Is inflammation good for the ischemic heart--perspectives beyond the ordinary.
In recent years, early reperfusion of the myocardial infarct has become the mainstay of optimal therapeutic management since it limits ventricular injury and infarct expansion and improves patient survival [14]. It has become clear that reperfusion promotes effective tissue repair and decreases ventricular remodeling even under circumstances where reperfusion is effected at too late a time to limit myocardial necrosis [4]. One of the striking differences between reperfused and non-reperfused myocardial infarctions is that the early intense inflammatory reaction which ensues immediately upon reperfusion has been demonstrated to potentially extend myocardial injury [9]. Substantial evidence suggests that this inflammatory reaction is important in tissue repair, leading to an obvious paradox with regard to the role of the inflammatory reaction. This communication takes the position that inflammatory injury occurring upon reperfusion of the infarcted myocardium results from the overwhelming of tissue defenses against inflammation resulting from the sudden entry of large amounts of neutrophils to an area of infarction where chemotactic factors have built up to high concentration. However, we hypothesize that inflammation fundamentally evolved as a protective mechanism to promote tissue healing and protect jeopardized myocardium. In this presentation, we will discuss our approach and data designed to evaluate potential protective roles of the inflammatory reaction after reperfusion.
Entman
M L
ML
Department of Medicine and Pediatrics, De Bakey Heart Center, Baylor College of Medicine and Methodist Hospital, Houston, Texas 77030, USA. mentman@bcm.tmc.edu
Youker
K A
KA
Frangogiannis
N
N
Lakshminarayanan
V
V
Nossuli
T
T
Evans
A
A
Kurrelmeyer
K
K
Mann
D L
DL
Smith
C W
CW
D000818:Animals; D004195:Disease Models, Animal; D004285:Dogs; D066298:In Vitro Techniques; D007249:Inflammation; D008407:Mast Cells / Q000166:cytology / Q000502:physiology*; D051379:Mice; D018345:Mice, Knockout; D009203:Myocardial Infarction / Q000503:physiopathology* / Q000628:therapy; D015425:Myocardial Reperfusion; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology; D009206:Myocardium / Q000166:cytology; D009504:Neutrophils / Q000166:cytology / Q000502:physiology*; D017382:Reactive Oxygen Species; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha