The Impact of VCAM-1 expression on left ventricular performance following acute coronary syndromes

TL;DR

This study shows that higher levels of VCAM-1, an inflammation marker, are linked to worse heart function and changes in patients with heart attacks.

Contribution

The study is the first to systematically examine the relationship between VCAM-1 levels and left ventricular remodeling in acute coronary syndrome patients.

Findings

Baseline VCAM-1 levels were significantly correlated with changes in left ventricular end-diastolic volume and ejection fraction.

Dynamic changes in VCAM-1 were also significantly associated with adverse left ventricular remodeling.

33.3% of patients showed a ≥10% increase in left ventricular end-diastolic volume at follow-up.

Abstract

Inflammatory pathways, particularly those involving vascular cell adhesion molecule-1 (VCAM-1), play a central role in post-ischemic myocardial remodeling. However, its relationship with left ventricle (LV) performance or volumetric changes has not been systematically examined. This study aimed to investigate the association between circulating VCAM-1 levels, LV volumes, and LV ejection fraction (LVEF), quantified using three-dimensional echocardiography (3-DE), in patients with acute coronary syndrome (ACS). All patients underwent comprehensive clinical evaluation and 3-DE assessment within the first 24 hours of hospital admission. Concurrently, a full panel of locally available laboratory tests was performed, including serum sampling for VCAM-1 analysis. A follow-up evaluation, comprising repeated biological and echocardiographic measurements, was conducted two months after the index event. A total of 90 patients with ACS (mean age 54 ± 9 years; 75 males) were included in the analysis. Among these, 30 patients (33.3%) had a ≥10% increase in left ventricular end-diastolic volume (LVEDV) at follow-up, indicative of adverse left ventricular remodeling. Baseline VCAM-1 levels were significantly correlated with subsequent changes in LVEDV and LVEF from admission to follow-up (r = -0.42, P < 0.05, and r = -0.43, P < 0.05, respectively). Furthermore, the dynamic changes in VCAM-1 between assessments also showed significant correlations with changes in LVEDV and LVEF (r = 0.41, P < 0.05; r = -0.46, P < 0.05). This study suggests that VCAM-1, an inflammatory biomarker, may be a prognostic indicator of LV remodeling and dysfunction in patients with acute coronary syndromes. The findings support further exploration of VCAM-1 for risk stratification and therapy.

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