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GW24-e0403 Autoantibodies against angiotensin II type 1 receptor-positive patients with heart failure have better clinical efficacy to perindopril treatment
  1. Du Qian1,
  2. Xin Wang1,
  3. Zhiyong Zhang1,
  4. Lin Xu1,
  5. Jiamei Liu1,
  6. Juan Zhang1,
  7. Hua Wang1,
  8. Jin Chen1,
  9. Guilin Ma1,
  10. Hakon Hakonarson2,
  11. Aihua Hu2,
  12. Lin Zhang1
  1. 1Heart Failure Center, Departments of cardiology, Capital Medical University, Chao-Yang Hospital, Beijing, China
  2. 2Children’s Hospital of Philadelphia Research Institute, University of Pennsylvania School of Medicine, Philadelphia, PA


Objectives Previously, we reported that autoantibodies specific for the angiotensin II type 1 receptor (anti-AT1-AR) is implicated in the pathogenesis of congestive heart failure (CHF). We hypothesised that the presence of anti-AT1-AR is associated with the left ventricular function of CHF patients in response to perindopril.

Methods Synthetic angiotensin II type 1 receptor (AT1-R) peptides were used as the target antigen. An ELISA was used to screen the sera of 156 CHF patients with NYHA class II-IV. The patients were then divided into positive or negative groups based on their anti-AT1-AR reactivity. Each patient of each group was subjected to an echocardiography and a 6-minute walk test. Performance at baseline and after one year of perindopril therapy with β-receptor blockers, diuretics, and digoxin were documented.

Results A total of 138 patients completed the final analysis in this study, including 82 patients with (+) anti-AT1-AR and 56 patients with (–) anti-AT1-AR. Compared to the patients with (–) anti-AT1-AR, patients with (+) anti-AT1-AR had a greater improvement in left ventricular end-diastolic, end-systolic dimensions, and ejection fraction (all P < 0.05). Similar trends were also observed in patients subjected to a 6-minute walk test (P < 0.05) after one year of perindopril therapy in combination with standard treatment. CHF patients that were (+) anti-AT1-AR responded better to target perindopril dose than those that were (–) anti-AT1-AR (P < 0.01). After 5 years of follow-up, there was no significant difference for hospitalisation, death, or cardiovascular failures between patients with (+) anti-AT1-AR and (–) anti-AT1-AR.

Conclusions Compared to (–) anti-AT1-AR, patients that were (+) anti-AT1-AR had a greater clinical therapeutic benefit on left ventricluar remodeling and function. This result potentially presents a novel biomarker of the renin-angiotensin-aldosterone system for assess of the level of receptor activation, as well as therapeutic intervention in patients with heart failure.

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