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Journal articles on the topic 'Peripheral vasculature; Cardiovascular; Coronary'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

Mai, Thi Thao, Manh-Cuong Vo, Tan-Huy Chu, Jin Young Kim, Chulhong Kim, Je-Jung Lee, Sung-Hoon Jung, and Changho Lee. "Pilot Study: Quantitative Photoacoustic Evaluation of Peripheral Vascular Dynamics Induced by Carfilzomib In Vivo." Sensors 21, no. 3 (January 27, 2021): 836. http://dx.doi.org/10.3390/s21030836.

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Carfilzomib is mainly used to treat multiple myeloma. Several side effects have been reported in patients treated with carfilzomib, especially those associated with cardiovascular events, such as hypertension, congestive heart failure, and coronary artery disease. However, the side effects, especially the manifestation of cardiovascular events through capillaries, have not been fully investigated. Here, we performed a pilot experiment to monitor peripheral vascular dynamics in a mouse ear under the effects of carfilzomib using a quantitative photoacoustic vascular evaluation method. Before and after injecting the carfilzomib, bortezomib, and PBS solutions, we acquired high-resolution three-dimensional PAM data of the peripheral vasculature of the mouse ear during each experiment for 10 h. Then, the PAM maximum amplitude projection (MAP) images and five quantitative vascular parameters, i.e., photoacoustic (PA) signal, diameter, density, length fraction, and fractal dimension, were estimated. Quantitative results showed that carfilzomib induces a strong effect on the peripheral vascular system through a significant increase in all vascular parameters up to 50%, especially during the first 30 min after injection. Meanwhile, bortezomib and PBS do not have much impact on the peripheral vascular system. This pilot study verified PAM as a comprehensive method to investigate peripheral vasculature, along with the effects of carfilzomib. Therefore, we expect that PAM may be useful to predict cardiovascular events caused by carfilzomib.

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2

Haines, David D., and Arpad Tosaki. "Role of Heme Oxygenases in Cardiovascular Syndromes and Co-morbidities." Current Pharmaceutical Design 24, no. 20 (October 11, 2018): 2322–25. http://dx.doi.org/10.2174/1381612824666180727110353.

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Cardiovascular Diseases (CVD), are the leading cause of human mortality worldwide and the focus of the intensive investigation is to characterize their pathogenesis. This review examines contribution to CVD of heme oxygenases (HOs), heat shock protein enzymes, comprising 3 isoforms: HO-1 (inducible), HO-2 (constitutively expressed) and HO-3 (function presently undefined), which constitute a primary endogenous countermeasure to oxidative tissue damage. Their role as CVD countermeasures is considered in the context of atherosclerosis, consequences of which are the leading cause of CVD deaths and from which 5 major syndromes may develop, namely: coronary artery disease and stroke, peripheral artery disease, kidney disease, cardiopulmonary disease and cerebrovascular disease. Over 75% of CVD deaths result from Coronary artery disease and stroke, with the severity of these conditions correlating with a systemic increase of the endogenous antioxidant bilirubin, produced by HO degradation of heme. Peripheral artery disease, (PAD) resulting from constricted arteries of the extremities is a painful and disabling condition, the severity of which correlates with elevated serum HO. Whether this represents an adaptive response or the enzyme is a contributor to PAD, remains to be determined. CVD symptoms, particularly hypertension, damage the vasculature and filtering structures of the kidneys and may be ameliorated by HO inducers. Interestingly, constitutive renal expression of HO-2 indicates that the enzyme is vital for healthy kidney function. Right ventricular hypertrophy and increased vascular resistance in blood vessels of the lungs exhibit mutually reinforcing positive feedback to result in cardiopulmonary heart disease, with morbidity and mortality resulting from associated inflammation and may be decreased with HO-1 inducers. Cerebrovascular disease, a major CVD complication affecting brain vasculature, with resulting susceptibility to stroke, maybe potently ameliorated by HO-1 inducers. Conclusion: Each of the six major categories of CVD exhibit features of pathogenesis that hold potential as future therapeutic targets, for modulated heme oxygenase activity.

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Mohler, Emile R., Lea Sarov-Blat, Yi Shi, Damir Hamamdzic, Andrew Zalewski, Colin MacPhee, Raul Llano, et al. "Site-Specific Atherogenic Gene Expression Correlates With Subsequent Variable Lesion Development in Coronary and Peripheral Vasculature." Arteriosclerosis, Thrombosis, and Vascular Biology 28, no. 5 (May 2008): 850–55. http://dx.doi.org/10.1161/atvbaha.107.154534.

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4

Wadhawan, Abhishek, Mark A. Reynolds, Hina Makkar, Alison J. Scott, Eileen Potocki, Andrew J. Hoisington, Lisa A. Brenner, et al. "Periodontal Pathogens and Neuropsychiatric Health." Current Topics in Medicinal Chemistry 20, no. 15 (June 1, 2020): 1353–97. http://dx.doi.org/10.2174/1568026620666200110161105.

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Increasing evidence incriminates low-grade inflammation in cardiovascular, metabolic diseases, and neuropsychiatric clinical conditions, all important causes of morbidity and mortality. One of the upstream and modifiable precipitants and perpetrators of inflammation is chronic periodontitis, a polymicrobial infection with Porphyromonas gingivalis (P. gingivalis) playing a central role in the disease pathogenesis. We review the association between P. gingivalis and cardiovascular, metabolic, and neuropsychiatric illness, and the molecular mechanisms potentially implicated in immune upregulation as well as downregulation induced by the pathogen. In addition to inflammation, translocation of the pathogens to the coronary and peripheral arteries, including brain vasculature, and gut and liver vasculature has important pathophysiological consequences. Distant effects via translocation rely on virulence factors of P. gingivalis such as gingipains, on its synergistic interactions with other pathogens, and on its capability to manipulate the immune system via several mechanisms, including its capacity to induce production of immune-downregulating micro-RNAs. Possible targets for intervention and drug development to manage distal consequences of infection with P. gingivalis are also reviewed.

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Zinkovska, S. M., E. K. Rodriguez, and D. A. Kirby. "Coronary and total peripheral resistance changes during sleep in a porcine model." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 2 (February 1, 1996): H723—H729. http://dx.doi.org/10.1152/ajpheart.1996.270.2.h723.

