alexa Commentary: On the Pathophysiology of Coronary Heart Disease
ISSN: 2472-4971

Journal of Medical & Surgical Pathology
Open Access

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Commentary

Commentary: On the Pathophysiology of Coronary Heart Disease

Mark I.M. Noble*

Department of Medicine and Therapeutics, University of Aberdeen, UK

*Corresponding Author:
Mark I.M. Noble
Department of Medicine and Therapeutics, University of Aberdeen
Polwarth Building, Foresterhill, berdeen AB25 2ZH, UK
Tel: 01674 840142
E-mail: [email protected]/[email protected]

Received date: June 07, 2017; Accepted date: June 15, 2017; Published date: June 21, 2017

Citation: Noble MIM (2017) Commentary: On the Pathophysiology of Coronary Heart Disease. J Med Surg Pathol 2:147. doi: 10.4172/2472-4971.1000147

Copyright: © 2017 Noble MIM. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

This article highlights some important aspects of the pathophysiology of coronary artery disease, namely:

• The distribution of lesions within the arterial tree at sites of low wall shear stress.

• The potential role of low flow-mediated arterial dilatation at sites of low wall stress.

• Low flow-mediated dilatation leads to low nitric oxide production by the arterial endothelium and consequent reduced protection against lesion formation.

• Flow-mediated dilatation is reduced by high lumenal glucose concentration.

• The role of the glycocalyx dysfunction in mediating flow-mediated dilatation and consequent reduced NO production by the arterial endothelium and cell adhesion.

• Stenoses cause convective acceleration of blood velocity and a consequent increase in platelet shear stress.

• Increased platelet shear stress activates platelets with release of serotonin.

• Serotonin activates more platelet activation via the 5HT2A platelet receptor causing a positive feedback and thrombus growth.

• Arterial thrombus growth is abolished by 5HT2A receptor antagonists, the key to improved treatment of the disease.

• One 5HT2A receptor antagonist has been shown in humans to be safe and to cause no excess bleeding from wounds.

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