Mediators of Inflammation

Mediators of Inflammation / 2005 / Article

Open Access

Volume 2005 |Article ID 654781 |

Fien Blancke, Marc J. Claeys, Philippe Jorens, Guy Vermeiren, Johan Bosmans, Floris L. Wuyts, Chris J. Vrints, "Systemic Inflammation and Reperfusion Injury in Patients With Acute Myocardial Infarction", Mediators of Inflammation, vol. 2005, Article ID 654781, 5 pages, 2005.

Systemic Inflammation and Reperfusion Injury in Patients With Acute Myocardial Infarction

Received15 Jul 2005
Accepted18 Aug 2005


Despite early recanalization of an occluded infarct artery, tissue reperfusion remains impaired in more than one-third of the acute myocardial infarction (AMI) patients owing to a process of reperfusion injury. The role of systemic inflammation in triggering this phenomenon is unknown. Proinflammatory factors (hs-CRP, TNF-α) and anti-inflammatory mediators (IL-1 receptor antagonist, IL-10) were measured in 65 patients during the acute phase of a myocardial infarction as well as in 11 healthy control subjects. Myocardial reperfusion injury was defined as the presence of persistent ST-segment elevation despite successful coronary intervention (50% of the initial value) and was observed in 28 patients. Systemic proinflammatory mediators (particularly hs-CRP and leukocytes) were higher in AMI patients compared to control subjects. Within the group of AMI patients, only serum TNF-α differed significantly between patients with versus without reperfusion injury: a median value of 25 versus 13 pg/mL was observed, respectively. Logistic regression analysis identified a high level of TNF-α as the most important independent determinant of reperfusion injury (P=.001), beyond total ischemic time (P=.01) and extent of jeopardized myocardium (P=.08). There was no correlation between the TNF-α level and the total ischemic time (P=.8) or the extent of jeopardized myocardium (P=.6). Systemic inflammation, in particular high levels of TNF-α, is strongly associated with the occurrence of reperfusion injury after successful recanalization. Our findings suggest that TNF-α is involved in the triggering and/or amplification of local inflammatory responses related to ischemia-reperfusion injury.

Copyright © 2005 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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