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Changes in autonomic tone in the vasculature during sleep may have important implications for silent ischemia and sudden cardiac death. Few models exist in which both cardiac output and coronary blood flow are continuously measured during natural sleep and autonomic mechanisms are assessed. Catheters were chronically implanted in the aorta to measure mean arterial pressure (MAP), and flow probes were placed on the ascending aorta and the circumflex coronary artery of 18 pigs. Electrodes determined sleep stage as either non-rapid eye movement (NREM) or rapid eye movement (REM) sleep. The MAP was 73 +/- 3 mmHg in the quiet awake state, did not change in NREM, and decreased to 64 +/- 2 mmHg in REM sleep (P < 0.05). In NREM sleep, heart rate did not change from awake state values of 136 +/- 8 beats/min but increased by 5 beats/min in REM sleep (P < 0.05). Coronary vascular resistance decreased from awake state values of 2.7 +/- 0.2 to 2.2 +/- 0.2 mmHg.ml-1.min in REM (P < 0.05); total peripheral resistance decreased from awake values of 0.061 +/- 0.004 mmHg.ml-1.min to 0.050 +/- 0.003 in REM sleep (P < 0.05). Those changes appear to have been mediated primarily by reduction of alpha-adrenergic activity. Spectral analysis of heart rate suggests that power in the high-frequency range (a presumed indicator of parasympathetic tone) was lower in REM sleep than NREM sleep.

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6

Nevitt, Chris, Grant McKenzie, Katelyn Christian, Jeff Austin, Sarah Hencke, James Hoying, and Amanda LeBlanc. "Physiological levels of thrombospondin-1 decrease NO-dependent vasodilation in coronary microvessels from aged rats." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 11 (June 1, 2016): H1842—H1850. http://dx.doi.org/10.1152/ajpheart.00086.2016.

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Aging and cardiovascular disease are associated with the loss of nitric oxide (NO) signaling and a decline in the ability to increase coronary blood flow reserve (CFR). Thrombospondin-1 (Thbs-1), through binding of CD47, has been shown to limit NO-dependent vasodilation in peripheral vascular beds via formation of superoxide (O2−). The present study tests the hypothesis that, similar to the peripheral vasculature, blocking CD47 will improve NO-mediated vasoreactivity in coronary arterioles from aged individuals, resulting in improved CFR. Isolated coronary arterioles from young (4 mo) or old (24 mo) female Fischer 344 rats were challenged with the NO donor, DEA-NONO-ate (1 × 10−7 to 1 × 10−4 M), and vessel relaxation and O2− production was measured before and after Thbs-1, αCD47, and/or Tempol and catalase exposure. In vivo CFR was determined in anesthetized rats (1–3% isoflurane-balance O2) via injected microspheres following control IgG or αCD47 treatment (45 min). Isolated coronary arterioles from young and old rats relax similarly to exogenous NO, but addition of 2.2 nM Thbs-1 inhibited NO-mediated vasodilation by 24% in old rats, whereas young vessels were unaffected. Thbs-1 increased O2− production in coronary arterioles from rats of both ages, but this was exaggerated in old rats. The addition of CD47 blocking antibody completely restored NO-dependent vasodilation in isolated arterioles from aged rats and attenuated O2− production. Furthermore, αCD47 treatment increased CFR from 9.6 ± 9.3 (IgG) to 84.0 ± 23% in the left ventricle in intact, aged animals. These findings suggest that the influence of Thbs-1 and CD47 on coronary perfusion increases with aging and may be therapeutically targeted to reverse coronary microvascular dysfunction.

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Chu, A., F. R. Cobb, P. O. Hagen, and J. J. Murray. "Effects of a stabilized endothelium-derived relaxing factor on the coronary vasculature in awake dogs." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 6 (December 1, 1989): H1895—H1899. http://dx.doi.org/10.1152/ajpheart.1989.257.6.h1895.

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The effects of a partially purified endothelium-derived relaxing factor (EDRF) stabilized by acidification from cultured bovine aortic endothelial cells stimulated with the calcium ionophore A23187 on coronary and peripheral vasculature were examined in five awake dogs. The dogs were chronically instrumented with miniature arterial dimension crystals and Doppler flow probes. Intracoronary or intra-arterial infusions of this EDRF induced a rapid (less than 15 s) significant increase in the proximal vessel diameter (P less than 0.02). The duration of proximal dilation response to this EDRF persisted up to 6 min, whereas the smaller changes in distal flow were more transient (less than 1 min). Similar but more pronounced changes in the proximal arterial dilation and distal flow occurred with infusion of nitroglycerin (0.4 mg). No vasoactive changes were observed during infusions of the control vehicle. The vasodilatory effects to this EDRF occurred in the absence of changes in aortic and left ventricular pressure, rate of pressure development (dP/dt), and heart rate. These data demonstrate that infusion of this partially purified relaxing factor from cultured endothelial cells causes vasodilation in vivo with a vasoactive profile similar to nitroglycerin. The biological effects of this EDRF persist significantly longer than the extreme lability of EDRF at neutral pH (approximately 6 s), consistent with its in vitro effects. Despite the demonstration of rapid inactivation of EDRF in vitro by hemoglobin, high oxygen tension, and plasma, the study shows that this EDRF can have significant in vivo vasoactive effects.

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8

Ozkaramanli Gur, Demet, Savas Guzel, Aydin Akyuz, Seref Alpsoy, and Niyazi Guler. "The role of novel cytokines in inflammation: Defining peripheral artery disease among patients with coronary artery disease." Vascular Medicine 23, no. 5 (April 11, 2018): 428–36. http://dx.doi.org/10.1177/1358863x18763096.

