://dx.doi.org/10.1016/0008-6363(95)00205-7.

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Jackson, G. "PHOSPHODIESTERASE 5 INHIBITION: EFFECTS ON THE CORONARY VASCULATURE." International Journal of Clinical Practice 55, no. 3 (April 2001): 183–88. http://dx.doi.org/10.1111/j.1742-1241.2001.tb11011.x.

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Kassab, Ghassan S., Edith Pallencaoe, Amy Schatz, and Yuan-Cheng B. Fung. "Longitudinal position matrix of the pig coronary vasculature and its hemodynamic implications." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 6 (December 1, 1997): H2832—H2842. http://dx.doi.org/10.1152/ajpheart.1997.273.6.h2832.

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Hemodynamic analysis of coronary blood flow must be based on a statistically valid geometric model of the coronary vasculature. We have previously developed a diameter-defined Strahler model for the arterial and venous trees and a network model for the capillaries. A full set of data describing the geometric properties of the porcine coronary vasculature was given. The order number, diameter, length, connectivity matrix [ m,n] (CM), and parallel-series features were measured for all orders of vessels of the right coronary artery (RCA), left anterior descending artery (LAD), left circumflex artery (LCX), and coronary venous system. The purpose of the present study is to present another feature of the branching pattern of the coronary vasculature: the longitudinal position matrix [ m,n] (LPM), whose component in row m and column n is the fractional longitudinal position of the branch point on vessels of order n at which vessels of order m branch off ( m ≤ n). The LPM of the pig RCA, LAD and LCX arterial trees, as well as the coronary sinusal and thebesian venous trees, are presented. The hemodynamic implications of the LPM are illustrated by comparing two kinds of circuits: one, the CM + LPM model, simulates the mean data on the morphology (diameters, lengths, and numbers), CM, and LPM of vessels, whereas the other, the CM model, simulates the mean data on the morphology and CM without considering the LPM. We found that the LPM affects the hemodynamics of coronary blood flow especially with regard to the nonuniformity or dispersion of flow distribution.

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Tangkawattana, P., M. Muto, T. Nakayama, A. Karkoura, S. Yamano, and M. Yamaguchi. "Prevalence, vasculature, and innervation of myocardial bridges in dogs." American Journal of Veterinary Research 58, no. 11 (November 1, 1997): 1209–15. http://dx.doi.org/10.2460/ajvr.1997.58.11.1209.

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SUMMARY Objective To report gross anatomic examination of the canine myocardial bridge (MB), a muscular band found above the coronary artery (CA), with respect to its occurrence, location, vascularization, and innervation. Sample Population 629 canine hearts obtained within 1 to 3 hours after euthanasia. Procedure After an incision was made at the left fifth intercostal space, the pericardial sac was cut open, and if an MB was present, the heart, lungs, and annexed structures were removed together and subsequently subjected to macroscopic examination of MB musculature and innervation after formalin fixation. Vascular casting was performed by use of methyl methacrylate perfusion. Results Of the 629 canine hearts examined, 189 (30%) had MB, occurrence of which was independent of sex, age, and breed. Among 13 MB-containing specimens examined in detail, there was great variation in thickness (0.11 to 2.24 mm; mean, 0.45 mm) of MB and distance (24 to 236 μm; mean, 103 μm) between the MB and the paraconal interventricular branch of the left CA (PIBL). One pair or 2 pairs of blood vessels from the PIBL supplied the MB muscle. Venous blood returned to the coronary circulation via the branches of the great coronary vein coursing on both sides of the PIBL, in close contact with the PIBL and the groove wall. The 2 veins rejoined at the upper portion of the PIBL and passed obliquely to the coronary groove under the left auricle, and finally drained the blood through the coronary sinus into the right ventricle. Innervation to the MB muscle was derived from nerve branches of the middle cervical ganglion and left vagus nerve. Conclusion Prevalence and localization of MB in dogs and human beings are similar. Vascularization of the MB muscle originates from the PIBL. The cervical ganglion and vagus nerve control the MB muscle. (Am J Vet Res 1997;58:1209–1215)

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Banerjee, Indroneal, John W. Fuseler, Colby A. Souders, Stephanie L. K. Bowers, and Troy A. Baudino. "The Role of Interleukin-6 in the Formation of the Coronary Vasculature." Microscopy and Microanalysis 15, no. 5 (August 27, 2009): 415–21. http://dx.doi.org/10.1017/s1431927609990353.

