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Relevant bibliographies by topics / Peripheral vasculature; Cardiovascular; Coronary

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Academic literature on the topic 'Peripheral vasculature; Cardiovascular; Coronary'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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

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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Peripheral vasculature; Cardiovascular; Coronary"

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Kneale, Barry J. "The influence of gender on forearm resistance vessel function." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312451.

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Reeves, Katherine Ann. "The cardiovascular actions of the isopropyl ester and other synthetic derivatives of palmitoyl carnitine." Thesis, University of Bath, 1995. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260252.

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Kmetz, John George II. "Differential Regulation of TRPV1 Channels in the Murine Coronary Vasculature by H2O2." Kent State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=kent1398336723.

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Davis, Griffith M. "Exposure to Nanomaterials Results in Alterations of Inflammatory and Atherosclerotic Signaling Pathways in the Coronary Vasculature of Wildtype Rodents." Thesis, University of North Texas, 2018. https://digital.library.unt.edu/ark:/67531/metadc1248468/.

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Cardiovascular disease (CVD) is the leading cause of death for people of most ethnicities on a global scale, and countless research efforts on the pathology of CVD has been well-characterized over the years. However, advancement in modern technologies, such as nanotechnology, has generated environmental and occupational health concerns within the scientific community. Current investigation of nanotoxicity calls into question the negative effects nanomaterials may invoke from their environmental, commercial, and therapeutic usage. As a result, further research is needed to investigate and characterize the toxicological implications associated with nanomaterial-exposure and CVD. We investigated the toxicity of multi-walled carbon nanotubes (MWCNT) and titanium dioxide (TiO2), which are two prominently used nanomaterials that have been previously linked to upregulation of inflammatory and atherogenic factors. However, the mechanistic pathways involved in these nanomaterials mediating detrimental effects on the heart and/or coronary vasculature have not yet been fully determined. Thus, we utilized two different routes of exposure in rodent models to assess alterations in proinflammatory and proatherogenic signaling pathways, which are represented in contrast throughout the dissertation. In our MWCNT study, we used C57Bl/6 mice exposed to MWCNTs (1 mg/m3) or filtered air (FA-Controls), via inhalation, for 6 hr/d for 14d. Conversely, intravenous TiO2 was administered to F344 male fisher rats, following 24h and 28d post-exposure to a single injection of TiO2-NPs (1 mg/kg), compared to control animals. MWCNT-exposed endpoints investigated the alterations in cholesterol transport, such as lectin-like oxidized low-density lipoprotein receptor (LOX)-1 and ATP-binding cassette transporter (ABCA)-1, inflammatory markers [tumor necrosis factor (TNF)-α], interleukin (IL)-1β/IL-6, nuclear-factor kappa-light-chain-enhancer of activated B cells (NF-κB) and signaling factors involved in activation of the pathway, as well as intracellular/vascular adhesion molecule(s) (VCAM-1, ICAM-1), and miRNAs (miR-221/-21/-1), associated with CVD, were analyzed in cardiac tissue and coronary vasculature. Cardiac fibrotic deposition, matrix-metalloproteinases (MMP)-2/9, and reactive oxygen species (ROS) were also assessed. TiO2-exposure endpoints also involved alterations on cholesterol transport proteins via LOX-1 and ABCA-1, factors of inflammation, namely intracellular macrophages and interleukin (IL)-1β, MMP-2/9 activity and protein expression, fibrotic deposition, and ROS generation were analyzed via quantitative detection or histologically in both cardiac tissue and coronary vasculature. Results from both studies found alterations in fibrotic deposition, upregulation in LOX-1 expression and MMP-2/9 activity, and ROS generation; with a concurrent decrease in ABCA-1 expression in cardiac tissue and coronary vasculature. Individually, MWCNT-exposed endpoints had shown induction of cardiac TNF-α, MMP-9, IκB Kinase (IKK)-α/β, and miR-221 mRNAs; as well as increased coronary expression of TNF-α and VCAM-1. TiO2 studies found increases in IL-1β and MMP-9 protein expression, as well as intracellular macrophage induction. Both studies also found, through pre-treatment of NADPH oxidase inhibitor, apocynin, resulted in attenuation of nanomaterial-exposure mediated ROS production; with nitric oxide synthase inhibitor, L-NNA, also showing attenuation, but only in our MWCNT-exposed inhalation study. The results from both studies have demonstrated, through different routes of administration, exposures, and rodent models; that exposure to nanomaterials can mediate signaling pathways involved in initiation and/or progression of CVD.