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Coronary artery disease (CAD) patients with concomitant peripheral artery disease (PAD) experience more extensive and calcified atherosclerosis, greater lesion progression and more common coronary events compared to patients with CAD only. To characterize the distinct features of this aggressive atherosclerotic disease, we studied novel cytokines that code different stages of atherogenesis. One hundred and eighty consecutive subjects (60 patients into each group of CAD+PAD, CAD and controls) were recruited among patients with stable angina pectoris scheduled for coronary angiography. An ankle–brachial index (ABI) ≤0.9 was determined as occlusive PAD. Fasting serum tumor necrosis factor (TNF)-like antigen 1A (TL1A) and its receptor death receptor 3 (DR3), NOGO-B (reticulon 4B) and its receptor NUS1, high-sensitivity C-reactive protein (hsCRP), A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) 1, 4, 5 and interleukin (IL) 6 levels were determined. Serum hsCRP and DR3/TL1A concentrations were similar and higher than controls in the CAD and CAD+PAD groups. Levels of NOGO-B and its receptor NUS1 were increased and ADAMTS-5 was decreased in patients with CAD+PAD. Independent predictors of ABI in multivariate analysis were smoking (B = −0.13, p = 0.04), NUS1 (B = −0.88, p < 0.001), ADAMTS-5 (B = 0.63, p < 0.001) and SYNTAX score (B = −0.26, p < 0.001). Similarly, smoking (OR = 5.5, p = 0.019), SYNTAX score (OR = 1.2, p < 0.001), NUS1 (OR = 14.4, p < 0.001), ADAMTS-5 (OR = 1.1, p < 0.001) and age (OR = 1.1, p = 0.042) independently predicted the involvement of peripheral vasculature in logistic regression. The diagnostic performance of these cytokines to discriminate CAD+PAD were AUC 0.79 ( p < 0.001) for NUS1 and 0.37 ( p = 0.013) for ADAMTS-5. We report herein that circulating cytokines can give clues to the ongoing atherosclerotic process and the extent of vascular involvement in which distinct features of ADAMTS-5 and NUS1 make them promising cytokines for future research.

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9

Bell, Dawn M., Thomas E. Johns, and Larry M. Lopez. "Endothelial Dysfunction: Implications for Therapy of Cardiovascular Diseases." Annals of Pharmacotherapy 32, no. 4 (April 1998): 459–70. http://dx.doi.org/10.1345/aph.17084.

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OBJECTIVE: To review current literature regarding endothelial dysfunction in cardiovascular diseases and examine implications of these findings for the treatment of various cardiovascular disorders. DATA SOURCE: A MEDLINE search of basic science articles pertinent to understanding the role of the endothelium in the atherosclerotic process and of clinical trials examining the presence and treatment of impaired endothelium-dependent vascular relaxation was conducted. STUDY SELECTION: Selected basic science articles and reviews were included to explain the foundation for subsequent clinical trials. All clinical trials examining the treatment of impaired endothelium-dependent vascular relaxation were reviewed. DATA SYNTHESIS: Endothelial dysfunction characterized by impaired endothelium-dependent vascular relaxation is an early physiologic event in atherogenesis. Endothelial dysfunction in peripheral vasculature serves as a marker for impairment in coronary arteries. Techniques for measuring endothelium-dependent vascular relaxation are specific and have a high positive predictive value for coronary artery disease, but low sensitivity. Various pharmacologic agents have been used in an attempt to improve endothelial function, but only lipid-lowering agents and estrogen supplementation have been shown to improve endothelium-dependent vascular relaxation consistently. Treatments used in patients with heart failure or hypertension fail to demonstrate consistent improvement. CONCLUSIONS: Endothelial dysfunction serves as a marker for cardiovascular disease, but pharmacologic treatment does not consistently restore normal endothelial function. Nevertheless, some of these agents are known to have positive clinical outcomes. Future research using these techniques will provide greater insight into the effects of many commonly used therapies for cardiovascular disease on the pathobiology of endothelial dysfunction. OBJETIVO: Revisar la literatura actual sobre la disfunción endotelial en enfermedades cardiovasculares y las implicaciones de estos hallazgos en el tratamiento de desórdenes cardiovasculares. FUENTES DE INFORMACION: A través de MEDLINE se realizó una búsqueda de artículos científicos relacionados al rol del endotelio en el proceso de aterosclerosis. En la búsqueda también se identificaron estudios clínicos sobre la detección y el tratamiento de disfunción en la relajación vascular dependiente del endotelio. SELECCIÓN DE FUENTES DE INFORMACIÓN: Se seleccionaron artículos de ciencias básicas y resúmenes de estudios para explicar la base de los estudios clínicos. Se revisaron todos los artículos de estudios clínicos que evaluaban el tratamiento de disfunción en la relajación vascular dependiente del endotelio. SÍNTESIS: La disfunción endotelial, caracterizada por una disfunción en la relajación vascular dependiente del endotelio, es un evento fisiológico que ocurre temprano en el proceso de aterogénesis. La disfunción del endotelio de la vasculatura periferal es un indicador de disfunción de las arterias coronarias. Las técnieas para medir la relajación vascular dependiente del endotelio son específicas y tienen un valor predictivo alto para enfermedad de las arterias coronarias pero una baja sensitividad. Se han utilizado varios agentes farmacológicos para tratar de mejorar la función endotelial, pero sólo los agentes antilipidémicos y el reemplazo de estrógenos han sido consecuentes en demostrar una mejoría en la relajación de la vasculatura dependiente de endotelio. Los tratamientos utilizados en los pacientes con fallo cardíaco e hipertensión no han sido consecuentes en demostrar una mejoría. CONCLUSIONES: La disfunción endotelial es un indicador de enfermedad cardiovascular. Aunque algunos agentes han demostrado obtener resultados clínicos positivos, el tratamiento farmacológico no ha sido consecuente en restaurar la función normal del endotelio. Existe la necesidad de realizar estudios clínicos que midan la relajación vascular que depende del endotelio. Estos podrán proveer mayor información sobre los efectos del tratamiento de enfermedades cardiovasculares en la disfunción del endotelio. OBJECTIF: Décrire les implications cliniques possibles de différents traitements pharmacologiques au niveau de la dysfunction endothéliale notée chez une population atteint d'ischémie myocardique, d'hyperlipidémie, d'hypertension, ou d'insuffisance cardiaque congestive. SOURCE: Les articles de science fondamentale examinant le róle de l'endothélium dans le processus athérosclérotique et les études cliniques évaluant l'effet de différents traitements phamacologiques pour rétablir à la normale la fonction endothéliale ont été identifiés et analysés. RÉSUMÉ: La dysfonction endothéliale caractérisée par un phénomène anormal de la relaxation vasculaire est un évènement physiologique précoce de l'athérogenèse. Ses principales manifestations sont en autre une concentration inadéquate soit du facteur de relaxation de l'endothélium, soit de l'oxide nitrique qui agit à titre de puissant vasodilatateur et d'inhibiteur de l'aggrégation plaquettaire, de la prolifération de cellules musculaires lisses, et de l'adhésion des monocytes. Plusieurs recherches ont démontré qu'une dysfonction endothéliale périphérique (telle que mesurée au niveau de l'artère brachiale) représente un marqueur d'une dysfonction endothéliale au niveau coronaire. La valeur prédictive de la dilatation brachiale pour estimer la dilatation coronaire est d'environ 95% bien que celle-ci ait une faible sensitivité. De tous les agents pharmacologiques testés, seuls les agents hypolipémiants et les suppléments d'oestrogènes semblent pouvoir améliorer la fonction endothéliale. Tous les autres traitements utilisés chez les patients hypertendus ou les insuffisants cardiaques n'ont pu démontrer à ce jour des résultats consistants. CONCLUSIONS: Plusieurs études préliminaires concluent qu'une dysfonction endothéliale périphérique constitue un marqueur pour les maladies cardiovasculaires. À ce jour, aucune thérapie ne semble pouvoir restorer cette fonction d'une façon non équivoque. Ce nouveau champ de recherche cardiovasculaire permettra possiblement d'établir un lien éventuel entre les effets endothéliaux et les effets bénéfiques cliniques des différents traitements pharmacologiques utilisés dans le domaine cardiovasculaire.

