COPD Morbidity, Mortality and Unrecognized, Untreated Thromboembolism

Morbidity and mortality in individuals with chronic obstructive pulmonary disease (COPD) are on the rise, due possibly to underrecognized and insufficiently treated thromboembolism than can develop in these patients. A review of data on the use of anticoagulation therapy among patients with exacerbations of COPD was recently published in the International Journal of Chronic Obstructive Pulmonary Disease.

Review authors sought to evaluate whether an insufficient approach to thromboembolic risk in patients with COPD is associated with higher rates of morbidity and mortality in this population, with the currently available data being scarce and fairly controversial. The pathogenesis of COPD has been shown to involve neutrophilic inflammation, as well as macrophages and CD8+ (cytotoxic) T lymphocytes. Epithelial cells and alveolar macrophages that elicit the release of cytokines and chemokines are activated by inhaled particles. These cytokines, in turn, inhibit plasminogen activators.

The systemic inflammation that is observed among patients with COPD can trigger various complications, particularly in the cardiovascular system. Chronic hypoxia and hypercapnia in individuals with COPD stimulate the hematopoietic function of the bone marrow to induce a compensatory elevation in the number of red blood cells, leading to increased blood viscosity and abnormal blood rheology. Vasoconstriction induced by chronic hypoxia in COPD may be associated with the development of pulmonary hypertension.

Another factor linked to the development of pulmonary vascular disease in patients with COPD is destruction of the lung parenchyma and the manifestation of emphysema, along with the loss of vascularity in surrounding tissue. The direct relationship between an increase in serum fibrinogen and the occurrence of cardiovascular events implies that the procoagulant state may generate atherothrombosis in patients with COPD. These findings suggest that thrombotic events are present in individuals with COPD because of a procoagulant status that is triggered by atherosclerotic vascular lesions.

Research has shown that treatment with low-molecular-weight heparin (LMWH) is associated with a considerable reduction in the incidence of deep vein thrombosis in individuals with many acute disorders, with the efficacy of LMWH being demonstrated in those with COPD. Superior improvements in arterial gasometry and lung function, as well as significant reductions in levels of D-dimers and blood clotting parameters, are associated with the use of anticoagulant therapy.

The investigators concluded that based on their review of existing data, early initiation of injectable anticoagulation treatment should be used in patients who are hospitalized with COPD exacerbations. Posthospitalization, the type of anticoagulant therapy to use in these individuals depends on the individual exacerbatory phenotype and its associated pathology. In those with an exacerbating phenotype and those linked to cardiovascular risk factors, the use of anticoagulant therapy is recommended on a long-term basis. Early diagnosis and long-term anticoagulant treatment in COPD may help increase rates of survival and improved prognosis. The use of extensive stratification-based studies of COPD is warranted to further explore the use of early anticoagulant therapy in this population of patients.

Disclosure: None of the study authors has declared affiliations with biotech, pharmaceutical, and/or device companies.  

Reference  

Petris OR, Cojocaru E, Fildan AP, Cojocaru C. COPD and anticoagulation therapy: time for a new approach? Int J Chron Obstruct Pulmon Dis. 2021;16:3429-3436. doi:10.2147/COPD.S340129