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Aortic stiffness and polymorphisms of collagen-1 type 1a gene in COPD patients


Journal of Lung, Pulmonary & Respiratory Research
Natalia Zakharchuk, Therapy department, Pacific State Medical University, Russia

Abstract

Currently the connection between chronic obstructive respiratory disease (COPD) and some cardiovascular and cerebrovascular diseases has been established. Vascular disorders in COPD become evident in the early stages of disease and can manifest from endothelial dysfunction to aortic mechanical property disturbance and cerebral circulation disorders. COPD is also known as a disease associated with smoking. A number of researchers have described pathophysiological mechanisms of vascular disorders and in particular arterial stiffening in COPD. A variety of theories have been proposed to explain these observations. Pathophysiological processes that increase arterial stiffness (both physiological and pathophysiological) involve remodeling cascades leading to disturbance of the structural and functional relationships between collagen and elastin in the arterial vascular wall. The main processes involved appear to be inflammatory, proteases and oxidative stress. New research suggests that the vascular dysfunction observed in COPD is associated with some specific genes. New data suggests that this is not just due to endothelial dysfunction, but a violation of the mechanical properties of the arterial vasculature, which is now considered an important component of the pathogenesis of COPD. Surplus aortic stiffness can contribute increasingly to cardiovascular event risk in COPD and is associated with changes in normal cerebral circulation and cognitive function. Research is focused on the study of genetic predisposition for vascular dysfunction in COPD. Various polymorphisms determining the connective tissue metabolism, production of nitric oxide, detoxification of xenobiotics and many others are now all thought relevant. Increasing of aortic stiffness is an important component of the amplification of cardiovascular risk events, coronary disorders and cerebral circulation in patients with COPD. Some polymorphisms are considered especially relevant, such as COL1A1 polymorphisms. It is now important to take into consideration the pathophysiological consequences of increasing arterial stiffness in COPD, which are schematically represented in our review.

Keywords

endothelial dysfunction, arterial stiffness, aorta, chronic obstructive pulmonary disease, genotype, cardiovascular risk, pathophysiology, left ventricular, collagen-1 type 1a gene

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