Risk In Chronic Obstructive Pulmonary Disease Research Articles

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.

Surrogates of Mortality in Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) remains a leading cause of disability and death in the United States. The identification and amelioration of systemic manifestations of COPD may improve long-term outcomes, including survival. These systemic manifestations often correlate with increased risk of mortality and may be considered surrogates of disease severity. Several potential clinical surrogates are evaluated, including airflow obstruction, dyspnea, malnutrition, hypoxemia, exercise capacity, lung hyperinflation, and anemia. The evidence in support of the impact of various COPD treatment modalities on systemic manifestations of COPD is also reviewed. Finally, the usefulness of measuring body mass index, degree of airflow obstruction, dyspnea, and exercise capacity in combination (the BODE index), as a measure of disease severity and mortality risk in COPD, is examined and found to be a simple-to-use tool for predicting COPD-related hospitalization and mortality.