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Opioid use associated with increased prevalence of AF
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Opioid use was independently associated with increased prevalence of atrial fibrillation in a new analysis from the Reasons for Geographic and Racial Differences in Stroke, or REGARDS, study.
Although opioid receptors are downregulated in animal models of AF, the association between opioid use and AF had not been analyzed in population-based studies, Waqas T. Qureshi, MD, and colleagues wrote in a research letter to JAMA Internal Medicine.
Qureshi, from the section on cardiology, department of internal medicine, Wake Forest School of Medicine in Winston-Salem, North Carolina, and colleagues examined the association between opioid use, which was determined by pill-bottle review during an in-home visit, and AF, which was identified by ECG and self-reported history of a previous diagnosis, in 24,632 participants (mean age, 65 years; 54% women; 40.2% black) from the REGARDS study.
They found that 7.7% of participants reported opioid use and 8.5% had AF. Of those using opioids, 41.3% were taking hydrocodone, 24.9% propoxyphene and 20% tramadol. Those using opioids were more likely to be female, to be black and to have CV comorbidities compared with nonusers, according to the researchers.
Qureshi and colleagues wrote that the prevalence of AF was higher in opioid users compared with nonusers (12.5% vs. 7.6%; P < .001) and that after adjustment for potential confounders, opioid use was associated with increased odds of AF (OR = 1.35; 95% CI, 1.16-1.57).
The results were consistent regardless of age, sex, race, presence of CHD, presence of hypertension or presence of diabetes, they wrote.
Further adjustment for benzodiazepine and alcohol use did not change the results (OR = 1.29; 95% CI, 1.11-1.51), according to the researchers.
When users of propoxyphene, which has known cardiotoxic effects, were excluded, the results did not change (OR = 1.33; 95% CI, 1.11-1.58), they wrote. Propoxyphene was withdrawn from the United States market in 2010, but REGARDS enrollment began in 2003.
“Endogenous opioid peptides open mitochrondrial potassium adenosine triphosphate channels, making mitochrondria resistant to oxidative stress during episodes of ischemia,” the researchers wrote. “Loss of this protective mechanism against oxidative stress may render atrial myocytes amenable to damage, leading to AF.”
Limitations of the study include its cross-sectional design, possibility of residual confounding by unmeasured factors, lack of data on opioid dosage and length of therapy and possibility of recall bias from a self-reported history of a previous diagnosis, they wrote. – by Erik Swain
Disclosure: The researchers report no relevant financial disclosures.
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