Relationship Between 25-Hydroxyvitamin D, Renin, and Collagen Remodeling Biomarkers in Atrial Fibrillation

Author:

Patel Dimpi12ORCID,Druck Aleksander1ORCID,Hoppensteadt Debra2,Bansal Vinod3,Brailovsky Yevgeniy4ORCID,Syed Mushabbar3,Fareed Jawed2ORCID

Affiliation:

1. Loyola University of Chicago, Stritch School of Medicine, Maywood, IL, USA

2. Hemostasis and Thrombosis Laboratories, Center of Translational Research and Education, Maywood, IL, USA

3. Loyola University Medical Center, Maywood, IL, USA

4. Center for Advanced Cardiac Care, Columbia University Medical Center, New York, NY, USA

Abstract

The interplay between vitamin D, the renin–angiotensin system (RAS), and collagen remodeling has been implicated in the pathogenesis of various cardiovascular diseases. This study sought to explore this relationship in atrial fibrillation (AF) by profiling plasma levels of 25-hydroxyvitamin D, RAS biomarkers, and collagen remodeling biomarkers using the enzyme-linked immunosorbent assay method. We hypothesized that 25-hydroxyvitamin D levels would inversely correlate with RAS biomarkers and that levels of RAS and collagen remodeling biomarkers would positively correlate with each other. Although our AF cohort (n = 37) did not exhibit decreased 25-hydroxyvitamin D levels compared to normal controls (n = 26), these levels inversely correlated with renin (Spearman r = −0.57, P = 0.005). Renin levels were elevated in patients with AF compared to normal controls (1233 ± 238 ng/mL vs 401 ± 27 ng/mL, P = 0.0002) and positively correlated with levels of matrix metalloproteinase 1 (MMP-1; Spearman r = 0.89, P = 0.01) and MMP-2 (Spearman r = 0.82, P = 0.03). These data suggest that 25-hydroxyvitamin D may influence RAS activation, and renin may help mediate the collagen remodeling process in AF. Understanding mediators of RAS dysregulation in AF may elucidate targets for therapeutic intervention to prevent collagen remodeling.

Funder

NIH Clinical Center

Publisher

SAGE Publications

Subject

Hematology,General Medicine

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