Fibroblast growth factor-23 and subclinical markers of cardiac dysfunction: The coronary artery risk development in young adults (CARDIA) study.

BACKGROUND: Elevated Fibroblast Growth Factor-23 (FGF23) levels have been associated with greater left ventricular mass (LVM) and heart failure. Whether higher FGF23 is associated with higher LVH prevalence and longitudinal changes in LVM and myocardial strain in middle-aged adults without cardiovascular disease (CVD) or chronic kidney disease (CKD) is unknown. METHODS: We studied 3,113 adults without CVD at baseline participating in the Year 25 (2010-2011) follow-up exam of the Coronary Artery Risk Development in Young Adults (CARDIA) study. We studied the association of Year 25 c-terminal FGF23 concentrations with indexed LVM (LVMI=LVM/height2.7), LVH and myocardial strain as assessed by speckle tracking strain echocardiography. Among the 2,758 (88.6%) participants who returned for the Year 30 examination, we also investigated the association of Year 25 FGF23 with 5 Year change in LVMI, strain parameters and incident LVH. RESULTS: The mean age was 50.0 (±3.6) years, 56.8% were female, 45.7% were Black and 6.4% had CKD. There was 6.0% LVH prevalence at Year 25. Mean 5 Year change in LVMI was 5.3 (±7.7) grams/meter. In multivariable models, FGF23 in the highest quartile was associated with greater odds of LVH at Year 25 compared to lower quartiles. [Odds Ratio 95% CI: 1.81 (1.28, 2.58)] with similar findings after exclusion of participants with CKD. There was no interaction between FGF23 and race (P = .18) or sex (P = .80). There was no association between FGF23 and global longitudinal strain. There was no association between FGF23 and 5 Year change in LVMI. There was no association between higher FGF23 and 5 year incident LVH. CONCLUSIONS: In a middle-aged adult population without known CVD or CKD, higher FGF23 was associated with greater odds of LVH, but not with greater increases in LVM over time. Further study is needed to elucidate whether FGF23 is a risk marker for underlying LVH or a mechanism for increased LVM over time in younger and middle-aged adult populations without CKD.