Role of beta-blocker therapy on the sympathetic effects in stroke heart syndrome.

IF 3.4 3区 医学 Q1 CLINICAL NEUROLOGY
Gabriele Prandin, Marcello Naccarato, Giovanni Furlanis, Laura Mancinelli, Federica Palacino, Emanuele Vincis, Magda Quagliotto, Edoardo Ricci, Luigi Cattaruzza, Paola Caruso, Paolo Manganotti
{"title":"Role of beta-blocker therapy on the sympathetic effects in stroke heart syndrome.","authors":"Gabriele Prandin, Marcello Naccarato, Giovanni Furlanis, Laura Mancinelli, Federica Palacino, Emanuele Vincis, Magda Quagliotto, Edoardo Ricci, Luigi Cattaruzza, Paola Caruso, Paolo Manganotti","doi":"10.1007/s10286-025-01139-3","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Sympathetic activation, inflammation, and neuro-endocrine response after an ischemic stroke contribute to the development of the stroke heart syndrome (SHS). One marker of SHS is a troponin \"rise and fall pattern\" > 30%. Among the beta-blocker drugs, the β1 antagonist class has a selective effect on the heart against sympathetic neurotransmitters. The aim of this study is to evaluate the possible role of pre-stroke chronic cardioselective β1 blocker treatment (B1B) in preventing SHS.</p><p><strong>Methods: </strong>We retrospectively analyzed data of 891 acute stroke patients admitted to the stroke unit at the University Hospital of Trieste (Italy) between 2018 and 2020. In total, 490 patients met the inclusion criteria. Clinical data, imaging characteristics and markers of cardiac injury (troponin I [TnI], N-terminal fragment of B type natriuretic peptide (NT-proBNP), and \"rise and fall pattern\" > 30%) and the chronic pre-stroke use of B1B were collected. We compared SHS against lack of SHS (no-SHS), subsequently examining the data through a multivariable analysis to determine possible SHS predictive factors.</p><p><strong>Results: </strong>No association between chronic B1B pre-stroke use and SHS (odds ratio [OR] 1.031; 95% confidence interval [CI] 0.636-1.672; p = 0.900) has been observed. The same result has been found in a sub-analysis on patients with chronic heart failure characterized by high NT-proBNP levels (> 900 pg/mL; n = 212), in which no association between chronic pre-stroke use of B1B and SHS (OR 0.807; 95% CI 0.449-1.451; p = 0.474) was identified.</p><p><strong>Conclusions: </strong>In our single-center retrospective cohort, a pre-stroke chronic B1B treatment seems not to prevent the development of SHS, including in patients with NT-proBNP > 900 pg/mL with chronic heart failure. These results should be confirmed by future randomized controlled trials to better understand the lack of effect of beta blockers on SHS.</p>","PeriodicalId":10168,"journal":{"name":"Clinical Autonomic Research","volume":" ","pages":""},"PeriodicalIF":3.4000,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical Autonomic Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s10286-025-01139-3","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Sympathetic activation, inflammation, and neuro-endocrine response after an ischemic stroke contribute to the development of the stroke heart syndrome (SHS). One marker of SHS is a troponin "rise and fall pattern" > 30%. Among the beta-blocker drugs, the β1 antagonist class has a selective effect on the heart against sympathetic neurotransmitters. The aim of this study is to evaluate the possible role of pre-stroke chronic cardioselective β1 blocker treatment (B1B) in preventing SHS.

Methods: We retrospectively analyzed data of 891 acute stroke patients admitted to the stroke unit at the University Hospital of Trieste (Italy) between 2018 and 2020. In total, 490 patients met the inclusion criteria. Clinical data, imaging characteristics and markers of cardiac injury (troponin I [TnI], N-terminal fragment of B type natriuretic peptide (NT-proBNP), and "rise and fall pattern" > 30%) and the chronic pre-stroke use of B1B were collected. We compared SHS against lack of SHS (no-SHS), subsequently examining the data through a multivariable analysis to determine possible SHS predictive factors.

Results: No association between chronic B1B pre-stroke use and SHS (odds ratio [OR] 1.031; 95% confidence interval [CI] 0.636-1.672; p = 0.900) has been observed. The same result has been found in a sub-analysis on patients with chronic heart failure characterized by high NT-proBNP levels (> 900 pg/mL; n = 212), in which no association between chronic pre-stroke use of B1B and SHS (OR 0.807; 95% CI 0.449-1.451; p = 0.474) was identified.

Conclusions: In our single-center retrospective cohort, a pre-stroke chronic B1B treatment seems not to prevent the development of SHS, including in patients with NT-proBNP > 900 pg/mL with chronic heart failure. These results should be confirmed by future randomized controlled trials to better understand the lack of effect of beta blockers on SHS.

受体阻滞剂治疗在卒中心脏综合征交感神经效应中的作用。
背景:缺血性卒中后交感神经激活、炎症和神经内分泌反应有助于卒中心脏综合征(SHS)的发展。SHS的一个标志是肌钙蛋白“上升和下降模式”(约30%)。在β受体阻滞剂药物中,β1拮抗剂类对心脏有选择性作用,对抗交感神经递质。本研究的目的是评估脑卒中前慢性心脏选择性β1阻滞剂治疗(B1B)在预防SHS中的可能作用。方法:回顾性分析2018年至2020年意大利的里雅斯特大学医院卒中病房收治的891例急性卒中患者的资料。共有490例患者符合纳入标准。收集临床资料、影像学特征、心脏损伤标志物(肌钙蛋白I [TnI]、B型利钠肽n端片段(NT-proBNP)、“起落模式”> 30%)及脑卒中前慢性使用B1B。我们比较了SHS和缺乏SHS(无SHS),随后通过多变量分析检查数据,以确定可能的SHS预测因素。结果:慢性B1B卒中前使用与SHS无相关性(优势比[OR] 1.031;95%置信区间[CI] 0.636-1.672;P = 0.900)。在以NT-proBNP水平高为特征的慢性心力衰竭患者的亚分析中也发现了相同的结果(bbb900 pg/mL;n = 212),其中慢性卒中前使用B1B与SHS无相关性(OR 0.807;95% ci 0.449-1.451;P = 0.474)。结论:在我们的单中心回顾性队列中,中风前慢性B1B治疗似乎不能预防SHS的发展,包括NT-proBNP bbb900 pg/mL合并慢性心力衰竭的患者。这些结果应该在未来的随机对照试验中得到证实,以更好地了解-受体阻滞剂对SHS缺乏作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Clinical Autonomic Research
Clinical Autonomic Research 医学-临床神经学
CiteScore
7.40
自引率
6.90%
发文量
65
审稿时长
>12 weeks
期刊介绍: Clinical Autonomic Research aims to draw together and disseminate research work from various disciplines and specialties dealing with clinical problems resulting from autonomic dysfunction. Areas to be covered include: cardiovascular system, neurology, diabetes, endocrinology, urology, pain disorders, ophthalmology, gastroenterology, toxicology and clinical pharmacology, skin infectious diseases, renal disease. This journal is an essential source of new information for everyone working in areas involving the autonomic nervous system. A major feature of Clinical Autonomic Research is its speed of publication coupled with the highest refereeing standards.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信