Objective Natriuretic peptides (NPs) are hormones with cardioprotective effects. NP levels vary by race; however, the pathophysiological consequences of lower NP levels are not well understood. We aimed to quantify the association between NPs and endothelial function as measured by flow-mediated dilation (FMD) and the contribution of NP levels to racial differences in endothelial function.
Methods In this cross-sectional study of 2938 Multi-Ethnic Study of Atherosclerosis participants (34% Caucasian, 20% African-American, 20% Asian-American and 26% Hispanic) without cardiovascular disease at baseline, multivariable linear regression models were used to examine the association between serum N-terminal pro-B-type NP (NT-proBNP) and natural log-transformed FMD. We also tested whether NT-proBNP mediated the relationship between race and FMD using the product of coefficients method.
Results Among African-American and Chinese-American individuals, lower NT-proBNP levels were associated with lower FMD, β=0.06 (95% CI: 0.03 to 0.09; p<0.001) and β=0.06 (95% CI: 0.02 to 0.09; p=0.002), respectively. Non-significant associations between NT-proBNP and FMD were found in Hispanic and Caucasian individuals. In multivariable models, endothelial function differed by race, with African-American individuals having the lowest FMD compared with Caucasians, p<0.001. Racial differences in FMD among African-Americans and Chinese-Americans were mediated in part by NT-proBNP levels (African-Americans, mediation effect: −0.03(95% CI: −0.05 to −0.01); Chinese-Americans, mediation effect: −0.03(95% CI: −0.05 to −0.01)).
Conclusions Lower NP levels are associated with worse endothelial function among African-Americans and Chinese-Americans. A relative NP deficiency in some racial/ethnic groups may contribute to differences in vascular function.
- cardiac risk factors and prevention
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Contributors All authors have substantially contributed to the study design, collection of data, analysis and interpretation, drafting the manuscript or critical revisions to the manuscript.
Funding This research was supported by contracts N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168 and N01-HC-95169 from the National Heart, Lung, and Blood Institute and by grants UL1-TR-000040 and UL1-TR-001079 from NCRR. This research was also supported by the National Heart, Lung, and Blood Institute grants K12 HL109019, 1K23HL128928-01A1, and the National Center for Advancing Translational Sciences of the National Institutes of Health award numbers UL1TR000445 (Vanderbilt University). Roche Diagnostics provided reagents for the measurement of NT-proBNP.
Competing interests LBD has received speaking fees from Roche and Critical Diagnostics, and consulting honoraria from Roche Diagnostics and Siemens Healthcare.
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement DKG had full access to all the data in the study and takes responsibility for its integrity and the data analysis.
Patient consent for publication Not required.