ETAR-AAs seropositivity in STEMI patients was associated with a 3.61-fold higher odds of cardiac arrest, especially in patients with smaller infarct size.
Are elevated levels of Endothelin-1 receptor type A agonistic autoantibodies associated with an increased risk of cardiac arrest in STEMI patients?
Elevated levels of ETAR-AAs at admission are associated with an increased risk of early cardiac arrest in STEMI patients, particularly those with smaller infarct sizes.
Absolute Event Rate: 0% vs 0%
Abstract Background cardiac arrest (CA) represents the most severe complication of ST-elevation myocardial infarction (STEMI). Endothelin-1 (ET-1) contribute to adverse prognosis after STEMI through vasoconstriction, myocardial inflammation and fibrosis. Its role has long been studied in CA and robust evidence shows that ET-1 released endogenously during ischemia is arrhythmogenic and elevated levels of ET-1 during acute ischemia predict resuscitation failure. Functional autoantibodies against ET-1 receptor type A (ETAR-AAs) bind to the same receptors as natural ligands, eliciting similar responses. In patients with STEMI, ETAR-AAs have been associated with microvascular obstruction, left ventricular remodeling and adverse prognosis. Purpose To assess the association between ETAR-AAs and CA in STEMI patients. Methods Consecutive STEMI patients who underwent primary percutaneous coronary intervention within 12 h after pain onset were enrolled in this prospective study. The levels of ETAR-AAs at the time of hospital admission were measured using an enzyme-linked immunosorbent assay (ELISA). Cardiac arrest was defined as the occurrence of pulseless ventricular tachycardia or ventricular fibrillation at presentation or within 12 hours after hospital admission. Autoantibody seropositivity was defined according to ELISA’s kit manufacturer’s instructions (levels 10 U/mL). Results 242 patients with STEMI were enrolled. The baseline characteristics of the patients are shown in Table 1. Of these, 105 (43.4%) were ETAR-AAs seropositive and 47 (19.4%) suffered from CA. Patients suffering from CA had significantly higher levels of ETAR-AAs than those without CA (11.0 7.2-19.9 versus 8.3 5.8-12.7; p=0.036; Figure 1A). CA was significantly more prevalent in seropositive than in seronegative patients (25.7% versus 14.6%; p=0.030; Figure 1B). At logistic regression, ETAR-AAs were significantly associated with CA (OR 1.04 1.02-1.07, p0.001) after adjustment for infarct related artery and peak troponin level. ETAR-AAs seropositivity was also significantly associated with CA (OR 3.61 1.68-8.23. Despite no significant interaction between ETAR-AAs and peak troponin levels, the association between ETAR-AAs and CA was stronger in patients with smaller infarct sizes (i.e., peak troponin level median). Among patients with smaller infarct size, the prevalence of CA was indeed significantly higher in ETAR-AAs seropositive than in seronegative (26.8% versus 6.8%; p=0.006; Figure 1C). The prevalence was not significantly different among patients with larger infarct sizes (29.8% in ETAR-AAs seropositive versus 16.7% in seronegative; p=0.12). Conclusions ETAR-AAs are associated with CA in the early phases of STEMI. This effect is more pronounced in patients with smaller infarct size. Our findings provide insights into the role of ETAR-AAs in the pathophysiology of arrhythmic complications of STEMI and pave the way for future studies on this topic.
Civieri et al. (Sat,) reported a other. ETAR-AAs seropositivity in STEMI patients was associated with a 3.61-fold higher odds of cardiac arrest, especially in patients with smaller infarct size.