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Correspondence
Tumour necrosis factor-α is a foe for patients with acute myocardial infarction
  1. Kai-Hu Shi1,2,
  2. Hui Tao1,2,
  3. Jun-Xu Wu1,2
  1. 1 Department of Cardiothoracic Surgery, The Second Hospital of Anhui Medical University, Hefei, China
  2. 2 Cardiovascular Research Center, Anhui Medical University, Hefei, China
  1. Correspondence to Dr Kai-Hu Shi, Department of Cardiothoracic Surgery, The Second Hospital of Anhui Medical University, Furong Road, Anhui Province, Hefei 230601, China; ayskh3{at}hotmail.com

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To the Editor Tumour necrosis factor-α (TNF-α) has been implicated in the development of acute myocardial infarction. The mechanisms of TNF-α on endothelial function and platelet activation in patients with acute myocardial infarction are still unclear. A recent article by Padfield et al 1 demonstrated that TNF-α antagonism is unlikely to be a beneficial therapeutic strategy in patients with acute myocardial infarction. And plasma TNF-α concentrations increased in all patients following etanercept. This result suggests that TNF-α may serve as a foe for acute myocardial infarction so far.

Other studies have been carried out with a similar aim. Fu et al 2 indicated that acute myocardial ischaemia and reperfusion increased TNF-α content. Otherwise, hawthorn leaves flavonoids could markedly inhibit the increase of TNF-α content induced by myocardial ischaemia and infarction. Furthermore, Qiao et al 3 found that delayed volatile anaesthetic preconditioning can protect against myocardial ischaemia and reperfusion injury. The underlying mechanisms may decrease the TNF-α expression. Moreover, Zhang et al 4 showed that plasma TNF-α concentrations in the myocardial infarction control group were significantly higher compared with those of the sham surgery group and coronary artery ligation group. What is more, Vaccarino et al 5 demonstrated that the relationship among genetically determined TNF-α production and increased levels of tissue damage is a marker of acute myocardial infarction. In addition, Prondzinsky et al 6 suggested that the inflammatory response in patients with acute myocardial infarction complicated by cardiogenic shock, as reflected by the inflammatory markers TNF-α, has been shown to be of prognostic value in estimating clinical outcome. Therefore, these show that TNF-α may also be regarded as an effective prevention for acute myocardial infarction.

These findings suggest that TNF-α may be a good clinical biomarker believed to reflect acute myocardial infarction. Therapeutic agents targeting TNF-α might result in innovative new therapies for acute myocardial infarction. In summary, we greatly enjoyed reading the article by Padfield et al 1 and believe TNF-α may be useful for the prevention and treatment of acute myocardial infarction.

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Footnotes

  • KHS and HT contributed equally to this letter.

  • Funding This project was supported by Anhui Provincial Natural Science Foundation (1308085MH117).

  • Provenance and peer review Not commissioned; internally peer reviewed.

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