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Liby, Tiera A. "The role of phosphoinositide 3-kinase (PI3K) in mediating mitogen and Simvastatin induced effects in the vasculature." Virtual Press, 2005. http://liblink.bsu.edu/uhtbin/catkey/1315171.

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Statins induce beneficial vascular effects. How statins induce beneficial vascular effects is yet to be determined. Here we examine Simvastatin and vascular endothelial growth factor (VEGF) acting through the phosphoinositide 3-kinase (PI3K) pathway in human coronary artery endothelial cells (HCAEC). While Simvastatin and VEGF both activated mediators in the PI3K pathway, the proteins and the rates of activation were not always consistent. This suggests that although Simvastatin and VEGF share a common PI3K pathway in HCAEC and similar vascular effects, the agonists diverge in the induction of cellular signaling cascades. Simvastatin also was shown to induce phosphoinositide 3, 4, 5-triphosphate (PIPS) organization and PI3K p110 gamma (y) perinuclear localization. Beneficial, non-lipid lowering effects of statins may occur through the PI3K pathway through activation of distinct mediators from those of VEGF. Better understanding of the pathways associated with statins is necessary for the discovery of better treatments for cardiovascular disease (CVD).
Department of Biology

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Goyal, Ayush. "Vasculature reconstruction from 3D cryomicrotome images." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:aa9e500b-a0a4-48f3-8cb8-e75bbcc775e9.

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Background: Research in heart disease can be aided by modelling myocardial hemodynamics with knowledge of coronary pressure and vascular resistance measured from the geometry and morphometry of coronary vasculature. This study presents methods to automatically reconstruct accurate detailed coronary vascular anatomical models from high-resolution three-dimensional optical fluorescence cryomicrotomography image volumes for simulating blood flow in coronary arterial trees. Methods: Images of fluorescent cast and bead particles perfused into the same heart comprise the vasculature and microsphere datasets, employed in a novel combined approach to measure vasculature and simulate a flow model on the extracted coronary vascular tree for estimating regional myocardial perfusion. The microspheres are used in two capacities - as fiducial biomarker point sources for measuring the image formation in order to accurately measure the vasculature dataset and as flowing particles for measuring regional myocardial perfusion through the reconstructed vasculature. A new model-based template-matching method of vascular radius estimation is proposed that incorporates a model of the optical fluorescent image formation measured from the microspheres and a template of the vessels’ tubular geometry. Results: The new method reduced the error in vessel radius estimation from 42.9% to 0.6% in a 170 micrometer vessel as compared to the Full-Width Half Maximum method. Whole-organ porcine coronary vascular trees, automatically reconstructed with the proposed method, contained on the order of 92,000+ vessel segments in the range 0.03 – 1.9 mm radius. Discrepancy between the microsphere perfusion measurements and regional flow estimated with a 1-D steady state linear static blood flow simulation on the reconstructed vasculature was modelled with daughter-to-parent area ratio and branching angle as the parameters. Correcting the flow simulation by incorporating this model of disproportionate distribution of microspheres reduced the error from 24% to 7.4% in the estimation of fractional microsphere distribution in oblique branches with angles of 100°-120°.

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Freisinger, Eva [Verfasser]. "Outcomes of Coronary and Peripheral Artery Disease in German Health Care Claims Data : Health Services Research in Cardiovascular Medicine / Eva Freisinger." Berlin : epubli, 2021. http://d-nb.info/1236472446/34.

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Llobera, Serentill Àlex. "Arteopatia perifèrica i factors de risc cardiovascular. Millora de la prevenció secundària dels pacients amb arteriopatia perifèrica en l'atenció primària." Doctoral thesis, Universitat de Girona, 2018. http://hdl.handle.net/10803/482107.