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10

Frie, Michael, and Mark Smith. "CRT-113 A Reproducible Animal Model of Calcified Atherosclerotic Plaque from a Cylindrical Bone Marrow Allograft Implanted in the Porcine Coronary and Peripheral Vasculature." JACC: Cardiovascular Interventions 6, no. 2 (February 2013): S36—S37. http://dx.doi.org/10.1016/j.jcin.2013.01.029.

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Indik, Julia H., Steven Goldman, and Mohamed A. Gaballa. "Oxidative stress contributes to vascular endothelial dysfunction in heart failure." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 4 (October 1, 2001): H1767—H1770. http://dx.doi.org/10.1152/ajpheart.2001.281.4.h1767.

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Congestive heart failure (HF) is characterized by inadequate nitric oxide (NO) production in the vasculature. Because NO is degraded by oxygen radicals, we hypothesized that NO is degraded faster in HF from inadequate peripheral arterial antioxidant reserves. HF was induced in male Sprague-Dawley rats by left coronary artery ligation. Vascular endothelial function was evaluated by measuring the NO-mediated vasorelaxation response to acetylcholine (ACh; 10−9–10−4M) in excised aortas. This was repeated with the free radical generator pyrogallol (20 μM) and again with pyrogallol and superoxide dismutase (SOD; 60 U/ml). Aortic and myocardial SOD activity was also determined. ACh-induced vasorelaxation was reduced in HF ( n = 9) compared with normal control rats ( n = 11; P < 0.001). Pyrogallol further reduced vasorelaxation in HF: 74 ± 11% at 10−4M ACh versus 58 ± 10% in normal control rats ( P < 0.004). There was a trend ( P = 0.06) toward reduced SOD activity in HF aortas. In conclusion, altered NO-dependent vasorelaxation in HF is in part due to excessive degradation of NO and is likely related to reduced vascular SOD activity.

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Stojković, Mirjana, and Miloš Žarković. "Subclinical Thyroid Dysfunction and the Risk of Cardiovascular Disease." Current Pharmaceutical Design 26, no. 43 (December 22, 2020): 5617–27. http://dx.doi.org/10.2174/1381612826666201118094747.

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The prevalence of subclinical hypothyroidism (SH) is 3-10%. The prevalence of subclinical hyperthyroidism (SHr) is 0.7-9.7%. Thyroid hormones affect cardiac electrophysiology, contractility, and vasculature. SH is associated with an increased risk of coronary heart disease (CHD), especially in subjects under 65. SHr seems to be associated with a slightly increased risk of CHD and an increase in CHD-related mortality. Both SH and SHr carry an increased risk of developing heart failure (HF), especially in those under 65. Both SH and SHr are associated with worse prognoses in patients with existing HF. SH is probably not associated with atrial fibrillation (AF). SHr, low normal thyroid-stimulating hormone (TSH) and high normal free thyroxine (FT4) are all associated with the increased risk of AF. An association between endothelial dysfunction and SH seems to exist. Data regarding the influence of SHr on the peripheral vascular system are conflicting. SH is a risk factor for stroke in subjects under 65. SHr does not increase the risk of stroke. Both SH and SHr have an unfavourable effect on cardiovascular disease (CVD) and all-cause mortality. There is a U-shaped curve of mortality in relation to TSH concentrations. A major factor that modifies the relation between subclinical thyroid disease (SCTD) and mortality is age. SH increases blood pressure (BP). SHr has no significant effect on BP. Lipids are increased in patients with SH. In SHr, high-density lipoprotein cholesterol and lipoprotein( a) are increased. SCTD should be treated when TSH is over 10 mU/l or under 0.1 mU/l. Treatment indications are less clear when TSH is between normal limits and 0.1 or 10 mU/L. The current state of knowledge supports the understanding of SCTD’s role as a risk factor for CVD development. Age is a significant confounding factor, probably due to age-associated changes in the TSH reference levels.

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Arrigo, Mattia, Quynh A. Truong, Duygu Onat, Jackie Szymonifka, Etienne Gayat, Heli Tolppanen, Malha Sadoune, et al. "Soluble CD146 Is a Novel Marker of Systemic Congestion in Heart Failure Patients: An Experimental Mechanistic and Transcardiac Clinical Study." Clinical Chemistry 63, no. 1 (January 1, 2017): 386–93. http://dx.doi.org/10.1373/clinchem.2016.260471.

