Baseline VCAM-1 predicts left ventricular dysfunction and cardiovascular outcomes after acute coronary syndromes

Background Growing evidence supports a central role of inflammation and immune activation in the pathophysiology of myocardial infarction. Endothelial inflammatory response is a key component of this process. Vascular cell adhesion molecule-1 (VCAM-1), a mediator of leukocyte–endothelium interaction, reflects endothelial dysfunction and immune activation in acute coronary syndromes (ACS). Purpose To assess the association between baseline soluble VCAM-1 (sVCAM-1), left ventricular systolic function assessed by three-dimensional echocardiography (3DE), and cardiovascular outcomes in patients with ACS. Methods This prospective, single-center, observational study included 150 consecutive ACS patients. Baseline sVCAM-1 levels were measured using ELISA at admission. Left ventricular volumes and ejection fraction were assessed by 3DE within 24 hours. Patients were followed for 4 years for major adverse cardiovascular events (MACE), defined as cardiovascular death, recurrent myocardial infarction, heart failure hospitalization, or unstable angina requiring revascularization. Correlation, ROC, and Kaplan–Meier survival analyses were performed. Results Mean age was 54.7 years, 35% were women, and STEMI was present in 64% of patients. Mean 3D-LVEF was 47.6%. During follow-up, 31 patients (21%) experienced MACE, and 8 (5.3%) died from cardiovascular causes. Baseline sVCAM-1 levels were inversely correlated with 3D-LVEF (r = −0.45, p = 0.04) (Figure 1A). ROC curve analysis demonstrated that baseline sVCAM-1, the optimal cut-off value derived from the Youden index being 4.76 (log10 scale), provided good discrimination for cardiovascular events (AUC 0.77, 95%CI 0.68–0.86) (Figure 1B). Kaplan–Meier analysis showed progressively lower event-free survival across increasing tertiles of sVCAM-1 (Figure 1C). Conclusions Baseline sVCAM-1 is associated with impaired left ventricular systolic function and adverse cardiovascular outcomes following acute coronary syndromes. These findings reinforce the central role of endothelial activation and persistent inflammation in the pathophysiology of post-infarction remodeling. sVCAM-1 may serve as a prognostic biomarker for risk stratification, but also as a potential tool to identify patients who could benefit from future targeted anti-inflammatory strategies.