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Cardiovascular risk factors control is low in peripheral artery disease patients. Leukocyte count over7.8 K/mcL or neutrophil count over 4.6 K/mcL are predictors of increased risk for heart coronary disease, cerebral vascular disease and all-cause mortality, independently of classical risk factors. Leukocyte and neutrophil count reclassifies risk and improves risk prediction in addition to classical risk factors. The improvements in cardiovascular risk factor control in peripheral artery disease patients with an audit and feedback intervention in primary care professionals are low. These improvements are more important when we talk about office procedures than in metabolic control of cardiovascular risk factors.
El control dels factors de risc cardiovascular en pacients amb malaltia arterial periférica en atenció primària és baix. El recompte de leucòcits major de7.8 K/mcL i el de neutrofils majors de 4.6 K/mcL són predictors d’un risc incrementat per malaltia coronaria cardiaca, malaltia cerebrovascular i mortalitat per totes les causes independentment dels factors de risc clàssics. El recompte de leucòcits i de neutròfils reclassifiquen els risc i milloren la predicció de risc afegits als factors de risc clàssics. Les millores en el control dels factors de risc cardiovascular en pacients amb malaltia arterial perifèrica mitjançant una intervenció d’audit i feedback en professionals d’atenció primària són baixes. Aquestes millores són més importants a nivell dels procediments en consulta que en el control metabòlic dels factors de risc cardiovascular.

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Howard, Dominic Peter James. "Extra-coronary arterial disease : incidence, projected future burden, risk factors and prevention." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:6ac90d2b-b919-45d4-abfd-2128efb31bc6.

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Vascular disease is the leading cause of death and disability worldwide. Incidence, risk factors, and outcome of coronary artery disease have been extensively studied, but there are fewer data on other forms of arterial disease, including carotid, aortic, visceral, and peripheral arterial disease. Although the burden of these diseases may be increasing due to the ageing population, we lack the most basic epidemiological data on which to base clinical decisions on individual patients (short and long-term prognosis); local service provision (current incidence and projected future burden); public health / screening initiatives (age and sex-specific incidence, risk factors, and outcome); and with which to assess current levels of primary prevention (pre-morbid risk factor control). Indeed, it is this lack of data, rather than a lack of treatments that is the greatest barrier to effective prevention. I have contributed to, cleaned, and analysed data from the Oxford Vascular Study, a prospective, population-based study (n=92,728) of all acute vascular events (2002-2012), and the Oxford Plaque Study, a carotid atherosclerosis biobank of over 1000 carotid plaques, in order to study these conditions. For acute aortic disease, I aimed to assess the risk factors associated with acute abdominal aortic aneurysms (AAA) and the population impact of the current UK AAA screening programme; and the incidence, risk factors, outcome, and projected future burden of acute aortic dissection. For acute peripheral arterial disease, I assessed the risk factors associated with premature onset and poor outcome, together with current levels of primary prevention. For symptomatic carotid artery disease, I studied the timing and benefits of surgical intervention in the current era; and went on to assess whether underlying carotid plaque morphology can be used to improve stroke risk stratification and help explain why ocular and cerebral stroke types have vast differences in future ipsilateral stroke risk. I found that compared with the current UK AAA screening strategy (one-off scan for men aged 65), screening of male smokers at 65 and all men at 75 would prevent nearly four-times as many deaths and three-times as many life-years lost with 21% fewer annual scans. I have also shown that incidence of acute aortic dissection is higher than previous estimates, a third of cases are out-of-hospital deaths, and uncontrolled hypertension is the most significant treatable risk factor for this condition. For acute peripheral arterial disease, the presence of multiple atherosclerotic risk factors are associated with premature onset, and severity of ischaemia, pre-morbid renal dysfunction, cardiac failure, and diabetes mellitus are predictive of future limb loss and survival. A significant proportion of acute peripheral events are AF-related in high risk patients who were not pre-morbidly anticoagulated despite having no contraindications and being at low risk of bleeding. Symptomatic carotid artery disease currently accounts for <10% of incident cerebrovascular events, and only 40% of these patients undergo surgical intervention. Due to improvements in medical therapy and on-going delays to intervention, little benefit is currently obtained from intervening in patients with <70% stenosis. Ipsilateral stroke risk is correlated with several carotid plaque features in a time-dependent manner, confirming the potential utility of plaque morphology in risk stratification. In addition, plaques from patients with cerebral events were significantly more unstable and inflammatory than from those with ocular events, helping explain differences in stroke risk between these groups. My findings advance the understanding of these conditions that form the backbone of modern vascular surgical practice, and I hope will improve prevention, clinical management, and outcome for patients with vascular disease.

