Reperfusion injury overview: Difference between revisions
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Revision as of 15:31, 19 August 2015
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Reperfusion injury Microchapters |
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Editors-In-Chief: Anjan K. Chakrabarti, M.D. [1]; C. Michael Gibson, M.S., M.D. [2]; Associate Editors-In-Chief: 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.
Risk Factors
Risk factors for reperfusion injury include hypertension with left ventricular hypertrophy, congestive heart failure, increased age, diabetes, and hyperlipidemia.
Natural History, Complications and Prognosis
Reperfusion injury may be responsible for about 50% of the total infarct size after an acute myocardial infarction as well as myocardial stunning, congestive heart failure and reperfusion arrhythmias such as ventricular arrhythmias.[1]