Use of bisphosphonate and risk of atrial fibrillation in older women with osteoporosis.

UNLABELLED: Concerns have been raised among clinicians and patients whether or not bisphosphonates increase the risk of atrial fibrillation. In this large cohort study, increased risk of atrial fibrillation was not found to be associated with bisphosphonate. In fact, bisphosphonate even showed a protective effect against cardiac arrhythmia compared to other osteoporosis medications. INTRODUCTION: Increased risk of atrial fibrillation among bisphosphonate users has been reported; however, the results from these studies are controversial. The purpose of this study was to evaluate the risk of atrial fibrillation associated with bisphosphonate use in older women. METHODS: We used the Korean Health Insurance Review and Assessment Service claims database from May 1, 2005 to June 30, 2006. Retrospective cohort analysis was conducted on women 65 years or older with newly diagnosed cases of osteoporosis (ICD 10 code: M80, M81) who had not previously taken any medications for osteoporosis. Bisphosphonate-exposed and non-exposed patients were followed until they were either diagnosed with atrial fibrillation (ICD 10 code: I48) or until the end of the study. The Cox proportional hazards model was used to calculate hazard ratios and the 95% confidence intervals. RESULTS: Atrial fibrillation was reported in 626 of the 120,319 patients (0.52%) treated with bisphosphonates and 66 of 9,863 patients (0.67%) treated with other osteoporosis medications. Overall hazard ratio for developing atrial fibrillation in the bisphosphonate-treated group was 0.52 (95% CIs, 0.29-0.91). In patients with a medication possession ratio greater than 0.7, the hazard ratio was lower (HR 0.41, 95% CIs 0.23-0.75). In the subgroup analysis, alendronate showed a statistically significant protective effect against the risk of atrial fibrillation with a hazard ratio of 0.75 (95% CI, 0.58-0.97). CONCLUSION: Among older Korean women with osteoporosis, bisphosphonate was found to have a protective effect against atrial fibrillation.

Cardiovascular effects of benzquinamide.

The cardiovascular effects of benzquinamide were evaluated in anesthetized dogs. Intravenous benzquinamide, 0.5 to 5 mg/kg, caused tachycardia, elevated blood norepinephrine levels, frequent ventricular arrhythmias, and brief hypotension. Ganglionic blockade by hexamethonium prior to administration of benzquinamide prevented the tachycardia and alterations in norepinephrine levels but prolonged the period of hypotension. In isolated mesenteric arterial preparations benzquinamide interfered with contractile force generated by potassium chloride, norepinephrine, and prostaglandin F2 alpha. It is concluded that benzquinamide directly relaxes vascular smooth muscle thereby producing in vivo reduced peripheral vascular resistance and hypotension, which are compensated for by reflex sympathetic activation.