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Abstract BACKGROUND Soluble CD146 (sCD146), is an endothelial marker with similar diagnostic power as natriuretic peptides in decompensated heart failure (HF). While natriuretic peptides are released by the failing heart, sCD146 may be released by veins in response to stretch induced by systemic congestion in HF. This study investigated the source, effects of vascular stress on release and prognostic properties of sCD146 in HF. METHODS In a peripheral venous stress study, plasma concentrations of sCD146 and N-terminal probrain natriuretic-peptide (NT-proBNP) were measured in 44 HF patients at baseline and after 90 min of unilateral forearm venous congestion. In addition, sCD146 and NT-proBNP were measured in peripheral vein (PV) and coronary sinus (CS) blood samples of 137 HF patients and the transcardiac gradient was calculated. Those patients were followed for major adverse cardiovascular events (MACE) during 2 years. RESULTS The induction of venous stress was associated with a pronounced increase in circulating concentrations of sCD146 in the congested arm (+60 μg/L) compared to the control arm (+16 μg/L, P = 0.025), while no difference in NT-proBNP concentrations was seen. In contrast to positive transcardiac gradient for NT-proBNP, median sCD146 concentrations were lower in CS than in PV (396 vs 434, P < 0.001), indicating a predominantly extracardiac source of sCD146. Finally, increased PV concentrations of sCD146 were associated with higher risk of MACE at 2 years. CONCLUSIONS Soluble CD146 is released from the peripheral vasculature in response to venous stretch and may reflect systemic congestion in chronic HF patients.

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Billups, Sarah J., and Barry L. Carter. "Mibefradil: A New Class of Calcium-Channel Antagonists." Annals of Pharmacotherapy 32, no. 6 (June 1998): 659–71. http://dx.doi.org/10.1345/aph.17323.

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OBJECTIVE: To describe the pharmacology, pharmacokinetics, and clinical efficacy of mibefradil compared with other agents used for hypertension and angina. DATA SOURCES: A MEDLINE search was performed for the period of January 1980 through September 1997 using the key terms mibefradil or Ro 40–5967. All articles written in English were considered for review. STUDY SELECTION AND DATA EXTRACTION: All clinical studies involving mibefradil were evaluated. Preclinical data were included if these data were not adequately represented in clinical (human) studies. DATA SYNTHESIS: Mibefradil is the first member of a new class of calcium-channel antagonists (CCAs) that block the T-type calcium channels. A long elimination half-life makes once-daily dosing feasible, and the drug's lack of negative inotropy and reflex tachycardia distinguishes it from other available CCAs. When administered at recommended dosages (50 or 100 mg once daily), mibefradil reduces blood pressure over 24 hours in patients with hypertension, improves exercise capacity, and relieves anginal symptoms in patients with chronic stable angina pectoris. CONCLUSIONS: Clinical studies have found that the antihypertensive effects of mibefradil are comparable with those of nifedipine, verapamil, and amlodipine, and more effective than those of diltiazem. These effects result from peripheral vasodilation and a slight reduction in heart rate. Selective vasodilation of the coronary vasculature makes it an effective antianginal agent when used alone or added to β-blocker therapy. Mibefradil demonstrates no significant effects on cardiac contractility, and no adrenergic stimulation resulting in reflex tachycardia. Therefore, it may have some advantages over currently available CCAs, especially in patients with congestive heart failure, although such advantages are unproven in published clinical trials. Ongoing clinical studies, including the Mortality Assessment in Congestive Heart Failure Trial (MACH-1) currently in progress, are needed to clarify mibefradil's place in cardiovascular therapy.

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Stamatelopoulos, Kimon, Marita Lyka, Christos Papamichail, Maria Roussou, Maria Gavriatopoulou, Constantinos Pamboucas, Evangelos Terpos, Meletios A. Dimopoulos, and Efstathios Kastritis. "Hemodynamic, Functional and Structural Markers of Vascular Involvement in Primary Systemic Light Chain (AL) Amyloidosis." Blood 124, no. 21 (December 6, 2014): 2029. http://dx.doi.org/10.1182/blood.v124.21.2029.2029.

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Abstract Light chain (AL) amyloidosis is characterized by the extracellular deposition of clonal light chain-derived amyloid fibrils in various tissues. Kidneys and heart are most commonly affected; clinically non detectable deposits in other tissues may also result in significant dysfunction. Amyloid deposits within the wall of the arteries or direct toxicity of light chains may cause arterial dysfunction in patients with AL amyloidosis, with cardiovascular consequences. Endothelial dysfunction, subclinical atherosclerosis of the carotid arteries and stiffening of the arterial tree are commonly found as deleterious vascular phenotypes and are considered surrogate markers of cardiovascular disease and outcome. Matrix metalloproteases, advanced glycation products, endothelial dysfunction and neuroendocrine signaling are implicated in arterial dysfunction and are affected in AL amyloidosis. However, arterial involvement in AL has not been evaluated thoroughly. In order to evaluate vascular dysfunction in patients with AL amyloidosis we evaluated non-invasively acquired markers which may be indicative of vascular involvement: hemodynamic [reflected waves and aortic blood pressures (BP)], functional [flow-mediated dilatation and carotid-femoral pulse wave velocity (PWV)] and structural [intima-media thickness (IMT) and the presence of plaques in the carotid arteries] markers of vascular damage were measured. Ninety-one (91) consecutive newly diagnosed patients with systemic AL were prospectively studied and compared to 91 controls matched 1:1 for traditional risk factors of cardiovascular disease (age, gender, smoking, hypertension, hyperlipidemia, diabetes) and for the presence of coronary artery disease. The median age of patients with AL was 65 years (range 40-83), 56% were males, 77% had renal and 57% cardiac involvement. Median NTproBNP was 1420 pg/ml, 25%, 49% & 26% were Mayo stage 1, 2 & 3 respectively, median eGFR was 66 ml/min/1.73 m2and median involved FLC (iFLC) level was 189 mg/L. First we compared indices of vascular damage between AL patients and matched controls: arterial stiffness (PWV: 10.4±3.0 vs 8.6±3.7 m/sec, p=0.002) and arterial wall thickness in the internal carotid artery (IMT: 0.76±0.21 vs 0.68±0.21 mm, p=0.017) were significantly higher in AL patients. Thus, subclinical vascular damage, independent from traditional factors of vascular dysfunction, is present in patients with AL. Peripheral systolic and diastolic blood pressure and aortic systolic, diastolic and pulse pressure (p≤0.001) and reflected waves (augmentation index (AI), p=0.045) were significantly lower in AL patients than in controls. After adjustment for NTproBNP levels, as a marker of cardiac dysfunction, the differences in blood pressures (systolic, diastolic and pulse pressure) remained significant (p≤0.008 for all). Thus, despite increased arterial stiffness, dysfunctional vasculature results in paradoxically lower systolic and diastolic blood pressure, a hallmark of AL amyloidosis, independently from the degree of cardiac dysfunction. We then examined possible associations of markers of AL with the indices of vascular dysfunction, after adjustment for risk factors of cardiovascular disease. The level of iFLCs was an independent determinant of lower peripheral systolic (p=0.021) and aortic systolic (p=0.009) and pulse pressure (p=0.013), hsTnT (p=0.016) and NTproBNP (p=0.001) levels were independent determinants of arterial stiffness (PWV). In a multivariate model mean blood pressure and NTproBNP were the only determinants of PWV. NTproBNP also correlated with the presence of plaques in the internal carotid arteries (p=0.006) independently of other risk factors of vascular disease. Thus, markers of cardiac dysfunction and the load of FLCs were associated with vascular dysfunction. Our results suggest vascular involvement in patients with AL amyloidosis, reflected at low aortic blood pressures, increased arterial stiffness and wall thickness in the internal carotid arteries. The association of the amount of light chains with aortic blood pressure suggests a role of the toxic light chain. The observed association of arterial stiffness with markers of heart involvement is indicative of a parallel process of heart and vascular injury in AL amyloidosis. Further research, to assess the clinical utility of markers of vascular damage in AL amyloidosis is needed. Disclosures No relevant conflicts of interest to declare.

