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Early Vascular and Bone Changes in COPD Tied to Heart Risk


CARDIFF, Wales -- Premature arterial stiffness and bone aging in patients with chronic obstructive pulmonary disease (COPD) may explain why they are at greater risk for cardiovascular disease, researchers reported.

CARDIFF, Wales, June 15 -- Premature arterial stiffness and bone aging in patients with chronic obstructive pulmonary disease may explain why cardiovascular disease may emerge, researchers here reported.

Furthermore, osteoporosis in COPD patients, a common complication of the disease, was linked to even greater arterial stiffening, Dennis J. Shale, M.D., of Cardiff University, and colleagues reported in the second June 2007 issue of the American Journal of Respiratory and Critical Care Medicine.

In a study of 75 clinically stable COPD patients (mean age 63) with various levels of airway obstruction, and 42 healthy smokers or ex-smoker controls who were free of cardiovascular disease, the researchers tested the hypothesis that COPD patients would have increased arterial stiffness, which would be associated with osteoporosis and systemic inflammation.

All participants underwent spirometry, measurement of aortic (carotid-femoral) pulse wave velocity and augmentation index, a measure of arterial stiffness, as well as dual-energy x-ray absorptiometry, and blood sampling for inflammatory mediators.

The mean aortic pulse wave velocity was greater in patients, 11.4 m/s, than in controls, 8.95 m/s, P

The strongest predictors of aortic pulse wave velocity in all participants were age (P1 (P0.05), mean arterial pressure (P

Study limitations included its cross-sectional design, which did not allow inferring causal relationships between COPD, systemic inflammation, arterial stiffness, and cardiovascular disease, but did show strong relationships that could be explored further.

In addition, this study was not powered to test the relationship between aortic pulse wave velocity and a large number of other independent variables. Also, some of the patients had hypertension and took vasodilating drugs, the researchers said, although the findings held up in subgroup analyses.

The excess cardiovascular risk in COPD may be due to increased arterial stiffness, which is related to airflow obstruction, systemic inflammation, and the presence of osteoporosis, investigators said.

These changes suggest that age-related bone and vascular changes occur and remain undetected in mild or early lung disease and may underlie the excess cardiovascular risk in COPD, they said.

The arterial stiffness changes as patients age are similar to those seen in type I diabetes, but the risk of premature excess cardiovascular disease in COPD is not appreciated, Dr. Shale and colleagues concluded.

In an accompanying editorial, Claus Vogelmeier, M.D., and Robert Bals, M.D., Ph.D., of Philipps-University in Marburg, Germany wrote that the study provides "important new information" on the relationship of cardiovascular disease to COPD.

Reviewing the significant study findings, Drs. Vogelmeier and Bals said that aortic pulse wave velocity, the most clinically relevant measure of arterial stiffness, independently predicted cardiovascular risk.

The more severe the flow limitation, the higher the pulse wave velocity values, Drs. Vogelmeier and Bals wrote. "Thus, they said, "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."

Commenting on the osteoporosis findings, the editorialists noted that although finding a relationship between osteoporosis and COPD is not new, the data linking osteoporosis to increased arterial stiffness provide important new information.

The editorial writers reported no financial disclosures.

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