Abstract 12646: Autoantibodies Targeting Endothelin Type-A Receptors Associate With no Reflow After ST-elevation Myocardial Infarction
Giovanni Civieri, Martina Perazzolo Marra, Giulia Masiero, Marta Vadori, Laura Iop, Emanuele Cozzi, Sabino Iliceto, Francesco Tona- Physiology (medical)
- Cardiology and Cardiovascular Medicine
Introduction: No-reflow (NR), where the coronary artery is patent after treatment of ST-elevation myocardial infarction (STEMI) but tissue perfusion is not restored, is associated with worse outcome. Although several mechanisms contributing to NR have been identified, its pathophysiology is still not completely understood. Autoantibodies activating endothelin-1 receptors type A (ETAR-AAs) exert their detrimental effects through vasoconstriction, fibrosis, and inflammation. Interestingly, all these factors are also involved in NR.
Hypothesis: We hypothesized that, after reopening of the epicardial coronary artery, the preexistence of ETAR-AAs might have detrimental effects on coronary microcirculation, resulting in microvascular obstruction (MVO) and, thus, NR.
Methods: Our prospective study was conducted at Padua University Hospital between January 2022 and December 2022. Consecutive patients with STEMI who underwent PPCI within 6 h after the onset of symptoms were enrolled. Blood samples were obtained from all patients within 12 hours after the admission for ETAR-AAs level measurement. MVO was assessed by cardiac magnetic resonance imaging, within 15 days after successful PPCI. The seropositive threshold was provided by the manufacturer (>10 U/ml).
Results: We recruited 50 patients with STEMI. MVO was observed in 24 patients (48%). ETAR-AAs were higher in patients with MVO (8.9 U/mL (interquartile range [IQR] 6.8-16.2 U/mL) vs. 5.7 U/mL [IQR 4.3-7.7 U/mL], p=0.002). The prevalence of MVO was higher in patients with ETAR-AAs seropositivity (72% vs. 38%, p=0.03). ETAR-AAs seropositivity was independently associated with MVO (OR 3.2, 95% CI 1.3-7.1; p=0.03).
Conclusions: ETAR-AAs concentration are associated with MVO in STEMI patients. These findings set the stage for a better pathophysiological understanding of NR and may open new options in the management of myocardial infarction.