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Books on the topic "Peripheral vasculature; Cardiovascular; Coronary"

1

Cardiovascular catheterization and intervention: A textbook of coronary, peripheral, and structural heart disease. New York: Informa Healthcare, 2010.

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Banerjee, Amitava, and Kaleab Asrress. Screening for cardiovascular disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0351.

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Screening involves testing asymptomatic individuals who have risk factors, or individuals who are in the early stages of a disease, in order to decide whether further investigation, clinical intervention, or treatment is warranted. Therefore, screening is classically a primary prevention strategy which aims to capture disease early in its course, but it can also involve secondary prevention in individuals with established disease. In the words of Geoffrey Rose, screening is a ‘population’ strategy. Examples of screening programmes are blood pressure monitoring in primary care to screen for hypertension, and ultrasound examination to screen for abdominal aortic aneurysm. The effectiveness and feasibility of screening are influenced by several factors. First, the diagnostic accuracy of the screening test in question is crucial. For example, exercise ECG testing, although widely used, is not recommended in investigation of chest pain in current National Institute for Health and Care Excellence guidelines, due to its low sensitivity and specificity in the detection of coronary artery disease. Moreover, exercise ECG testing has even lower diagnostic accuracy in asymptomatic patients with coronary artery disease. Second, physical and financial resources influence the decision to screen. For example, the cost and the effectiveness of CT coronary angiography and other new imaging modalities to assess coronary vasculature must be weighed against the cost of existing investigations (e.g. coronary angiography) and the need for new equipment and staff training and recruitment. Finally, the safety of the investigation is an important factor, and patient preferences and physician preferences should be taken into consideration. However, while non-invasive screening examinations are preferable from the point of view of patients and clinicians, sometimes invasive screening tests may be required at a later stage in order to give a definitive diagnosis (e.g. pressure wire studies to measure fractional flow reserve in a coronary artery). The WHO’s principles of screening, first formulated in 1968, are still very relevant today. Decision analysis has led to ‘pathways’ which guide investigation and treatment within screening programmes. There is increasing recognition that there are shared risk factors and shared preventive and treatment strategies for vascular disease, regardless of arterial territory. The concept of ‘vascular medicine’ has gained credence, leading to opportunistic screening in other vascular territories if an individual presents with disease in one territory. For example, post-myocardial infarction patients have higher incidence of cerebrovascular and peripheral arterial disease, so carotid duplex scanning and measurement of the ankle–brachial pressure index may be valid screening approaches for arterial disease in other territories.

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3

Tomanek, Robert J. Coronary Vasculature: Development, Structure-Function, and Adaptations. Springer, 2012.

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Coronary Vasculature: Development, Structure-Function, and Adaptations. Springer, 2012.

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5

Covic, Adrian, Mugurel Apetrii, Luminita Voroneanu, and David J. Goldsmith. Vascular calcification. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0120_update_001.

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Vascular calcification (VC) is a common feature of patients with advanced CKD and it could be, at least in part, the cause of increased cardiovascular mortality in these patients. From a morphologic point of view, there are at least two types of pathologic calcium phosphate deposition in the arterial wall—namely, intima calcification (mostly associated with atherosclerotic plaques) and media calcification (associated with stiffening of the vasculature, resulting in significantly adverse cardiovascular outcomes). Although VC was viewed initially as a passive phenomenon, it appears to be a cell-mediated, dynamic, and actively regulated process that closely resembles the formation of normal bone tissue, as discovered recently. VC seems to be the result of the dysregulation of the equilibrium between promoters and inhibitors. The determinants are mostly represented by altered calcium and phosphorus metabolism, secondary hyperparathyroidism, vitamin D excess, high fibroblast growth factor 23, and high levels of indoxyl sulphate or leptin; meanwhile, the inhibitors are vitamin K, fetuin A, matrix G1a protein, osteoprotegerin, and pyrophosphate. A number of non-invasive imaging techniques are available to investigate cardiac and vascular calcification: plain X-rays, to identify macroscopic calcifications of the aorta and peripheral arteries; two-dimensional ultrasound for investigating the calcification of carotid arteries, femoral arteries, and aorta; echocardiography, for assessment of valvular calcification; and, of course, computed tomography technologies, which constitute the gold standard for quantification of coronary artery and aorta calcification. All these methods have a series of advantages and limitations. The treatment/ prevention of VC is currently mostly around calcium-mineral bone disease interventions, and unproven. There are interesting hypotheses around vitamin K, Magnesium, sodium thiosulphate and other potential agents.