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Sato, Yayoi, Yuichi Ohki, Haruyo Akiyama, Hiroyuki Daida, Beate Heissig, and Koichi Hattori. "Administration of Low-Dose Cyclophosphamide Reduces Progression of Atherosclerosis in Mice by Controlling the Cellular Microenvironment." Blood 106, no. 11 (November 16, 2005): 4452. http://dx.doi.org/10.1182/blood.v106.11.4452.4452.

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Abstract Atherosclerosis develops as a result of multiple inflammatory-fibroproliferative responses and is the primary cause of heart disease and stroke in Western countries. Circulating BM-derived progenitor cells (CFU-Cs or EPCs) can regenerate injured vasculature by accelerating reendothelialization and limiting atherosclerotic lesion formation. Risk factors for coronary artery disease like age and diabetes reduce the number and functional activity of these cells, thus limiting the regenerative capacity. The impairment of stem/progenitor cells by risk factors may contribute to atherosclerotic disease progression. High leukocyte counts, and especially neutrophils, a marker of inflammation have been shown to be an independent risk factor and prognostic indicator of future cardiovascular outcomes. Cyclophosphamide (CY) is a synthetic antineoplastic drug, which reduces white blood cell counts (WBC), especially neutrophils, and under certain circumstances can promote hematopoietic progenitor (colony forming unit-cells, CFU-C) mobilization from the bone marrow (BM) into the circulation. We hypothesized that administration of CY limits atherosclerotic lesion formation by decreasing inflammation-associated cells, and by increasing circulating BM-derived progenitors cells. Apolipoprotein E knockout (ApoE−/ −) mice were fed a high cholesterol diet and received different doses of CY in their drinking water (37.5mg/kg/day, 18.75mg/kg/day, 9.375mg/kg/day or nothing). To control for possible effects on progenitor release a control experiment was set up in which C57/B6 received the highest CY in their drinking water (37.5mg/kg/day) or remained untreated. Peripheral blood was drawn from mice every other week. Peripheral blood mononuclear cells (PBMCs) were isolated and subjected to cultures to detect EPCs and CFU-Cs. In CY-treated mice, WBC and neutrophil counts decreased within the first 10 days after the start of the treatment as compared to non-treated controls, and stayed low over the course of the experiment (until day 70). When apoE mice receiving a high-cholesterol diet were treated with CY, the number of circulating CFU-Cs doubled, whereas no major change was found in the c57Bl/6 control group receiving only Cy. EPCs were not detectable at any time point in the CY or control apoE group. Aortic atherosclerotic tree lesion areas were approximately 50% smaller in apoE-KO mice receiving CY in their drinking water after 12 weeks on a high-cholesterol diet than control animals. Most strikingly, apoE-KO mice treated with CY showed a prolonged survival rate as compared to untreated controls. The presence of macrophage-derived foam cells is a hallmark of the atherosclerotic lesion, and an increase in their content promotes plaque instability. Immunohistochemical analysis revealed that the number of macrophages was reduced in plaques of CY-treated animals, indicating that plaques in these might be more stable. Vascular endothelial growth factor (VEGF) is expressed in atherosclerotic plaques from local macrophages and can induce metalloproteinase-9 (MMP-9). Plasma VEGF levels were lower in the CY-treatment group, coinciding with a decrease in MMP-9 plasma levels. This study demonstrates the potential clinical use of a myelosuppressive agent for the treatment of a benign, but not less “malignant” deadly disease like atherosclerosis.

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Buxhofer-Ausch, Veronika, Heinz Gisslinger, Juergen Thiele, Bettina Gisslinger, Hans-Michael Kvasnicka, Leonhard Müllauer, Sophie Frantal, et al. "Risk Factors for Thrombosis in WHO-Defined Early/Prefibrotic Myelofibrosis: An International Study of 264 Patients,." Blood 118, no. 21 (November 18, 2011): 3846. http://dx.doi.org/10.1182/blood.v118.21.3846.3846.

