ArticleJAMA network open2021
Association of Angiotensin II Type 1 Receptor Agonistic Autoantibodies With Outcomes in Patients With Acute Aortic Dissection.
Article in JAMA network open, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Article
- The role of complement in normal pregnancy and preeclampsia.Frontiers in immunology · 2025Review
- The short-chain fatty acid butyrate exerts a specific effect on VE-cadherin phosphorylation and alters the integrity of aortic endothelial cells.Frontiers in cell and developmental biology · 2023Article
- Changes of Serum D-Dimer, NT-proBNP, and Troponin I Levels in Patients with Acute Aortic Dissection and the Clinical Significance.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Single-Cell RNA Sequencing Reveals Smooth Muscle Cells Heterogeneity in Experimental Aortic Dissection.Frontiers in genetics · 2022Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Importance: Angiotensin II is significantly associated with the pathogenesis of acute aortic dissection. Angiotensin II type 1 receptor agonistic autoantibodies (AT1-AAs) can mimic the effect of angiotensin II. Objective: To investigate the association between AT1-AAs and all-cause and cause-specific mortality risk in patients with acute aortic dissection. Design, Setting, and Participants: A total of 662 patients with clinically suspected aortic dissection from 3 medical centers in Wuhan, China, were enrolled in this cohort study from August 1, 2014, to July 31, 2016. Of these, 315 patients were included in the 3-year follow-up study. Follow-up was mainly performed via telephone interviews and outpatient clinic visits. Data analysis was conducted from March 1 to May 31, 2020. Main Outcomes and Measures: The primary outcomes of interest were all-cause mortality, death due to aortic dissection, and late aortic-related adverse events. Results: The full study cohort included 315 patients with AAD (mean [SD] age, 56.2 [12.7] years; 230 men [73.0%]). Ninety-two patients (29.2%) were positive for AT1-AAs. The mortality of AT1-AA-positive patients was significantly higher than that of AT1-AA-negative patients (40 [43.5%] vs 37 [16.6%]; P < .001). The mortality risk in AT1-AA-positive patients was always significantly higher than that in AT1-AA-negative patients in patients with both type A and type B dissection. Multivariable analysis showed that the risk of AT1-AA-positive patients for type A dissection was significantly higher than that of AT1-AA-negative patients (odds ratio [OR], 1.88; 95% CI, 1.12-3.13; P = .02). The Cox proportional hazards regression model showed a significant increase of all-cause mortality risk (OR, 2.27; 95% CI, 1.44-3.57; P < .001) and late aortic-related adverse events (OR, 1.58; 95% CI, 1.06-2.36; P = .03) among AT1-AA-positive patients during the follow-up period compared with AT1-AA-negative patients. Conclusions and Relevance: This cohort study first detected AT1-AAs in patients with acute aortic dissection. The presence of AT1-AAs was associated with significantly higher all-cause and cause-specific mortality during a follow-up period of 3 years. The antibodies may be a risk factor for aortic dissection.
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