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Mukherjee, Debabrata, Eric R. Bates, David J. Moliterno, Richard A. Lange, and Marco Roffi. Cardiovascular Catheterization and Intervention. Taylor & Francis Group, 2020.

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7

Bowker, Lesley K., James D. Price, Ku Shah, and Sarah C. Smith. Cardiovascular. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198738381.003.0010.

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This chapter provides information on the ageing cardiovascular system, chest pain, stable angina, acute coronary syndromes, myocardial infarction, hypertension, treatment of hypertension, presentation of arrhythmias, management of arrhythmias, atrial fibrillation, rate/rhythm control in atrial fibrillation, stroke prevention in atrial fibrillation, bradycardia and conduction disorders, common arrhythmias and conduction abnormalities, heart failure assessment, acute heart failure, chronic heart failure, dilemmas in heart failure, heart failure with preserved left ventricular function, valvular heart disease, peripheral oedema, preventing venous thromboembolism in an older person, peripheral vascular disease, gangrene in peripheral vascular disease, and vascular secondary prevention.

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8

Mukherjee, Debabrata, Eric R. Bates, David J. Moliterno, Richard A. Lange, and Marco Roffi. Cardiovascular Catheterization and Intervention: A Textbook, Second Edition. Taylor & Francis Group, 2017.

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9

Prevention of Cardiovascular Disease: Atherosclerosis, Carotid Artery Disease, Cerebral Artery Disease/Stroke, Coronary Artery Disease, Peripheral Artery Disease and Hypertension. iUniverse, Inc., 2005.

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Vlachopoulos, Charalambos, and Nikolaos Ioakeimidis. Erectile dysfunction as a marker and predictor of cardiovascular disease. Edited by Charalambos Vlachopoulos. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0245.

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Erectile dysfunction (ED) is defined as the inability to obtain or maintain a penile erection to support satisfactory sexual performance. It is considered an early manifestation of generalized vascular disease and recognized as a marker of increased cardiovascular risk both acutely and chronically by predicting all-cause mortality, cardiovascular mortality, coronary events, stroke, and peripheral artery disease in men with and without known coronary artery disease. The link between ED and cardiovascular disease might reside in the interaction between androgen level, chronic inflammation, and cardiovascular risk factors that determine endothelial dysfunction and atherosclerosis both in the penile and coronary circulation. Because penile artery size is smaller compared with coronary arteries, the same degree of endothelial dysfunction and atherosclerotic burden causes a more significant reduction of blood flow in erectile tissues compared with that in coronary circulation. From a clinical standpoint, because ED may precede cardiovascular disease, it can be used as an early marker to identify men at higher risk of cardiovascular events. The average 3-year time period between the onset of ED symptoms and a cardiovascular event offers the opportunity for detailed cardiological assessment and intensive treatment of risk factors.

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Book chapters on the topic "Peripheral vasculature; Cardiovascular; Coronary"

1

Bauer, Barbara, Robert A. Kloner, and Karin Przyklenk. "Preconditioning and the Coronary Vasculature." In Developments in Cardiovascular Medicine, 61–72. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2602-5_4.

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Chilian, William M., Robert J. Tomanek, and Melvin L. Marcus. "The Coronary Vasculature During Myocardial Hypertrophy." In Developments in Cardiovascular Medicine, 87–105. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2041-8_5.

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Fail, Peter S., and Vinod Nair. "Imaging of the Peripheral Vasculature and Carotid Arteries." In Atlas of Cardiovascular Computed Tomography, 205–20. London: Springer London, 2017. http://dx.doi.org/10.1007/978-1-4471-7357-1_12.

