Exploring the prognostic significance of antiphospholipid antibody in acute myocardial infarction: insights from clinical study and mechanism.

Abstract

BACKGROUND: Acute myocardial infarction (AMI) remains a major cause of morbidity and mortality. Besides traditional cardiovascular risk factors, autoimmune components such as antiphospholipid antibodies (aPL) have been implicated, but their prognostic role in AMI is unclear. OBJECTIVES: This study investigated the prognostic significance of aPL in patients with AMI and explored potential mechanisms. METHODS: This study consecutively enrolled 777 patients with AMI and detected aPL. Cox proportional hazard models assessed cardiovascular event risk. For mechanistic insights, an antiphospholipid syndrome (APS) myocardial infarction mouse model was developed, and bulk RNA sequencing was performed on human coronary artery endothelial cells (HCAECs) stimulated with APS immunoglobulin G. RESULTS: Compared with the aPL-negative group, patients in the aPL-positive group were significantly younger (62.0 [54.0-69.0] vs 52.0 [44.0-60.0] years; P < .001). aPL-positive AMI group had higher incidence of thrombosis (199 [27.3%] vs 22 [46.8%]; P = .007) and fewer traditional risk factors such as hypertension and hyperlipidemia. During a mean follow-up of 18.8 months, aPL positivity was significantly associated with future cardiovascular events (adjusted hazards ratio, 2.28; 95% CI, 1.26-4.12; P = .006). In the mouse model, the APS group exhibited accelerated disease progression and higher thrombosis rates. Neutrophil-related chemokines were upregulated in APS immunoglobulin G-stimulated HCAECs, consistent with increased neutrophil infiltration and neutrophil extracellular traps formation in vivo. CONCLUSION: Our findings suggest that patients with aPL-positive AMI represent a distinct AMI subset with worse outcomes. They may benefit from additional therapies beyond standard treatment. Neutrophil-driven inflammatory pathways could be a potential underlying mechanism.