SEMA3A is a predictive biomarker of primary ventricular fibrillation complicating STEMI - 25/06/24
, Simon Leboube b, Ahmad Hayek c, Camille Brun d, Cyril Prieur e, Kevin Gardey a, Francis Bessière f, Nathan Mewton g, Gabriel Bidaux h, Claire Crola Da Silva d, Philippe Chevalier i, Thomas Bochaton jRésumé |
Introduction |
Ventricular fibrillation (VF) during acute myocardial infarction (MI) remains a significant concern, affecting approximately 10% of MI patients. Despite advances in post-MI management, survival with intact neurological function is below 5%. Neural and electrical remodeling, driven by elevated sympathetic activity and nerve growth factor (NGF) levels, contribute to myocardial electrical instability after MI. Overexpression of Semaphorin3A (SEMA3A), a sympathetic nerve growth regulator, has shown promise in limiting ventricular arrhythmias in animal models of acute MI.
Objective |
Our study aimed at investigating the association between systemic SEMA3A levels and VF occurrence during the acute phase of MI before revascularization.
Method |
From 2016 to 2022, 339 ST-elevation myocardial infarction (STEMI) patients undergoing percutaneous coronary intervention (PCI) were enrolled. Blood samples were collected before coronary angiography, and SEMA3A levels were measured using enzyme-linked immunosorbent assay (ELISA). Left ventricular ejection fraction (LVEF) was assessed using transthoracic echocardiography, while infarct size (IS) was measured at 1month with cardiac magnetic resonance imaging (CMR). Statistical analysis employed Mann–Whitney's test, with a P-value<0.05 considered statistically significant.
Results |
Among 339 patients, 28 (8.2%) experienced primary VF (PVF). SEMA3A levels at admission were significantly lower in the PVF group (1463.0pg/mL [IQR: 351.8–2492.0]) compared to the non-PVF group (2097.0pg/mL [IQR: 1208.0–3358.0], P=0.03) (Fig. 1). SEMA3A level<1658pg/mL was associated with an increased risk of VF (adjusted odds ratio=2.7 CI [1.2–6.3], P=0.02) after logistic regression analysis considering age, gender, LVEF and ischemic time and anterior localization of MI.
Conclusion |
Our findings reveal, for the first time in humans, lower SEMA3A levels in patients experiencing VF during acute MI. Since our study design cannot confirm causation, prospective studies are needed to elucidate SEMA3A's role in early post-MI sympathetic nerve sprouting and its implications in arrhythmogenesis. Yet, SEMA3A holds promise as a therapeutic target for malignant arrhythmias during STEMI.
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Vol 117 - N° 6-7S
P. S178 - juin 2024 Retour au numéro
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