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      The Role of Septal Perforators and “Myocardial Bridging Effect” in Atherosclerotic Plaque Distribution in the Coronary Artery Disease

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          Summary

          The distribution of atherosclerotic plaque burden in the human coronary arteries is not uniform. Plaques are located mostly in the left anterior descending artery (LAD), then in the right coronary artery (RCA), circumflex branch (LCx) and the left main coronary artery (LM) in a decreasing order of frequency. In the LAD and LCx, plaques tend to cluster within the proximal segment, while in the RCA their distribution is more uniform. Several factors have been involved in this phenomenon, particularly flow patterns in the left and right coronary artery. Nevertheless, it does not explain the difference in lesion frequency between the LAD and the LCx as these are both parts of the left coronary artery. Branching points are considered to be the risk points of atherosclerosis. In the LCx, the number of side branches is lower than in the LAD or RCA and there are no septal perforators with intramuscular courses like in the proximal third of the LAD and the posterior descending artery (PDA). We hypothesized that septal branches generate disturbed flow in the LAD and PDA in a similar fashion to the myocardial bridge (myocardial bridging effect). This coronary architecture determines the non-uniform plaque distribution in coronary arteries and LAD predisposition to plaque formation.

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          Most cited references71

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          The role of shear stress in the pathogenesis of atherosclerosis.

          Although the pathobiology of atherosclerosis is a complex multifactorial process, blood flow-induced shear stress has emerged as an essential feature of atherogenesis. This fluid drag force acting on the vessel wall is mechanotransduced into a biochemical signal that results in changes in vascular behavior. Maintenance of a physiologic, laminar shear stress is known to be crucial for normal vascular functioning, which includes the regulation of vascular caliber as well as inhibition of proliferation, thrombosis and inflammation of the vessel wall. Thus, shear stress is atheroprotective. It is also recognized that disturbed or oscillatory flows near arterial bifurcations, branch ostia and curvatures are associated with atheroma formation. Additionally, vascular endothelium has been shown to have different behavioral responses to altered flow patterns both at the molecular and cellular levels and these reactions are proposed to promote atherosclerosis in synergy with other well-defined systemic risk factors. Nonlaminar flow promotes changes to endothelial gene expression, cytoskeletal arrangement, wound repair, leukocyte adhesion as well as to the vasoreactive, oxidative and inflammatory states of the artery wall. Disturbed shear stress also influences the site selectivity of atherosclerotic plaque formation as well as its associated vessel wall remodeling, which can affect plaque vulnerability, stent restenosis and smooth muscle cell intimal hyperplasia in venous bypass grafts. Thus, shear stress is critically important in regulating the atheroprotective, normal physiology as well as the pathobiology and dysfunction of the vessel wall through complex molecular mechanisms that promote atherogenesis.
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            Update on myocardial bridging.

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              Calcification in atherosclerosis: bone biology and chronic inflammation at the arterial crossroads.

              Dystrophic or ectopic mineral deposition occurs in many pathologic conditions, including atherosclerosis. Calcium mineral deposits that frequently accompany atherosclerosis are readily quantifiable radiographically, serve as a surrogate marker for the disease, and predict a higher risk of myocardial infarction and death. Accelerating research interest has been propelled by a clear need to understand how plaque structure, composition, and stability lead to devastating cardiovascular events. In atherosclerotic plaque, accumulating evidence is consistent with the notion that calcification involves the participation of arterial osteoblasts and osteoclasts. Here we summarize current models of intimal arterial plaque calcification and highlight intriguing questions that require further investigation. Because atherosclerosis is a chronic vascular inflammation, we propose that arterial plaque calcification is best conceptualized as a convergence of bone biology with vascular inflammatory pathobiology.
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                Author and article information

                Journal
                Pol J Radiol
                Pol J Radiol
                Pol J Radiol
                Polish Journal of Radiology
                International Scientific Literature, Inc.
                1733-134X
                1899-0967
                2015
                16 April 2015
                : 80
                : 195-201
                Affiliations
                [1 ]3 rd Department of Cardiology, Medical University of Silesia, Silesian Center for Heart Diseases, Zabrze, Poland
                [2 ]Department of Mechanical Engineering, University of Sheffield, Sheffield, U.K.
                [3 ]Department of Diagnostic Imaging, Medical University of Silesia, Silesian Center for Heart Diseases, Zabrze, Poland
                [4 ]Department of Mechanical Engineering Fundamentals, Faculty of Mechanical Engineering and Computer Science, University of Bielsko-Biała, Bielsko-Biała, Poland
                Author notes
                Author’s address: Jarosław Wasilewski, 3 rd Department of Cardiology, Medical University of Silesia, Silesian Centre for Heart Diseases, M. Curie-Skłodowska 9 Str., 41-800 Zabrze, Poland, e-mail: jaroslaw-wasilewski@ 123456wp.pl
                [A]

                Study Design

                [B]

                Data Collection

                [C]

                Statistical Analysis

                [D]

                Data Interpretation

                [E]

                Manuscript Preparation

                [F]

                Literature Search

                [G]

                Funds Collection

                Article
                893227
                10.12659/PJR.893227
                4404747
                25922625
                e25c2f36-bc93-4164-ab2c-2fce20173abb
                © Pol J Radiol, 2015

                This is an open access article. Unrestricted non-commercial use is permitted provided the original work is properly cited.

                History
                : 07 December 2014
                : 19 December 2014
                Categories
                Review Article

                Radiology & Imaging
                atherosclerosis,haemodynamics,myocardial bridge,septal branch
                Radiology & Imaging
                atherosclerosis, haemodynamics, myocardial bridge, septal branch

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