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Premature Vascular and Bone Changes Occur in COPD Patients

Researchers in the United Kingdom have found that patients with COPD, or chronic obstructive pulmonary disease, have greater arterial stiffness. The researchers also found that those COPD patients with osteoporosis, a common complication of the respiratory disease, had even greater arterial stiffness. These premature signs of aging may explain why COPD patients are at greater risk for cardiovascular disease.

Their research results appear in the second issue for June 2007 of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.

Dennis J. Shale, M.D., of the Department of Respiratory Medicine at Cardiff University in the United Kingdom, and eight associates studied 75 clinically stable COPD patients who had various levels of airway obstruction, and 42 smoker or ex-smoker control subjects who did not have cardiovascular disease or COPD.

All participants in the study underwent spirometry to determine lung function, had their aortic pulse wave velocity measured along with another indirect measurement of arterial stiffness, took bone mineral density tests of their spine and hips, and had their blood sampled for inflammatory mediators.

COPD, the fourth leading cause of death in the United States and the world, involves persistent obstruction of the airways caused by emphysema or chronic bronchitis. In most instances, both conditions result from years of smoking cigarettes.

Though the exact link between COPD and arterial stiffness was not identified by the researchers, they did find elevated levels of inflammation markers in those with COPD. Other researchers have demonstrated that inflammatory processes are involved in arteriosclerosis, the cardiovascular disease commonly known as hardening of the arteries.

There is also evidence that inflammation plays a role in osteoporosis. In this study, patients with osteoporosis had the greatest a rterial stiffness. Increased arterial stiffness was present in patients with COPD over a wide range of severity of airway obstruction and was greatest in those with osteoporosis, said Dr. Shale. Our findings indicate vascular changes predictive of cardiovascular disease occur and remain undetected in mild or early lung disease and may underlie the excess cardiovascular risk in COPD.

The researchers noted that age was an important factor influencing arterial stiffness, a problem that reflects the increasing rigidity of the aortic artery. The average age of the study cohort was 63. The increased arterial stiffness in patients within each decade is similar to changes seen in type I diabetes mellitus and suggest that age-related vascular changes occur prematurely in COPD, as compared with disease-free individuals, said Dr. Shale. However, unlike diabetes mellitus, the risk of premature excess cardiovascular disease in COPD is not appreciated.

At the beginning of the study, none of the participants had a history of heart disease or possessed cardiovascular symptoms. Of the 75 COPD patients studied, 18 had osteoporosis, while among the controls, only two individuals suffered from abnormal loss of bony tissue. Also, those who had osteoporosis of the hip had a greater aortic pulse wave velocity than those without the hip problem.

In an editorial on the study in the same issue of the journal, Claus Vogelmeier, M.D., and Robert Bals, M.D., of Philipps-University, Marburg in Germany, said that the study provides important new information on the relationship of cardiovascular disease and COPD.

They noted that aortic pulse wave velocityconsidered the most clinically relevant measure of arterial stiffnesshas been shown to predict cardiovascular outcome in various populations. The authors also highlighted the studys correlation of pulse wave velocity and COPD severity as important.

The more severe the flow limit ation, the higher the pulse wave velocity values, wrote Drs. Vogelmeier and Bals. Thus, COPD may induce arterial stiffness, which in turn may promote vascular remodeling, thickening of arterial walls and plaque formation. The process may start in the early stages of COPD and worsen with the decline of lung function.

The editorialists also commented on osteoporosis, which was the second focus of the study: The authors found that bone mineral density was lower in patients with COPD than in control subjects. Among the patients with COPD, 32 percent had osteoporosis and this was not restricted to those with severe COPD.

Although the editorialists termed the relationship between COPD and osteoporosis in the study was not novel, they noted that those patients with osteoporosis also had the greatest arterial stiffness valuesa new finding.

They concluded that future research is necessary to uncover further relationships between this studys findings and accelerated aging processes in COPD, which might then be avoided.


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