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Barbeau, Gérald R., and George S. Abela. "Clinical Experience with Peripheral and Coronary Laser Angioplasty." In Developments in Cardiovascular Medicine, 257–71. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4613-1489-9_17.

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Tabib, A., and R. Loire. "Pathology of Peripheral and Coronary Vessels in AIDS Patients." In Cardiovascular Disease in AIDS, 65–73. Milano: Springer Milan, 2009. http://dx.doi.org/10.1007/978-88-470-0761-1_5.

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de Groot, J. Eric, J. Wouter Jukema, Alexander D. Montauban van Swijndregt, A. D. J. van Boven, Aeilko H. Zwinderman, Rob G. A. Ackerstaff, Anton F. W. van der Steen, Nicolaas Bom, Kong I. Lie, and Albert V. G. Bruschke. "Is peripheral B-mode ultrasound a substitute for coronary arteriography?" In Developments in Cardiovascular Medicine, 145–56. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0291-6_11.

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Drobinski, G., D. Brisset, F. Philippe, D. Kremer, G. Montalescot, and D. Thomas. "Therapeutic Ultrasound Peripheral and Coronary Angioplasty Using the Angioson System." In Developments in Cardiovascular Medicine, 213–27. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1243-7_13.

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8

Hoffman, Julien I. E. "Basic Anatomy and Physiology of the Heart, and Coronary and Peripheral Circulations." In Pediatric Cardiovascular Medicine, 46–70. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781444398786.ch4.

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Kroon, A. A., and A. F. H. Stalenhoef. "Effect of aggressive versus conventional lipid-lowering treatment on coronary and peripheral atherosclerosis: design and baseline characteristics of the LDL-Apheresis Atherosclerosis Regression Study (LAARS)." In Developments in Cardiovascular Medicine, 193–202. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0143-8_17.

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Stoia, M. A., A. D. Farcaș, F. P. Anton, A. I. Roman, and L. A. Vida-Simiti. "Comparative Analysis of Cardiovascular Risk Profile, Cardiac and Cervical Arterial Ultrasound in Patients with Chronic Coronary and Peripheral Arterial Ischemia." In International Conference on Advancements of Medicine and Health Care through Technology; 12th - 15th October 2016, Cluj-Napoca, Romania, 53–56. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-52875-5_12.

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Conference papers on the topic "Peripheral vasculature; Cardiovascular; Coronary"

1

Boutsianis, Evangelos, Thomas Frauenfelder, Hitendu Dave, Jurg Grunenfelder, Simon Wildermuth, Gregor Zund, Marko Turina, Dimos Poulikakos, and Yiannis Ventikos. "Cardiovascular Haemodynamic Simulations of Anatomically Accurate Coronaries." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-42728.

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The present study is devoted to the investigation of the pulsatile blood flow within the first few vessels of the Left Coronary Artery (LCA) vasculature of an anatomically accurate porcine coronary tree. Transient computational fluid dynamics simulations were performed under realistic pulsatile volume inflow boundary conditions. The numerical results have provided a comprehensive collection of information regarding the haemodynamics within the LCA and its major branches, namely the Left Anterior Descending (LAD) and the Left Circumflex (LCX) arteries. The underlying principle of developing computational techniques, which would eventually allow for the realistic simulation of the vascular haemodynamics of patients, lies on the capacity of such tools for predictive diagnostics and non-invasive, hence simulation-based, surgical planning.

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Chen, Jenny, Jessica S. Coogan, Hyun Jin Kim, and Charles A. Taylor. "Pressure and Flow Characterization for Different Idealized Models of Stenotic Coronary Arteries." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19329.

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Coronary artery disease is one of the leading causes of death worldwide. This year, an estimated 785,000 Americans will have a new coronary attack [1]. Treatment of coronary artery disease varies from medication alone to cardiovascular surgery. Treatment regimens depend on the number and hemodynamic significance of stenoses present. In this study, we created idealized models of stenotic coronary arteries with varying geometric properties and simulated flow and pressure in coronary stenoses using a novel computational method including a three-dimensional model of an idealized coronary artery coupled to a lumped parameter model of the heart at the inlet and a lumped parameter model of the distal coronary vasculature at the outlet.

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3

Wang, Roy, Rudolph L. Gleason, and Luke Brewster. "Diameter Constriction Reduces Intramural Circumferential Stress Gradient in the Vein Under Arterial Pressures." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80797.