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AbstractThe formation and the patterning of the coronary vasculature are critical to the development and pathology of the heart. Alterations in cytokine signaling and biomechanical load can alter the vascular distribution of the vessels within the heart. Changes in the physical patterning of the vasculature can have significant impacts on the relationships of the pressure-flow network and distribution of critical growth and survival factors to the tissue. Interleukin-6 (IL-6) is a pleiotropic cytokine that regulates several biological processes, including vasculogenesis. Using both immunohistological and cardioangiographic analyses, we tested the hypothesis that IL-6-loss will result in decreased vessel density, along with changes in vascular distribution. Moreover, given the impact of vascular patterning on pressure-flow and distribution mechanics, we utilized non-Euclidean geometrical fractal analysis to quantify the changes in patterning resulting from IL-6-loss. Our analyses revealed that IL-6-loss results in a decreased capillary density and increase in intercapillary distances, but does not alter vessel size or diameter. We also observed that the IL-6−/− coronary vasculature had a marked increase in fractal dimension (D value), indicating that IL-6-loss alters vascular patterning. Characterization of IL-6-loss on coronary vasculature may lend insight into the role of IL-6 in the formation and patterning of the vascular bed.

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Kumar, Mukesh, Muhammad Naeem Mengal, Taimur Asif Ali, and Rizwan Qurban Ali Khawaja. "Nightmare of Coronary Wire Loop Jail from Side Branch to Main Vessel during Primary Percutaneous Coronary Interventions." Pakistan Journal of Cardiovascular Intervention 2, no. 1 (June 1, 2022): 35–39. http://dx.doi.org/10.58889/pjcvi.2.35.39.

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Background: Guide wire breakage and entrapment inside the coronary circulation are rare but extremely dangerous complications of coronary intervention that can be life-threatening by resulting in embolization of thrombi, perforation of the coronary vasculature, and thrombus development. Case Presentation: A male patient who developed a complication of left circumflex artery guide wire looped and trapped under left anterior descending artery (LAD) stent during Primary PCI and went for emergency cardiac surgery for removal. Management & Results: Guide wire entrapment during the intervention should always consider this as a risk factor, especially when intervening in the tortuous coronary vasculature, and it is important to keep several wires, snare wires, and a surgical team on board as a backup. Conclusion: Although guide wire entanglement infrequently occurs during interventions, interventionists should always be on the lookout for it, especially in patients with convoluted coronary arteries. Before working on these patient's coronary arteries, it's essential to have a surgical team, lots of wires, and snare wires on hand. These preventative measures may be effective in reducing death and morbidity under adverse conditions.

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Keelan, Jonathan, Emma M. L. Chung, and James P. Hague. "Simulated annealing approach to vascular structure with application to the coronary arteries." Royal Society Open Science 3, no. 2 (February 2016): 150431. http://dx.doi.org/10.1098/rsos.150431.

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Do the complex processes of angiogenesis during organism development ultimately lead to a near optimal coronary vasculature in the organs of adult mammals? We examine this hypothesis using a powerful and universal method, built on physical and physiological principles, for the determination of globally energetically optimal arterial trees. The method is based on simulated annealing, and can be used to examine arteries in hollow organs with arbitrary tissue geometries. We demonstrate that the approach can generate in silico vasculatures which closely match porcine anatomical data for the coronary arteries on all length scales, and that the optimized arterial trees improve systematically as computational time increases. The method presented here is general, and could in principle be used to examine the arteries of other organs. Potential applications include improvement of medical imaging analysis and the design of vascular trees for artificial organs.

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Männer, Jörg. "Embryology of congenital ventriculo-coronary communications: a study on quail-chick chimeras." Cardiology in the Young 10, no. 3 (May 2000): 233–38. http://dx.doi.org/10.1017/s1047951100009161.