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Abstract Abstract 3846 INTRODUCTION There is strong evidence indicating that the clear-cut separation of prefibrotic primary myelofibrosis (PMF) from essential thrombocythemia (ET) by consequent application of the World Health Organization (WHO) 2008 criteria is reflected in different, well defined clinical pictures and divergent prognoses (Barbui et al, JCO 2011,Thiele et al, Blood 2011). Very recently the specific risk profile for arterial and venous thrombosis in WHO- diagnosed ET was published (Carobbio et al, Blood 2011). In PMF so far all published data on vascular events were exclusively based on overt disease manifestations until now there are no data available regarding prefibrotic stages. Consequently, we aimed to evaluate the corresponding risk profile of patients with WHO-diagnosed prefibrotic PMF. METHODS A total number of 264 patients with WHO-defined prefibrotic PMF derived from either the Medical University of Vienna or an International Database (Barbui et al, JCO 2011) were studied. Nonfatal thrombotic events considered in this study were reported as rates per 100 patient-years and included transient ischemic attacks, thrombotic cerebrovascular accidents, coronary artery disease, myocardial infarction, peripheral arterial disease, deep vein thrombosis of peripheral vasculature, pulmonary embolism, and abdominal large vein thrombosis. Cardiovascular risks factors considered, comprised of arterial hypertension, diabetes mellitus and tobacco use. To evaluate risk factors for total thrombosis and for arterial and venous events in particular multivariate Cox- regression analysis including the co-variables sex, age, previous thrombotic event, laboratory parameters measured at diagnosis and need for cytoreductive and/or antiplatelet therapy during follow-up was calculated. P values less than 0.05 were considered as statistically significant. RESULTS After a median follow- up of 5.8 years (range0.0 – 27.2), the total rate of non fatal thrombotic events was 2.1% patient-years (95% CI, 1.5–2.8); the incidence of arterial events was higher (1.7% patient- years) than of venous events (0.6% patient-years).Considering thrombosis in general a higher white blood cell (WBC) count enhances the risk significantly (p=0.005; HR 1.15). This is also true in arterial events in particular (p=0.047; HR 1.12). A lower platelet count is associated with a higher risk for thrombotic events; for thrombosis in general this association is of borderline significance (p=0.056; HR 0.99), for arterial thrombosis in particular of significance (p= 0.042; HR 0.99). A lower hemoglobin level is associated with a higher risk for venous thrombosis (p=0.007; HR 0.59). CONCLUSION Leukocytosis appears as a risk factor for thrombosis in general and also for arterial thrombosis in particular in WHO-diagnosed prefibrotic PMF. Moreover, higher platelet counts seem to decrease significantly the risk for thrombotic events in general and arterial thrombosis in particular. Anemia is associated with a higher risk for venous thrombosis. These observations are partly in line with recently published findings in WHO-diagnosed ET (Carobbio et al,2011) and might indicate the existence of a specific risk profile for thrombotic events in prefibrotic PMF. This is the first study reporting data on the risk profile for thrombosis in WHO-diagnosed prefibrotic PMF. Certainly these findings ask for validation in a larger patient population. Disclosures: Gisslinger: Novartis: Speakers Bureau; Celgene Austria: Research Funding, Speakers Bureau; AOP-Orphan Pharmaceuticals AG: Speakers Bureau. Vannucchi:Novartis: Honoraria.

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Reilly, Dermot F., Elizabeth J. Westgate, and Garret A. FitzGerald. "Peripheral Circadian Clocks in the Vasculature." Arteriosclerosis, Thrombosis, and Vascular Biology 27, no. 8 (August 2007): 1694–705. http://dx.doi.org/10.1161/atvbaha.107.144923.

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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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20

Hughes, A., G. Martin, S. Thom, and P. Sever. "Dopaminergic Mechanisms in Human Peripheral Vasculature." Journal of Hypertension 3, no. 6 (December 1985): 664–65. http://dx.doi.org/10.1097/00004872-198512000-00024.

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21

Criqui, Michael H., and Joachim H. Ix. "Highs and Lows in the Peripheral Vasculature." Journal of the American College of Cardiology 59, no. 4 (January 2012): 408–9. http://dx.doi.org/10.1016/j.jacc.2011.10.861.

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22

Auerbach, Eric G., and Edward T. Martin. "Magnetic resonance imaging of the peripheral vasculature." American Heart Journal 148, no. 5 (November 2004): 755–63. http://dx.doi.org/10.1016/j.ahj.2004.04.045.

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23

Reardon, Lindsay, Andrew O. Maree, and Michael de Moor. "Moyamoya Disease with Peripheral Pulmonary Artery Stenoses and Coronary Artery Fistulae." Case Reports in Medicine 2009 (2009): 1–2. http://dx.doi.org/10.1155/2009/840904.

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Moyamoya is a progressive disorder of the cerebral vasculature. Our report describes a rare case of Moyamoya disease with distal peripheral pulmonary artery stenoses and coronary fistulae in a 12-year-old Caucasian female patient.

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24

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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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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27

Mulvany, M. J., and C. Aalkjaer. "Calcium Metabolism and Structure in the Peripheral Vasculature." Journal of Cardiovascular Pharmacology 12, Supplement (1988): 134. http://dx.doi.org/10.1097/00005344-198800125-00024.

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28

Mulvany, M. J., and C. Aalkjaer. "Calcium Metabolism and Structure in the Peripheral Vasculature." Journal of Cardiovascular Pharmacology 12 (1988): 134. http://dx.doi.org/10.1097/00005344-198806125-00024.

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29

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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30

Avery, Joseph C., Darren T. Beck, Darren P. Casey, Paloma D. Sardina, and Randy W. Braith. "Enhanced external counterpulsation improves peripheral resistance artery blood flow in patients with coronary artery disease." Applied Physiology, Nutrition, and Metabolism 39, no. 3 (March 2014): 405–8. http://dx.doi.org/10.1139/apnm-2013-0309.

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Enhanced external counterpulsation (EECP) increases coronary artery perfusion and improves endothelium-dependent vasodilation in peripheral muscular conduit arteries. It is unknown whether vasodilatory capacity is improved in the peripheral resistance vasculature. Here we provide novel evidence from the first randomized, sham-controlled study that EECP increases peak limb blood flow and improves endothelium-dependent vasodilation in both calf and forearm resistance arteries in patients with coronary artery disease.

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31

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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32

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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33

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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34

Murarka, Shishir, and Richard R. Heuser. "Chronic total occlusions in peripheral vasculature: techniques and devices." Expert Review of Cardiovascular Therapy 7, no. 10 (October 2009): 1283–95. http://dx.doi.org/10.1586/erc.09.107.

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35

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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36

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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Teragawa, Hiroki, Chikage Oshita, and Tomohiro Ueda. "The Myocardial Bridge: Potential Influences on the Coronary Artery Vasculature." Clinical Medicine Insights: Cardiology 13 (January 2019): 117954681984649. http://dx.doi.org/10.1177/1179546819846493.

