Abstract
Patients with chronic obstructive pulmonary disease (COPD) show systemic consequences, such as chronic systemic inflammation leading to changes in the airway, airway penetrability, and endothelial function. Endothelial dysfunction is characterized by a list of alterations of endothelium towards reduced vasodilation, proinflammatory state, detachment and apoptosis of endothelial cells, and development of atherosclerosis. COPD-induced endothelial dysfunction is associated with elevated cardiovascular risk. The increment of physical activities such as pulmonary rehabilitation (PR) training have a significant effect on COPD, thus, PR can be an integrative part of COPD treatment. In this narrative review the focus is on the function of endothelial inflammatory mediators [cytokines, chemokines, and cellular proteases] and pulmonary endothelial cells and endothelial dysfunction in COPD as well as the effects of dysfunction of the endothelium may play in COPD-related pulmonary hypertension. The relationship between smoking and endothelial dysfunction is also discussed. The connection between different pulmonary rehabilitation programs, arterial stiffness and pulse wave velocity (PWV) is presented. Endothelial dysfunction is a significant prognostic factor of COPD, which can be characterized by PWV. We discuss future considerations, like training programs, as an important part of the treatment that has a favorable impact on the endothelial function.
Highlights
The factors that drive pulmonary hypertension are the following: systemic inflammation, impaired lung function accompanied by lung inflammation, and hypoxic vasoconstriction
This persistent pulmonary inflammatory response is driven by the increment of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in Chronic obstructive pulmonary disease (COPD) patients; pulmonary artery stiffness, pulmonary hypertension, and cor pulmonale are often associated with respiratory diseases, such as COPD [141,142]
These findings clearly indicate that Cigarette smokeand (CS) exposure damages endothelial cells in vitro; these findings are ignored or treated clinically irrelevant apart from the fact that they support the idea that emphysema is, to some extent, a vascular abnormality
Summary
Botond Szucs 1,† , Csilla Szucs 2,† , Mate Petrekanits 3 and Janos T.
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