Study finds higher risk of cardiovascular and cerebrovascular disease in COPD patients, suggests spread of inflammation may be a factor.
Chronic obstructive pulmonary disease (COPD) is rampant globally and is the third leading cause of death in the United States. Its comorbidities—myocardial infarction, arrhythmia, and multiple organ system disease—are well documented and increase risk of all-cause mortality and cardiovascular mortality in COPD sufferers. Since many of these diseases have similar etiologies (smoking in particular), this is not surprising.
Researchers from the Cleveland Clinic recognized that while clinicians have adequate tools to predict short-term risk for COPD patients they have few tools to predict lifetime or long-term risk. They saw a need for a systematic risk stratification algorithm that clinicians could use with COPD patients. As a first step, they compared the prevalence of self-reported cardiovascular and cerebrovascular disease (CCVD) between patients with COPD and patients who did not have COPD. Their study results
were published online ahead of print on July 2, 2014, in the American Journal of Preventive Medicine
These researchers analyzed pooled National Health and Nutrition Examination Survey (NHANES) 2007-2010 data in May 2012 and April 2013 and calculated the Framingham risk score for patients without self-reported CCVD. Patients were classified as high short-term risk, low short-term/high lifetime risk, and low short-term/low lifetime risk for future CCVD.
COPD and non-COPD groups self-reported CCVD at rates of 20% and 7.4%, respectively. COPD was an independent risk factor for prevalent self-reported CCVD.
The researchers isolated patients who did not have CCVD and predicted their future CCVD risk. The results varied widely depending on whether or not patients had comorbid COPD. In the non-COPD group, 18.9% had high short-term risk, 62.7% had low short-term/high lifetime risk, and 18.4% had low short-term/low lifetime risk. In the COPD group, corresponding prevalence estimates were 35.8%, 53.2%, and 11.1%, respectively. Thus, risk of future CCVD was significantly higher in the COPD group.
Men and women had significantly different risk factor profiles for future CCVD. The researchers speculate that women’s circulating estrogens create a vigorous airway inflammatory reaction which leads to an imbalance between cigarette smoke toxin formation and removal.
This study replicated the results of several others that found that smoking is not the sole determinant of increased CCVD risk in COPD patients. The researchers note that atherosclerotic CCVD’s hallmark is endothelial dysfunction, a problem strongly related to inflammation. They indicate local pulmonary inflammation in COPD may spread to the systemic circulation, possibly leading to extensive endothelial dysfunction in multiple vascular beds. They also discuss other potential mechanisms, include pulmonary hypertension and increased sympathetic nervous system stimulation.