Key result
Women with SCAD show 60% AT1R and ETAR autoantibody seropositivity vs STEMI or healthy controls.
Why the study?
Spontaneous coronary artery dissection is an uncommon cause of acute myocardial infarction in women with unclear pathophysiology, and the prevalence of endothelial-targeting autoantibodies had not been investigated.
Is there a higher prevalence of AT1R and ETAR autoantibodies in women with SCAD and acute myocardial infarction compared to women with STEMI or healthy controls?
Case-Control (n=30)
Is there a higher prevalence of AT1R and ETAR autoantibodies in women with SCAD and acute myocardial infarction compared to women with STEMI or healthy controls?
Absolute Event Rate: 60% vs 10%
p-value: p=0.03
Women with SCAD and acute myocardial infarction have a significantly higher prevalence of AT1R and ETAR autoantibodies compared to STEMI patients and healthy controls, suggesting a potential autoimmune role in SCAD pathophysiology.
AIMS: 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 AAs in SCAD-affected female patients. METHODS AND RESULTS: Female patients diagnosed at coronary angiography with myocardial infarction and SCAD were consecutively enrolled. Autoantibodies targeting angiotensin-II receptor type 1 and ETAR-AA titres and seropositivity prevalence were compared between SCAD patients, ST-elevation myocardial infarction (STEMI) patients, and healthy women. Ten women with SCAD and 20 age-matched controls (10 women with 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 AA titre 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). CONCLUSION: Autoantibodies targeting angiotensin-II receptor type 1 and ETAR-AA 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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Civieri et al. (2023) conducted a case-control in Spontaneous coronary artery dissection (SCAD) with acute myocardial infarction (n=30). AT1R and ETAR autoantibodies vs. Healthy women and women with STEMI was evaluated on Seropositivity for AT1R-AAs and ETAR-AAs (p=0.03). Seropositivity for AT1R and ETAR autoantibodies was significantly higher in women with SCAD (60%) compared to healthy women (10%, P=0.03) or women with STEMI (10%, P=0.03).
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