Mechanisms of atherothrombosis in chronic obstructive pulmonary disease.
Patients affected by chronic obstructive pulmonary disease (COPD) have an increased risk of atherothrombotic acute events, independent of smoking and other cardiovascular risk factors. As a consequence, myocardial ischemia is a relevant cause of death in these patients. We reviewed studies concerning the potential mechanisms of atherothrombosis in COPD. Bronchial inflammation spreads to the systemic circulation and is known to play a key role in plaque formation and rupture. In fact, C-reactive protein blood levels increase in COPD and provide independent prognostic information. Systemic inflammation is the first cause of the hypercoagulable state commonly observed in COPD. Furthermore, hypoxia is supposed to activate platelets, thus accounting for the increased urinary excretion of platelet-derived thromboxane in COPD. The potential metabolic risk in COPD is still debated, in that recent studies do not support an association between COPD and diabetes mellitus. Finally, oxidative stress contributes to the pathogenesis of COPD and may promote oxidation of low-density-lipoproteins with foam cells formation. Retrospective observations suggest that inhaled corticosteroids may reduce atherothrombotic mortality by attenuating systemic inflammation, but this benefit needs confirmation in ongoing randomized controlled trials. Physicians approaching COPD patients should always be aware of the systemic vascular implications of this disease.
Fimognari
Filippo Luca
FL
Health Centre for Elderly, Chair of Geriatrics, University Campus Bio Medico, Rome, Italy.
Scarlata
Simone
S
Conte
Maria Elisabetta
ME
Incalzi
Raffaele Antonelli
RA
D050197:Atherosclerosis / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D006801:Humans; D018384:Oxidative Stress / Q000502:physiology; D015539:Platelet Activation / Q000502:physiology; D029424:Pulmonary Disease, Chronic Obstructive / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D013927:Thrombosis / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy