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Published on: January 28, 2020
Kinetics and prognostic value of soluble VCAM-1 in ST-segment elevation myocardial infarction patients
Ahmad Hayek1, Alexandre Paccalet2, Laura Mechtouff3
1Intensive Cardiological Care Division, Louis Pradel Hospital, Hospices Civils de Lyon, Bron, France.
Insights
High levels of soluble vascular cell adhesion molecule-1 (sVCAM-1) after ST-elevation myocardial infarction (STEMI) predict poor clinical outcomes. This biomarker indicates endothelial activation and may guide future therapeutic strategies.
Area of Science:
- Cardiology
- Biomarkers
- Inflammation
Background:
- Soluble vascular cell adhesion molecule-1 (sVCAM-1) is a marker of endothelial activation and inflammation.
- Its role in predicting clinical outcomes after ST-elevation myocardial infarction (STEMI) remains controversial.
Purpose of the Study:
- To assess sVCAM-1 kinetics post-STEMI.
- To evaluate the prognostic value of sVCAM-1 for clinical outcomes.
Main Methods:
- Prospective enrollment of 251 STEMI patients undergoing coronary revascularization.
- sVCAM-1 serum levels measured by ELISA at multiple time points (admission, 4h, 24h, 48h, 1 month).
- Cardiac MRI for infarct size (IS) and LVEF at 1 month; 12-month clinical outcome follow-up.
Main Results:
- sVCAM-1 levels increased significantly from admission to 1 month and correlated with IS and LVEF.
- Elevated sVCAM-1 at 48 hours (H48) predicted adverse clinical events (HR=2.6, p=0.02).
- H48 sVCAM-1 demonstrated good discrimination for composite endpoints (AUC=0.67, p=0.004), superior to creatine kinase.
Conclusions:
- Elevated sVCAM-1 levels in STEMI patients are associated with adverse clinical outcomes.
- sVCAM-1 serves as an early post-myocardial infarction biomarker.
- sVCAM-1 may represent a target for future therapeutic interventions.
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.
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