The potential role of endothelial dysfunction and platelet activation in the development of thrombotic risk in COPD patients.

Despite lack of knowledge in the field, several studies have underlined the role of endothelium dysfunction and platelet activation as significant players in the development and progression of chronic obstructive pulmonary disease (COPD). Indeed, endothelium plays a crucial role in vascular homeostasis and impairment, due to the inflammation process enhanced by smoking. Chronic inflammation and endothelial dysfunction have been proved to drive platelet activity. Consequently, thrombotic risk is enhanced in COPD, and might explain the higher percentage of cardiovascular death in such patients. Areas covered: This review aims to clarify the role of endothelium function and platelet hyper-activity as the pathophysiological mechanisms of the increased thrombotic risk in COPD. Expert commentary: In COPD patients, chronic inflammation does not impact only on lung parenchyma, but potentially involves all systems, including the endothelium of blood vessels. Impaired endothelium has several consequences, such as reduced vasodilatation capacity, enhanced blood coagulation, and increased platelet activation resulting in higher risk of thrombosis in COPD patients. Endothelium dysfunction and platelet activation are potential targets of therapy in patients with COPD aiming to reduce their risk of cardiovascular events.