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{{Reperfusion injury}}
{{Reperfusion injury}}


'''Editors-In-Chief:''' {{AC}}; [[C. Michael Gibson]], M.S., M.D. [mailto:Mgibson@perfuse.org]
'''Editors-In-Chief:''' {{AC}}; [[C. Michael Gibson]], M.S., M.D. [mailto:Mgibson@perfuse.org]; [[User:Kashish Goel|Kashish Goel, M.D.]]


==Overview==
==Overview==
'''Reperfusion injury''' refers to damage to [[tissue (biology)|tissue]] caused when [[blood]] supply returns to the tissue after a period of [[ischemia]]. The absence of [[oxygen]] and [[nutrient]]s from blood creates a condition in which the restoration of [[circulatory system|circulation]] results in [[inflammation]] and [[oxidation|oxidative]] damage through the induction of [[oxidative stress]] rather than restoration of normal function.
The introduction and wide application of reperfusion strategies in patients with [[STEMI]] has significantly reduced the mortality rate over last decade. Despite this, the rate of 30-day mortality remains high and about 25% of the patients develop [[heart failure]]. One of the mechanisms responsible for this is '''Reperfusion injury'''. Reperfusion injury refers to myocardial cell death secondary to restoration of blood flow to the [[ischemia|ischemic]] myocardium. The absence of [[oxygen]] and [[nutrient]]s from blood creates a condition in which the restoration of [[circulatory system|circulation]] results in [[inflammation]] and [[oxidation|oxidative]] damage through the induction of [[oxidative stress]] rather than restoration of normal function. Few of the animal studies show that [[reperfusion injury]] may be responsible for approximately 50% of the final infarct size in [[STEMI]] patients<ref name="pmid17855673">{{cite journal |author=Yellon DM, Hausenloy DJ |title=Myocardial reperfusion injury |journal=N. Engl. J. Med. |volume=357 |issue=11 |pages=1121–35 |year=2007 |month=September |pmid=17855673 |doi=10.1056/NEJMra071667 |url=}}</ref>. Recent advances in understanding of the pathophysiologic process behind reperfusion injury and treatment targets have provided opportunities to reduce mortality.


==References==
==References==

Revision as of 16:49, 17 May 2012

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Editors-In-Chief: Anjan K. Chakrabarti, M.D. [1]; C. Michael Gibson, M.S., M.D. [2]; Kashish Goel, M.D.

Overview

The introduction and wide application of reperfusion strategies in patients with STEMI has significantly reduced the mortality rate over last decade. Despite this, the rate of 30-day mortality remains high and about 25% of the patients develop heart failure. One of the mechanisms responsible for this is Reperfusion injury. Reperfusion injury refers to myocardial cell death secondary to restoration of blood flow to the ischemic myocardium. The absence of oxygen and nutrients from blood creates a condition in which the restoration of circulation results in inflammation and oxidative damage through the induction of oxidative stress rather than restoration of normal function. Few of the animal studies show that reperfusion injury may be responsible for approximately 50% of the final infarct size in STEMI patients[1]. Recent advances in understanding of the pathophysiologic process behind reperfusion injury and treatment targets have provided opportunities to reduce mortality.

References

  1. Yellon DM, Hausenloy DJ (2007). "Myocardial reperfusion injury". N. Engl. J. Med. 357 (11): 1121–35. doi:10.1056/NEJMra071667. PMID 17855673. Unknown parameter |month= ignored (help)