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AbstractVentriculo-coronary arterial communications are rare congenital heart defects which have been explained traditionally on the basis of abnormal persistence of such communications found in the normal developing heart. Recent studies, however, have suggested that these embryonic communications might be an incidental finding rather than a normal feature. Thus, it has been suggested that congenital ventriculo-coronary communications do not represent remnants of normal embryonic vessels, but rather represent acquired lesions. In the present study, hearts were constructed in embryonic chicks in which the coronary vasculature was almost completely derived from a quail-donor. After immunohistochemical staining of the quail-derived coronary endothelium, chimeric hearts were analysed with respect to the presence of embryonic ventriculo-coronary communications, and with respect to the origin of these structures from either coronary arteries or endocardium. The results demonstrate the normal presence of ventriculo-coronary communications in avian embryonic hearts. They show, furthermore, that these structures are of coronary endothelial origin. The findings are in accord with the traditional view on the pathogenesis of congenital ventriculo-coronary communications. The roles of elevated ventricular pressure, abnormal remodelling of the developing myocardium, and of abnormal growth of the coronary vasculature are discussed relative to the pathogenesis of congenital ventriculo-coronary communications.

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Merkus, Daphne, Anna K. Brzezinska, Cuihua Zhang, Shuichi Saito, and William M. Chilian. "Cardiac myocytes control release of endothelin-1 in coronary vasculature." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 5 (May 2005): H2088—H2092. http://dx.doi.org/10.1152/ajpheart.00522.2003.

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α-Adrenergic vasoconstriction in the coronary circulation is mediated through α-adrenoceptors on cardiac myocytes and subsequent release of endothelin, a very potent, long-lasting vasoconstrictor. Recent studies found that adult cardiac myocytes do not express the preproendothelin gene. Thus we hypothesized that α-adrenoceptor stimulation on the cardiac myocytes results in the production of an endothelin-releasing factor, which stimulates the coronary vasculature to produce endothelin. We tested this hypothesis by using an in vitro model in which isolated adult rat cardiac myocytes can be stimulated with an α-adrenoceptor agonist (phenylephrine). Their bathing fluid is then transferred to isolated coronary arterioles, and vasoactive responses are measured. To identify the source of endothelin, the endothelin-converting enzyme inhibitor phosphoramidon was added to either the myocytes or the isolated arterioles. Phenylephrine enhanced the vasoconstrictor properties of the myocyte bathing fluid. Administration of phosphoramidon (in either the presence or the absence of phenylephrine) to the myocytes had no effect on the vasoactive properties of the bathing fluid. In contrast, administration of phosphoramidon to the isolated arteriole before administration of the bathing fluid converted vasoconstriction to vasodilation, similar to the effect of the endothelin A receptor antagonist JKC-301, indicating that the endothelin is indeed produced by the coronary vasculature. Administration of the angiotensin type 1 receptor antagonist losartan to the vessel bath enhanced vasodilation to the bathing fluid of the phenylephrine-treated but not control myocytes. In conclusion, during α-adrenergic activation cardiac myocytes release a factor, probably angiotensin II, that stimulates the vascular production of endothelin. Although the physiological implications of this mechanism are not obvious, this may represent a protective mechanism that integrates neuronal vasoconstrictor mechanisms with myocardial metabolism, which minimizes periods of both coronary underperfusion and overperfusion.

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Liu, Xiaolei, and Guillermo Oliver. "New insights about the lymphatic vasculature in cardiovascular diseases." F1000Research 8 (October 29, 2019): 1811. http://dx.doi.org/10.12688/f1000research.20107.1.

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The heart contains a complex network of blood and lymphatic vessels. The coronary blood vessels provide the cardiac tissue with oxygen and nutrients and have been the major focus of research for the past few decades. Cardiac lymphatic vessels, which consist of lymphatic capillaries and collecting lymphatic vessels covering all layers of the heart, transport excess fluid from the interstitium and play important roles in maintaining tissue fluid balance. Unlike for the coronary blood vessels, until a few years ago, not much information was available on the origin and function of the cardiac-associated lymphatic vasculature. A growing body of evidence indicates that cardiac lymphatic vessels (lymphatics) may serve as a therapeutic cardiovascular target.

