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CVD Diagnosis Raises Hip Fracture Risk 'Considerably'


 

The risk for hip fracture rises steeply after patients have a major cardiovascular event, most likely because of genetic factors common to both vascular and bone disorders, a Swedish study has shown.

In a population-based study of nearly 32,000 twins in Sweden, the rate of hip fracture rose “considerably” in both men and women following any of several cardiovascular disease (CVD) diagnoses. Most of that increase appeared to be explained “by genes or by early environmental sharing” rather than individual lifestyle habits or other individual-specific environmental factors, said Dr. Ulf Sennerby of Uppsala (Sweden) University and associates.

“We advocate that individuals with a recent diagnosis of CVD should have their future fracture risk evaluated with clinical risk factors and bone scans,” such as the recently established 10-year probability using the FRAX (the World Health Organization's fracture risk assessment tool) algorithm, they noted.

The researchers used data from an extensive twin registry to examine the relation between CVD events and hip fracture. It included twin pairs who were born between 1914 and 1944 and were subsequently followed from the age of 50 years. It identified 31,936 pairs in which one twin developed CVD or hip fracture by Dec. 31, 2005.

The crude absolute rate of hip fractures in the cohort was 12.6 per 1,000 person-years after a diagnosis of heart failure, 12.6 per 1,000 person-years after a stroke, 6.6 per 1,000 person-years after a diagnosis of peripheral atherosclerosis, and 5.2 per 1,000 person-years after a diagnosis of ischemic heart disease, compared with 1.2 per 1,000 person-years for those without a CVD diagnosis.

All CVD diagnoses were associated with a higher risk of hip fracture independent of other CVD diagnoses and other comorbidities, the investigators said (JAMA 2009;302:1666-73).

The association was stronger in women than in men, but it was significant in both sexes.

Co-twins of subjects who had CVD also were at increased risk of sustaining hip fracture during follow-up, even if they had not had a cardiovascular event. For example, co-twins of subjects who had heart failure were at fourfold higher risk of fracturing a hip, compared with co-twins of subjects with no CVD.

The risk of hip fracture was higher in identical twins who had such “pseudoexposure” and lower in fraternal twins, indicating that an as-yet unidentified genetic factor predisposes people to both vascular and bone disorders, Dr. Sennerby and his associates said.

A subgroup of 24,598 subjects participated in telephone interviews to assess anthropomorphic, lifestyle, and medical factors. The inclusion of these factors into the data analysis did not materially change the results.

It is possible that “specific genes involved in cellular mechanisms shared by the vasculature and bone” may eventually explain this association between CVD and hip fracture, the authors wrote. “Matrix proteins supporting bone, vessel walls, and the myocardium [may] be of special relevance.

Dr. Sennerby reported no financial conflicts of interest.

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