Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/126616
Citations
Scopus Web of Science® Altmetric
?
?
Type: Journal article
Title: Prolonged suppression of the anti-oxidant/anti-inflammatory effects of BNP post-Takotsubo syndrome
Author: Liu, S.
Ngo, D.
Chirkov, Y.
Stansborough, J.
Chong, C.
Horowitz, J.D.
Citation: ESC Heart Failure, 2020; 7(5):2250-2257
Publisher: Wiley Open Access
Issue Date: 2020
ISSN: 2055-5822
2055-5822
Statement of
Responsibility: 
Saifei Liu, Doan Ngo, Yuliy Chirkov, Jeanette Stansborough, Cher‐Rin Chong John D. Horowitz
Abstract: AIMS:Takotsubo syndrome (TTS) episodes are primarily initiated by 'pulse' release of catecholamines inducing neutrophil infiltration and myocardial inflammation in susceptible individuals (largely ageing women). Evidence of myocardial inflammation and associated energetic impairment persists for ≥ 3 months post-acute TTS episodes, suggesting the existence of additional 'perpetuating' mechanisms. The effects of B-type natriuretic peptide (BNP) in suppressing superoxide (O2 - ) release from neutrophils are transiently impaired in acute heart failure. We also evaluated the extent and duration of BNP-induced suppression of O2 - release post-TTS. METHODS AND RESULTS:TTS patients were studied acutely (n = 34) and 3 months thereafter (n = 13) and compared with control subjects (n = 25). O2 - generation from neutrophils, triggered by N-formyl-methionyl-leucyl-phenylalanine and phorbol myristate acetate, and its suppression by BNP, were measured in vitro. Determinants of variability in BNP effect were sought via univariate and multivariate analyses. Relative to control subjects, in TTS patients, BNP suppression of both phorbol myristate acetate and N-formyl-methionyl-leucyl-phenylalanine-induced O2 - release was impaired acutely (P < 0.05 for both); this did not improve over the 3-month recovery period, despite treatment with conventional anti-failure medication in 85% of patients. No significant correlates of BNP effect (other than TTS) were identified. CONCLUSIONS:(1) While TTS is associated with marked and prolonged release of BNP, there is virtually total loss of the ability of BNP to suppress neutrophil O2 - release and its impact on tissue inflammation. (2) BNP responses do not recover for at least 3 months post-attacks, suggesting that this might contribute to perpetuation of myocardial inflammation in TTS patients.
Keywords: BNP; Neutrophils; Superoxide; Takotsubo syndrome
Rights: © 2020 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
RMID: 1000022972
DOI: 10.1002/ehf2.12729
Appears in Collections:Medicine publications

Files in This Item:
There are no files associated with this item.


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.