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37

Vials, Amanda J., and Geoffrey Burnstock. "Effects of pyrimidines on the guinea-pig coronary vasculature." British Journal of Pharmacology 110, no. 3 (November 1993): 1091–97. http://dx.doi.org/10.1111/j.1476-5381.1993.tb13926.x.

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Mickelson, Judith K., Paul J. Simpson, Charles V. Jackson, and Benedict R. Lucchesi. "Protection of Myocardial Function and Coronary Vasculature by Streptokinase." Journal of Cardiovascular Pharmacology 12, no. 2 (August 1988): 186–95. http://dx.doi.org/10.1097/00005344-198808000-00009.

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39

Roux, E., M. Deloume, R. Markovic, M. Gosak, M. Marhl, C. Duplàa, and T. Couffinhal. "Quantitative analysis of 3D imaging of mouse coronary vasculature." Archives of Cardiovascular Diseases Supplements 9, no. 2 (April 2017): 215. http://dx.doi.org/10.1016/s1878-6480(17)30533-5.

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Kennedy, Jennifer A., Puneet Mohan, Maria A. Pelle, Steven R. Wade, and John D. Horowitz. "The effects of perhexiline on the rat coronary vasculature." European Journal of Pharmacology 370, no. 3 (April 1999): 263–70. http://dx.doi.org/10.1016/s0014-2999(99)00106-5.

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Harrison, Michael R. M., Jeroen Bussmann, Ying Huang, Long Zhao, Arthela Osorio, C. Geoffrey Burns, Caroline E. Burns, Henry M. Sucov, Arndt F. Siekmann, and Ching-Ling Lien. "Chemokine-Guided Angiogenesis Directs Coronary Vasculature Formation in Zebrafish." Developmental Cell 33, no. 4 (May 2015): 442–54. http://dx.doi.org/10.1016/j.devcel.2015.04.001.

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42

Marszalek, Richard J., R. John Solaro, and Beata M. Wolska. "Coronary arterial vasculature in the pathophysiology of hypertrophic cardiomyopathy." Pflügers Archiv - European Journal of Physiology 471, no. 5 (October 29, 2018): 769–80. http://dx.doi.org/10.1007/s00424-018-2224-y.

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Maresca, David, Mafalda Correia, Olivier Villemain, Alain Bizé, Lucien Sambin, Mickael Tanter, Bijan Ghaleh, and Mathieu Pernot. "Noninvasive Imaging of the Coronary Vasculature Using Ultrafast Ultrasound." JACC: Cardiovascular Imaging 11, no. 6 (June 2018): 798–808. http://dx.doi.org/10.1016/j.jcmg.2017.05.021.

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Kolesová, Hana, Martin Bartoš, Wan Chin Hsieh, Veronika Olejníčková, and David Sedmera. "Novel approaches to study coronary vasculature development in mice." Developmental Dynamics 247, no. 8 (July 1, 2018): 1018–27. http://dx.doi.org/10.1002/dvdy.24637.

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Nanka, Ondrej, Petra Krizova, Michal Fikrle, Michal Tuma, Milan Blaha, Milos Grim, and David Sedmera. "Abnormal Myocardial and Coronary Vasculature Development in Experimental Hypoxia." Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology 291, no. 10 (October 2008): 1187–99. http://dx.doi.org/10.1002/ar.20738.

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Nanka, Ondrej, Petra Krizova, Michal Fikrle, Michal Tuma, Milan Blaha, Milos Grim, and David Sedmera. "Abnormal Myocardial and Coronary Vasculature Development in Experimental Hypoxia." Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology 291, no. 10 (October 2008): spc1. http://dx.doi.org/10.1002/ar.20790.

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CANNAN, CHARLES R., STUART T. HIGANO, DAVID R. HOLMES, KIRK N. GARRATT, and AMIR LERMAN. "Beyond the Coronary Angiogram: Further Evaluation of the Coronary Vasculature and Endothelial Function." Journal of Interventional Cardiology 9, no. 2 (April 1996): 153–61. http://dx.doi.org/10.1111/j.1540-8183.1996.tb00610.x.

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Khayyal, M. A., C. Eng, D. Franzen, J. A. Breall, and E. S. Kirk. "Effects of vasopressin on the coronary circulation: reserve and regulation during ischemia." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 4 (April 1, 1985): H516—H522. http://dx.doi.org/10.1152/ajpheart.1985.248.4.h516.

