Systemic inflammation and reperfusion injury in patients with acute myocardial infarction.
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-alpha ) 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 (> or = 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-alpha 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-alpha 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-alpha level and the total ischemic time (P = .8) or the extent of jeopardized myocardium (P = .6). Systemic inflammation, in particular high levels of TNF-alpha , is strongly associated with the occurrence of reperfusion injury after successful recanalization. Our findings suggest that TNF-alpha is involved in the triggering and/or amplification of local inflammatory responses related to ischemia-reperfusion injury.
Blancke
Fien
F
Department of Cardiology, Antwerp University Hospital, University of Antwerp, Edegem, Belgium.
Claeys
Marc J
MJ
Jorens
Philippe
P
Vermeiren
Guy
G
Bosmans
Johan
J
Wuyts
Floris L
FL
Vrints
Chris J
CJ
D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D004562:Electrocardiography; D006801:Humans; D007249:Inflammation; D016753:Interleukin-10 / Q000097:blood / Q000276:immunology; D007962:Leukocytes / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000276:immunology* / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000276:immunology* / Q000473:pathology; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000276:immunology
D017472:Receptors, Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D002097:C-Reactive Protein