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38

Wang, Sarah B., Paul Mitchell, Gerald Liew, Tien Yin Wong, Kevin Phan, Aravinda Thiagalingam, Nichole Joachim, George Burlutsky, and Bamini Gopinath. "A spectrum of retinal vasculature measures and coronary artery disease." Atherosclerosis 268 (January 2018): 215–24. http://dx.doi.org/10.1016/j.atherosclerosis.2017.10.008.

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39

Miličić, Davor, Nina Jakuš, and Dora Fabijanović. "Microcirculation and Heart Failure." Current Pharmaceutical Design 24, no. 25 (November 8, 2018): 2954–59. http://dx.doi.org/10.2174/1381612824666180625143232.

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The idea of coronary microcirculation playing a role in the pathophysiology of heart failure dates from decades ago, with authors hypothesizing that structural and functional alterations in the coronary microcirculation could potentially contribute to heart failure. It is known that in a wide range of primary cardiomyopathies, from dilated to hypertrophic, there are pathological alterations in myocardial vasculature structure and function, playing a role in the clinical course of the disease. Needless to say, many patients with normal epicardial coronary arteries can suffer from coronary microvascular dysfunction, that could lead to a wide variety of clinical problems – from impaired functional capacity to stable and unstable angina, Takotsubo syndrome, myocardial infarction with normal coronary arteries and can also end up with either acute or chronic heart failure. Furthermore, nowadays, it has been recognized that pathophysiology of the heart failure with preserved ejection fraction (HFpEF) is mainly due to the myocardial microcirculatory impairment. In heart failure with reduced ejection fraction (HFrEF) neurohumoral mechanisms affecting the peripheral vasculature have been identified as important factors in the development and progression of heart failure, leading to unfavourable remodelling, and thus some of them being important treatment targets. Among many new clinical scenarios where both myocardial and peripheral microcirculation play an important role, raising field of implantable continuous flow assist devices opens many questions and implies better understanding of their effects of microcirculation, as they usually lead to the improvement of end organ dysfunction caused by previous heart failure, which is probably through the positive effects of peripheral microcirculation.

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40

Stekiel, Thomas A., Zeljko J. Bosnjak, and William J. Stekiel. "Effects of General Anesthetics on Regulation of the Peripheral Vasculature." Seminars in Cardiothoracic and Vascular Anesthesia 7, no. 3 (September 2003): 311–31. http://dx.doi.org/10.1177/108925320300700307.

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41

Mancio, Jennifer, Evangelos K. Oikonomou, and Charalambos Antoniades. "Perivascular adipose tissue and coronary atherosclerosis." Heart 104, no. 20 (May 31, 2018): 1654–62. http://dx.doi.org/10.1136/heartjnl-2017-312324.

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Adipose tissue (AT) is no longer viewed as a passive, energy-storing depot, and a growing body of evidence supports the concept that both quantitative and qualitative aspects of AT are critical in determining an individual’s cardiometabolic risk profile. Among all AT sites, perivascular AT (PVAT) has emerged as a depot with a distinctive biological significance in cardiovascular disease given its close anatomical proximity to the vasculature. Recent studies have suggested the presence of complex, bidirectional paracrine and vasocrine signalling pathways between the vascular wall and its PVAT, with far-reaching implications in cardiovascular diagnostics and therapeutics. In this review, we first discuss the biological role of PVAT in both cardiovascular health and disease, highlighting its dual pro-atherogenic and anti-atherogenic roles, as well as potential therapeutic targets in cardiovascular disease. We then review current evidence and promising new modalities on the non-invasive imaging of epicardial AT and PVAT. Specifically, we present how our expanding knowledge on the bidirectional interplay between the vascular wall and its PVAT can be translated into novel clinical diagnostics tools to assess coronary inflammation. To this end, we present the example of a new CT-based method that tracks spatial changes in PVAT phenotype to extract information about the inflammatory status of the adjacent vasculature, highlighting the numerous diagnostic and therapeutic opportunities that arise from our increased understanding of PVAT biology.

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42

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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43

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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44

Gresele, Paolo. "Coronary and peripheral artery atherosclerosis." Journal of Cardiovascular Medicine 19 (February 2018): e72-e74. http://dx.doi.org/10.2459/jcm.0000000000000557.

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45

Lluri, Gentian, Vincent Huang, Marlin Touma, Xiaoqian Liu, Andrew W. Harmon, and Atsushi Nakano. "Hematopoietic progenitors are required for proper development of coronary vasculature." Journal of Molecular and Cellular Cardiology 86 (September 2015): 199–207. http://dx.doi.org/10.1016/j.yjmcc.2015.07.021.

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46

Yucel, E. Kent. "Magnetic resonance angiography and the peripheral vasculature: how useful is it?" Nature Clinical Practice Cardiovascular Medicine 2, no. 3 (March 2005): 136–37. http://dx.doi.org/10.1038/ncpcardio0131.

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47

Lei, Xun-Lan, and George C. Y. Chiou. "Studies on Cardiovascular Actions of Salvia miltiorrhiza." American Journal of Chinese Medicine 14, no. 01n02 (January 1986): 26–32. http://dx.doi.org/10.1142/s0192415x86000053.

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Cardiovascular actions of S. miltiorrhiza (SM) were studied on systemic blood pressure in the rat. Langendorff cardiac preparation in the guinea pig, and four types of vasculature in the dog including coronary, renal, femoral, and mesenteric arteries. SM induced dose-related hypotension without changing heart rate. The hypotension was antagonized by atropine, propranolol, and chlorpheniramine plus cimetidine. In the isolated whole-heart preparation, SM increased coronary blood flow significantly for 15 min and positive inotropic action for 3 min after pulse injection. SM relaxed all arteries at low concentration (3.0 mg/ml) and contracted all but the coronary artery at higher concentration (10.0 mg/ml). The coronary artery relaxed at all doses of SM tested.

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48

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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49

Lüscher, Thomas F. "Coronary and peripheral interventions: an update." European Heart Journal 37, no. 14 (April 7, 2016): 1085–87. http://dx.doi.org/10.1093/eurheartj/ehw107.

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50

Vecht, Romeo J. "Coronary and peripheral angiography and angioplasty." International Journal of Cardiology 30, no. 3 (March 1991): 369–70. http://dx.doi.org/10.1016/0167-5273(91)90025-k.

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