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Coronary and peripheral artery diseases are a leading cause of morbidity and mortality in developed countries. For severe cases, surgical intervention to bypass the disease using autologous vessels continues to be the preferred choice of treatment. These bypass vessels are typically obtained from the venous vasculature. Despite the superior long-term patency of veins over synthetic grafts, one-year failure rates approach 30–40% in both the coronary and peripheral systems [1–2]. Still, bypass surgery remains the recommended therapy for most persons with severe arterial blockages [3]. As the number of bypass procedures increase and patients receiving bypasses live longer, improving the lifetime of bypass grafts is increasingly important.

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4

Solanki, Roshni, Rebecca Gosling, Vignesh Rammohan, Rodney Hose, Patricia Lawford, Julian Gunn, Paul Morris, and Yousef Ahmed. "16 Assessing the accuracy of a novel in silico imaging tool for the 3D reconstruction of coronary vasculature in the context of virtual fractional flow reserve." In British Cardiovascular Society Annual Conference ‘Digital Health Revolution’ 3–5 June 2019. BMJ Publishing Group Ltd and British Cardiovascular Society, 2019. http://dx.doi.org/10.1136/heartjnl-2019-bcs.15.

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5

Liu, J. L., Y. Qian, K. Itatani, T. Miyakoshi, A. Murakami, M. Ono, R. Shiurba, K. Miyaji, and M. Umezu. "An Approach of Computational Hemodynamics for Cardiovascular Flow Simulation." In ASME-JSME-KSME 2011 Joint Fluids Engineering Conference. ASMEDC, 2011. http://dx.doi.org/10.1115/ajk2011-03057.

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Computational fluid dynamics (CFD) is one of available methods to quantitatively evaluate the treatments of cardiovascular disease. However, currently, applications of this technology to cardiac surgery are few due to the complexity of performing physiological simulation. Here, we used CFD to study the outcome of the Norwood surgical procedure for palliating hypoplastic left heart syndrome in a 33-month-old child. The Reynolds number for post-surgical flow calculated at the peak of systole was about 4000, consistent with turbulent flow. During diastole, by contrast, the flow reduced to low speed, suggesting the strong transition flow from systole to diastole. Therefore, to improve the simulation of transitional flow, we determined that time step intervals of 10−5 second were best in using the k–ε turbulence model. We also develop a new boundary condition to simulate blood pressure wave reflection from peripheral vessels in order to physiologically capture pressure recovery and correctly obtained flow through each arch-branch and flow pattern in the coronary. Then we computed time-varying energy losses, local pressure, and wall shear stress at the anastomosis to evaluate the surgical outcome. The results suggest the time step and boundary conditions that take account of pressure wave reflection improve simulation of cardiovascular flow.

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6

Riel, Louis-Philippe, Steven Dion, Martin Brouillette, Simon Bérubé, Marc-Antoine Despatis, and Étienne Bousser. "Characterization of Calcified Plaques Retrieved From Occluded Arteries and Comparison With Potential Artificial Analogues." In ASME 2014 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/imece2014-38152.

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Cardiovascular disease is the leading cause of death worldwide. This disease includes chronic total occlusion (CTO), which is a complete blockage of an artery. Unlike partial occlusions, CTOs are difficult to cross percutaneously using conventional guidewires (thin and flexible wires) because of the fibrotic and calcified nature of the blockage. The lack of data regarding the mechanical properties of CTO limits the development of new technologies in the field of percutaneous coronary intervention (PCI) and percutaneous peripheral intervention (PPI). In this study, calcified plaques retrieved from occluded arteries are analyzed in order to better understand their mechanical properties and to help propose an artificial analogue. Calcified plaques samples were collected from the superficial femoral artery wall within one hour following a lower limb amputation surgery. These samples were studied to determine their composition and mechanical properties. The same characterization procedures were performed on various potential artificial analogues. These analogues include three plaster materials and dense hydroxyapatite blocks. The results were then compared with those of the calcified plaques in order to determine the more favorable analogue. This mechanical analysis and the proposal of a potential analogue for the calcified plaques found in occluded arteries could benefit the development of new technologies and devices in the field PCI and PPI.

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