Kinetics and prognostic value of soluble VCAM-1 in ST-segment elevation myocardial infarction patients

Abstract

Background: Soluble vascular cell adhesion molecule-1 (sVCAM-1) is a biomarker of endothelial activation and inflammation. There is still controversy as to whether it can predict clinical outcome after ST-elevation myocardial infarction (STEMI). Our aim was to assess the sVCAM-1 kinetics and to evaluate its prognostic predictive value.

Method: We prospectively enrolled 251 consecutive STEMI patients who underwent coronary revascularization in our university hospital. Blood samples were collected at admission, 4, 24, 48 h and 1 month after admission. sVCAM-1 serum level was assessed using ELISA assay. All patients had cardiac magnetic resonance imaging at 1-month for infarct size (IS) and left ventricular ejection fraction (LVEF) assessment. Clinical outcomes were recorded over 12 months after STEMI.

Results: sVCAM-1 levels significantly increased from admission up to 1 month and were significantly correlated with IS, LVEF, and LV end-systolic and diastolic volume. (H48 area under curve (AUC) ≥ H48 median) were associated with an increased risk of adverse clinical events during the 12-month follow-up period with a hazard ratio (HR) = 2.6 (95% confidence interval [CI] of ratio = 1.2-5.6, p = .02). The ability of H48 AUC for sVCAM-1 to discriminate between patients with or without the composite endpoint was evaluated using receiver operating characteristics with an AUC at 0.67 (0.57-0.78, p = .004). This ability was significantly superior to H48 AUC creatine kinase (p = .03).

Conclusions: In STEMI patients, high sVCAM-1 levels are associated with a poor clinical outcome. sVCAM-1 is an early postmyocardial infarction biomarker and might be an interesting target for the development of future therapeutic strategies.

Keywords: STEMI; VCAM-1; acute coronary syndrome; cell adhesion molecules; inflammation.

Figure 1

(A) sVCAM‐1 kinetics in STEMI patients within the first month (n = 251 patients). (B) Level of sVCAM‐1 in patients with or without adverse clinical events (all‐cause death, MI, stroke, and hospitalization for heart failure) during the first 12 months after MI (n = 251 patients). (C) Adverse clinical events according to AUC for sVCAM‐1 secretion within 48 h (n = 251 patients). (D) ROC for discriminating patients with or without a composite endpoint (adverse clinical event). ***p < .001, ****p < .0001. AUC, area under curve; CK, creatine kinase; MI, myocardial infarction; ROC, receiver operating characteristic; sVCAM‐1, soluble VCAM‐1; STEMI, ST‐segment elevation myocardial infarction

Figure 2

(A) Violin plot of sVCAM‐1 serum level at admission in STEMI patients. **p < .01. (B) Adverse clinical events (all‐cause death, myocardial infarction, stroke and hospitalization for heart failure) according to sVCAM‐1 at admission. STEMI, ST‐segment elevation myocardial infarction; sVCAM‐1, soluble vascular cell adhesion molecule‐1

Figure 3

Central illustration: Graphical presentation summarizing the putative key role of sVCAM‐1 after ST‐elevation segment myocardial infarction. MI, myocardial infarction; MMP, matrix metalloproteinase; oxLDL, oxidized low‐density lipoprotein; sVCAM‐1, soluble vascular cell adhesion molecule 1