Fibroblast Growth Factor-23 and Incident Atrial Fibrillation: The Multi-Ethnic Study of Atherosclerosis (MESA) and the Cardiovascular Health Study (CHS)
Do circulating levels of fibroblast growth factor-23 (FGF-23) correlate with incidence of atrial fibrillation (AF)?
Circulating FGF-23 concentrations were measured in 6,398 MESA (Multi-Ethnic Study of Atherosclerosis) and 1,350 CHS (Cardiovascular Health Study) trial participants with incident AF, all free of clinical cardiovascular disease at baseline.
During approximately 8.0 years of median follow-up, 291 and 229 incident AF events were observed in the MESA and CHS trials, respectively. In multivariable analyses, each two-fold higher FGF-23 concentration was associated with a 41% higher risk of incident AF in MESA (hazard ratio [HR], 1.41; p = 0.003) and a 30% higher risk of incident AF in CHS (HR, 1.30; p = 0.016). Serum phosphate concentration was associated with incident AF in MESA (HR, 1.15 per 0.5 mg/dl, p = 0.023), but not in CHS. In MESA, an association of low estimated glomerular filtration rate (GFR) with incident AF was partially attenuated by adjusting for FGF-23.
The authors concluded that higher circulating FGF-23 concentration is associated with incident AF and may, in part, explain the link between chronic kidney disease and AF.
Impaired renal function is increasingly recognized as a risk factor for left ventricular hypertrophy (LVH), diastolic dysfunction, and atrial fibrillation. Renal disease affects many factors that could contribute to this link, including FGF-23 levels, which rise in the setting of reduced GFR. FGF-23 has been shown to induce LVH directly, in addition to its effects on urinary phosphate excretion and vitamin D production. This study provides additional support for a role of FGF-23 in promoting a very common adverse cardiovascular event, AF. Further studies will be necessary to determine whether FGF-23 is a mediator or marker of AF.
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