Spontaneous coronary artery dissection in women with acute myocardial infarction: is there a new role for autoimmunity?

spontaneous coronary artery dissection (SCAD) is an uncommon cause of acute myocardial infarction in women and has an unclear pathophysiology. Autoantibodies (AAs) targeting angiotensin-II receptor type 1 (AT1R) and endothelin-1 receptor type A (ETAR) have known detrimental effects on endothelial function. We investigated the prevalence of these autoantibodies in SCAD-affected female patients. female patients diagnosed at coronary angiography with myocardial infarction and SCAD were consecutively enrolled. AT1R-AAs and ETAR-AAs titers and seropositivity prevalence were compared between SCAD patients, STEMI patients, and healthy women. ten women with SCAD and 20 age-matched controls (10 women with ST-elevation myocardial infarction (STEMI) and 10 healthy women) were included. Six out of 10 (60%) women with myocardial infarction and SCAD were seropositive for AT1R-AAs and ETAR-AAs. In contrast, only one (10%) healthy woman and one (10%) STEMI patient were seropositive for AT1R-AAs (p = 0.03 and p = 0.03, respectively). One STEMI patient was seropositive for ETAR-AAs, while none of the healthy women was found to be seropositive (p = 0.03 and p = 0.01, respectively). The median autoantibody titer was significantly higher in SCAD patients than in healthy women (p = 0.01 for AT1R-AAs; p = 0.02 for ETAR-AAs) and STEMI patients (p < 0.001 for AT1R-AAs; p = 0.002 for ETAR-AAs). AT1R-AAs and ETAR-AAs seropositivity is significantly higher in SCAD women with myocardial infarction than in healthy women or female patients with STEMI. Our findings, corroborated by previous data in the literature and biological plausibility, suggest a possible role for AT1R-AAs and ETAR-AAs in the pathophysiology of SCAD in women with acute myocardial infarction and should warrant further studies with larger sample sizes.

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