DENVER — Mild renal impairment constitutes an important new predictor of new-onset atrial fibrillation, Dr. Nicholas S. Peters reported at the annual meeting of the Heart Rhythm Society.
The most likely pathophysiologic mechanism for this association involves the elevated renin-angiotensin-aldosterone system activity characteristic of mild renal dysfunction. Such a mechanism, in turn, gives rise to a readily testable hypothesis that drugs that block renin-angiotensin-aldosterone overactivity—ACE inhibitors, angiotensin receptor blockers, and aldosterone blockers such as spironolactone—may reduce the incidence of new-onset atrial fibrillation (AF), according to Dr. Peters of Imperial College London.
He reported on 203 consecutive patients with new-onset AF and 781 without AF who were enrolled in the Imperial College New AF Study, a prospective epidemiologic study of AF in a community setting.
The mean serum creatinine level was significantly higher in patients presenting with their first episode of AF (94 micromol/L) than in controls (83 micromol/L). The AF patients had a mean estimated glomerular filtration rate (eGFR) of 68 mL/min per 1.73 m
An eGFR of less than 60 mL/min per 1.73 m
An association between milder degrees of renal impairment and the atrial arrhythmia has not previously been reported, according to Dr. Peters.
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