Perspective:

Earlier studies have demonstrated an association between angiotensin II and the angiotensin II type 1 receptor (AT1-R) in the pathogenesis of aortic dissection. AT1-R agonistic autoantibodies (AT1-AAs), previously identified among patients with refractory hypertension, can partially mimic the effect of angiotensin II, promoting the proliferation of vascular smooth muscle cells and aortic wall stiffening; and potentially stimulate the production of matrix metalloproteinases, which are involved in the pathogenesis of aortic dissection. This cohort study from three centers in China found that approximately 29% of patients with acute aortic dissection had AT1-AAs, and that the presence of AT1-AAs was associated with higher all-cause mortality risk and a higher risk of late aortic-related adverse events at 3 years. Although limited by a relatively small number of patients presumably of a single dominant ethnicity and by relatively short follow-up, the findings are provocative and suggest an association between AT1-AAs and risk among patients with acute aortic dissection. Additional study is required to address whether AT1-AAs detected outside the setting of acute aortic dissection pose a risk for the future development of aortic dissection.