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In 18 dogs, intracoronary infusion of vasopressin produced a 40% reduction in coronary flow without significantly affecting systemic hemodynamics. The blood flow reduction occurred in a uniform transmural pattern without evidence of a gradient. The reduction in coronary flow resulted in a decrease in regional contractility as determined by isometric strain gauge arches. The decrease in regional contractility was transiently reversed by bolus injection of adenosine into the perfusion line. This suggests that the reduction of blood flow due to vasopressin was causing ischemia. Evidence for ischemia was also supported by measurements of local vein and tissue lactate production. Despite the apparently ischemic conditions, the vascular bed demonstrated evidence for significant reserve and regulation. Pressure-flow relationships performed under control and during vasopressin infusion demonstrated that the coronary vasculature retained its ability to regulate or defend a given level of coronary flow over a range of coronary perfusion pressures. Vasopressin produced a mild decrease in the peak hyperemic flow after a 15-s coronary occlusion and shortened the duration of reactive hyperemia. These overall findings are compatible with a predominant vasoconstrictor effect on the distal coronary vasculature. A role for a myogenic factor in the control of the coronary circulation is suggested, which is amplified by vasopressin.

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Goland, Javier, Ezequiel Yasuda, Martín Monteverde, and Silvia Garbugino. "Catheter fragment retrieved from an arterial branch of the right middle cerebral artery." Surgical Neurology International 10 (June 28, 2019): 129. http://dx.doi.org/10.25259/sni-171-2019.

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Background: Cerebral emboli is a rare complication of endovascular procedures and foreign bodies in the cerebrovascular system can lead to stroke. When an intravascular foreign body is identified, endovascular retrieval should be attempted due to its high success rate and minimal morbidity. Case Description: A 59-year-old male patient underwent cine-coronario-graphy through a trans-radial approach because of angina. During the study, a 6Fr catheter fragment ruptured, detached and migrated to a right middle cerebral artery branch. We recovered it with a coronary balloon. Conclusion: A coronary angioplasty balloon is an option for retrieving foreign objects or device fragments that have migrated into cerebral vasculature.

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Roth, D. M., F. C. White, O. Mathieu-Costello, B. D. Guth, G. Heusch, C. M. Bloor, and J. C. Longhurst. "Effects of left circumflex Ameroid constrictor placement on adrenergic innervation of myocardium." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 6 (December 1, 1987): H1425—H1434. http://dx.doi.org/10.1152/ajpheart.1987.253.6.h1425.

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We evaluated the adrenergic innervation of the swine and canine myocardium after placement of an Ameroid constrictor around the left circumflex coronary artery (LCX). Fluorescent histochemistry was used to identify adrenergic nerve terminals in the myocardium and coronary vasculature. Ameroid occlusion of the proximal LCX in 10 pigs for 3 wk resulted in 6 +/- 1% infarction as well as myocardial ischemia in the left circumflex region of pigs studied during exercise. However, placement of the Ameroid constrictor did not significantly alter the surface density of the nerve terminals in the LCX region of myocardium when compared with innervation of control hearts. Histological examination of the coronary arterial adrenergic innervation in Ameroid-occluded pigs revealed that coronary vessels in the circumflex region of the heart were innervated. Similarly, in seven LCX Ameroid-occluded dogs, no significant decrease in adrenergic innervation of the LCX region of myocardium was observed when compared with control dogs. In contrast LCX Ameroid-occluded pigs demonstrated significant (P less than 0.01) denervation of the left anterior descending (LAD) region of myocardium when compared with control animals. The close proximity of adrenergic nerve bundles in the proximal LAD region indicates that denervation of the myocardium supplied by the LAD may result from the dissection and/or fibrosis associated with placement of the Ameroid constrictor on the proximal LCX. Our results suggest that placement of an Ameroid constrictor on the proximal LCX does not significantly alter the adrenergic innervation of the LCX-perfused myocardium or its associated coronary vasculature. However, denervation of LAD-perfused myocardium and its vasculature may result.

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Journal articles on the topic 'Coronary vasculature'

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