The following article is a part of conference coverage from AHA Scientific Sessions 2020, held virtually from November 13 to 17, 2020. The team at the Clinical Advisor will be reporting on the latest news and research conducted by leading experts in cardiology. Check back for more from the AHA 2020.
Fibroblast growth factor 23 (FGF23) levels may be associated with lower left ventricular (LV) systolic function, higher LV mass, and lower left atrial (LA) function in the long term, according to study results presented at the American Heart Association (AHA) Scientific Sessions 2020, held virtually from November 13 to 17, 2020.
In this prospective, community-based cohort Multi-Ethnic Study of Atherosclerosis (MESA), researchers examined the association between cardiac magnetic resonance- (CMR) evaluated LV measures and LA mechanical function and serum FGF23 levels at baseline (ie, between 2000 and 2002) and at the 10-year follow-up (ie, between April 2010 and February 2012) in 2276 participants. LV mass and volumes and LV ejection fractions were measured using commercially available software. LA volumes were quantified using multimodality tissue-tracking software.
After adjusting for covariates, an independent association was established between FGF23 and: higher LV mass (β coefficient per 1 standard deviation [SD] higher, 1.14; 95% CI, 0.16-2.12; P =.02), worse LV global circumferential strain (β coefficient per 1 SD higher, 0.15; 95% CI, 0.05-0.25; P =.003), worse LV midwall circumferential strain (β coefficient per 1 SD higher, 0.20; 95% CI, 0.08-0.31; P =.001), and lower LA total emptying fraction (β coefficient per 1 SD higher, 0.20; 95% CI, 0.08-0.31; P =.001). There were no significant associations between FGF23 levels and the presence of myocardial scar or traditional measures of LV function. Associations between FGF23 levels and LV systolic and LA function were observed for all races and regardless of glomerular filtration rate.
This study was limited due to the exclusion of many participants from the original cohort, who tended to have a higher prevalence of cardiovascular risk factors, and the fact that the extent of diastolic function could not be assessed.
“These findings provide mechanistic support for the role of FGF23 in the development of overt [heart failure], substantiate the strong association between FGF23 and [heart failure] with preserved ejection fraction (HFpEF), and suggest that FGF23 may drive HFpEF through distinct effects upon the myocardium,” the researchers concluded. “Further investigation is required to understand if therapeutic reduction in FGF23 can alter derangements in cardiac function and prevent progression to overt cardiovascular disease.”
Disclosure: Several study authors declared affiliations with the pharmaceutical industry. Please see the original reference for a full list of authors’ disclosures.
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Patel RB, Ning H, de Boer IH, et al. Fibroblast growth factor 23 and long-term cardiac function. Presented at: AHA Scientific Sessions 2020; November 13-17, 2020. Presentation 240.
This article originally appeared on The Cardiology Advisor