Abstract

We used a population-based case-control study in women and linkage to the Swedish in-patient register to examine if there is an increased risk of hip fracture after a cardiovascular disease. There was a substantially increased risk of hip fracture after a diagnosis of a cardiovascular disease. Recent data have indicated that cardiovascular diseases (CVDs) might have a relationship to osteoporosis, which may explain the increased risk of mortality after hip fracture. It is uncertain, however, whether there is an increased risk of fracture after any cardiovascular disease and in subgroups of CVDs. The objective of this study was to determine whether there are associations between CVD and future hip fracture risk. Knowledge of the risk pattern would lead to better understanding of common pathologic pathways of osteoporosis and CVD. We conducted a population-based case-control study of 1,327 incident hip fracture cases and 3,170 randomly selected population controls among women 50-81 years old in Sweden. Information on cardiovascular and other diseases before the fracture was obtained by linkage to the Swedish National Inpatient Register. Odds ratios (OR) and 95% confidence intervals (CI) where calculated by unconditional logistic regression. Before study entry, CVDs were diagnosed more than twice as commonly among fracture cases (25%) as among controls (12%). Also, after adjustment for variables including several chronic diseases, we found a doubled risk of hip fracture after a CVD event (OR 2.38; 95% CI 1.92-2.94). There was a gradient increase in risk of hip fracture with increasing number of hospitalizations for CVD and highest fracture risk occurred the first year after the CVD event. Hypertension, heart failure, and cerebrovascular lesions remained independent risk factors, with 2- to 3-fold increases in odds ratios, even after mutual adjustments for other CVDs. There was a substantially increased risk of hip fracture in women after a diagnosis of a CVD, a finding compatible with the concept of common pathologic pathways for osteoporotic fractures and CVD.

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