Article Text

PDF
Correspondence
Tumour necrosis factor-α antagonism: a potential therapeutic target for prevention of arrhythmogenesis in the setting of acute myocardial infarction?
  1. Kenan Yalta,
  2. Nasir Sivri,
  3. Bilal Geyik,
  4. Ertan Yetkin
  1. Cardiology Department, Trakya Üniversity, Edirne, Turkey
  1. Correspondence to Professor Kenan Yalta, Cardiology Department, Trakya Üniversity, Edirne 778765, Turkey; kyalta{at}gmail.com

Statistics from Altmetric.com

To the Editor In their recently published elegant article,1 Padfield et al have reported potential cardiovascular effects of tumour necrosis factor α (TNF-α) antagonism in patients with non-ST elevation acute myocardial infarction. In this first in human study, the authors have demonstrated that a single dose of etanercept (a TNF-α antagonist) infusion might blunt systemic inflammatory response, but might appear to enhance platelet aggregation along with its neutral effects on fibrinolytic and peripheral vasomotor functions in these patients 24h after infusion suggesting that TNF-α antagonism should not be regarded as a promising therapeutic strategy in the setting of acute myocardial infarction (AMI).1 We also agree that currently, this strategy should be regarded with caution in the setting of acute coronary syndrome (ACS). However, as described below, based on the multifaceted nature of systemic inflammation and its detrimental effects, modulation of cytokine response in conditions with heightened …

View Full Text

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Linked Articles