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.