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Prevention of atrial fibrillation (AF) is an urgent unmet clinical need given its association with a higher risk of stroke, heart failure and death. Known risk factors for AF include age, hypertension, body mass index and diabetes as well as markers of systemic inflammation; all of which likely contribute to the high prevalence of this dysrhythmia in our aging, increasingly obese, population. However, there currently are no established biomarkers to help in assessment of AF risk. Adiponectin is an adipocyte-generated hormone with lower levels seen with increased adiposity. Adiponectin has insulin sensitizing, anti-inflammatory and anti-atherosclerotic effects in experimental studies suggesting that, at least in theory, a lower adiponectin level might increase the likelihood of adverse cardiovascular outcomes, including AF. Paradoxically, previous clinical studies have reported the exact opposite finding for coronary disease, heart failure and all cause mortality, with mixed results for the association between adiponectin levels and AF.
In this issue of Heart, Macheret and colleagues (see page 1368) hypothesized that these seemingly contradictory findings might be due to a U-shaped relationship between adiponectin and incident AF. To test this hypothesis, they measured adiponectin levels in 3190 older adults (mean age 74±5 years) from the population based Cardiovascular Health Study, who were free of AF, atrial flutter or known cardiovascular disease at study entry. Based on analysis of the 886 incident AF events at 11.4 years of follow-up, with adjustment for both potential cofounders and putative mediators of AF, they did not find the hypothesized U-shaped association. Instead, higher (not lower) …
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