Serum VCAM-1 Levels and Incident Heart Failure

NT-proBNP Levels Reduced With Spironolactone
NT-proBNP Levels Reduced With Spironolactone
Higher serum levels of VCAM-1 may be associated with incident HFpEF.

This article is part of Cardiology Advisor‘s coverage of AHA Scientific Sessions 2020.

Higher serum levels of vascular cell adhesion molecule-1 (VCAM-1) may be associated with incident heart failure with preserved ejection fraction (HFpEF), according to study results presented at the American Heart Association (AHA) Scientific Sessions 2020, held virtually from November 13 to 17, 2020.

VCAM-1 levels are used to assess endothelial activation, and VCAM-1 has been found to play a role in the pathogenesis of HFpEF. In this study, the data of patients with incident heart failure  who were enrolled in the Multi-Ethnic Study of Atherosclerosis (MESA) study conducted between 2002 and 2004, and for whom serum VCAM-1 levels were obtained during the MESA study period (n=2297) were examined at follow-up. The primary outcome of this study was incident heart failure, and secondary outcomes were heart failure subtypes of HFpEF and heart failure with reduced ejection fraction (HFrEF).

Over a median follow-up of 14.4 years, there were 102 (4.4%) total heart failure events, 65 of which (64%) were incident hospitalization for HFpEF, and 37 (36%) were incident hospitalization for HFrEF. Higher VCAM-1 levels at baseline were found to be associated with a higher risk for incident heart failure hospitalizations in unadjusted analyses. After adjusting for covariates, each doubling of VCAM-1 level was associated with a 94% increased risk for heart failure (hazard ratio [HR] 1.94; 95% CI, 1.17-3.23; P =.01). The association between VCAM-1 level and incident heart failure was found to be stronger among current and former smokers compared with never-smokers (HR, 3.19; 95% CI, 1.66-6.14 vs HR, 1.12; 95% CI, 0.54-2.33; P =.03, respectively).

Study limitations include the fact that patients who were excluded due to lack of VCAM-1 measurement represented a higher-risk group with more cardiovascular risk factors, which may have led to biased results.

“Taken together, our findings substantiate the potential pathogenic roles of endothelial activation, cellular adhesion molecules, and microvascular coronary inflammation in driving symptomatic HFpEF and HF hospitalization,” concluded the study authors. “Therapies aimed to reduce endothelial activation and specifically VCAM-1 may prevent incident HF among patients at risk.”

Disclosure: Several study authors declared affiliations with the pharmaceutical industry. Please see the original reference for a full list of authors’ disclosures.


Patel RB, Colangelo LA, Bielinski SJ, et al. Circulating vascular cell adhesion molecule-1 and incident heart failure: the multi-ethnic study of atherosclerosis (MESA). Presented at: AHA Scientific Sessions 2020 Virtual Meeting; November 13-17, 2020. Presentation 2424.

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