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Invited Commentary
January 2017

Cardiovascular Medications and Fractures: Dodging Complexity

Author Affiliations
  • 1Duke University School of Medicine, Durham, North Carolina
  • 2The Durham Veterans Affairs Geriatric Research Education and Clinical Center, Durham, North Carolina
JAMA Intern Med. 2017;177(1):77-78. doi:10.1001/jamainternmed.2016.7040

The American computer scientist Alan Perlis wrote, “Fools ignore complexity. Pragmatists suffer it. Some can avoid it. Geniuses remove it.”1(p 10) Geriatricians (a pragmatic bunch) will tell you that the associations between medications and geriatric syndromes, such as osteoporotic fractures, are inherently complex and often involve trade-offs between benefits in one system and harms in another. Patients with low bone density and/or fractures have a higher risk of cardiovascular disease and vice versa; common pathophysiologic pathways have been postulated. Medications used to treat cardiovascular disease, including β-blockers, angiotensin system–blocking medications, calcium channel blockers, and thiazide diuretics, have been hypothesized to positively and negatively affect bone metabolism.2 These same medications may increase falls through changes in blood pressure, heart rate, and (in the case of angiotensin-converting enzyme inhibitors [ACEis]) muscle metabolism; fall risk may vary by class. One in 10 falls results in an osteoporotic fracture. Given the high prevalence of low bone density (55%) and cardiovascular disease (>70%) in people older than 65 years, it would be foolish to ignore the complex interaction between cardiovascular medications and osteoporotic fractures.

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