Background Anti-angiotensin II receptor subtype 1 (AT1 receptor) autoantibodies have previously been shown in sera of hypertensive patients. This study assessed whether anti-AT1-receptor autoantibody in serum is correlated with the efficacy of an AT1-receptor blocker (ARB; candesartan)-based regimen in hypertensive patients after 8 weeks of treatment.
Design The Study of Optimal Treatment in Hypertensive Patients with Anti-AT1-Receptor Autoantibodies is a multicentre, randomised, blinded endpoint, open-label, parallel-group comparison clinical trial conducted in five centres in Wuhan, China. Treatment is designed as stepwise added-on therapy to reduce blood pressure (BP) <140/90 mm Hg. 512 patients with moderate to severe primary hypertension were randomly assigned to an 8-week treatment with either ARB (candesartan)-based regimen (n=257) or ACE inhibitor (imidapril)-based regimen (n=255).
Results Systolic and diastolic BP was reduced significantly in both treatment groups. The candesartan-based regimen achieved a significantly greater systolic BP reduction than imdapril (30.8±10.3 vs 28.8±10.3 mm Hg, p=0.023). In those anti-AT1 receptor autoantibody-positive hypertensive patients, the mean systolic BP at baseline was higher than in the anti-AT1 receptor autoantibody-negative group (160.5±16.5 vs 156.2±17.7 mm Hg; p=0.006). The mean BP reduction was greater in the candesartan-based regimen than the imidapril-based regimen (−35.4±9.8/16.9±6.9 vs −29.4±9.8/14.2±6.9 mm Hg; p=0.000 and 0.002, respectively), and more patients on imidapril required add-on medications to achieve BP control (94% vs 86%; p=0.03). No correlation was observed between the titre of anti-AT1 receptor autoantibody and the efficacy of candesartan-based therapy. In those anti-AT1 receptor autoantibody-negative patients similar BP lowering was reached in the candesartan and the imidapril-based regimens.
Conclusions An ARB-based regimen is more effective in BP lowering than an ACE inhibitor-based regimen in the presence of anti-AT1 receptor autoantibodies.
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Funding This study was supported by the Clinical Key Program of the Chinese Ministry of Public Health (programme no. 9707237), National Natural Science Foundation of China (programme no. 30600235) and partly supported by a foundation of the Takeda Pharmaceuticals (Tianjin, China) Co. Ltd.
Competing interests None.
Patient consent Obtained.
Ethics approval This study was conducted with the approval of the medical ethics committees of Tongji Medical College.
Provenance and peer review Not commissioned; externally peer reviewed.
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