Reperfusion injury natural history: Difference between revisions
Jump to navigation
Jump to search
Kashish Goel (talk | contribs) No edit summary |
Kashish Goel (talk | contribs) No edit summary |
||
| Line 2: | Line 2: | ||
'''Editors-In-Chief:''' {{AC}}; [[C. Michael Gibson]], M.S., M.D. [mailto:Mgibson@perfuse.org]; '''Associate Editors-In-Chief: '''[[User:Kashish Goel|Kashish Goel, M.D.]] | '''Editors-In-Chief:''' {{AC}}; [[C. Michael Gibson]], M.S., M.D. [mailto:Mgibson@perfuse.org]; '''Associate Editors-In-Chief: '''[[User:Kashish Goel|Kashish Goel, M.D.]] | ||
==Overview== | ==Overview== | ||
Hypothetical assessment of reperfusion injury and change in its natural history with myocardial protective methods is presented in [[Reperfusion injury medical therapy|medical therapy]] section. Animal studies have shown that [[reperfusion injury]] may be responsible for about 50% of the total infarct size after an acute [[myocardial infarction]]. | Hypothetical assessment of reperfusion injury and change in its natural history with myocardial protective methods is presented in [[Reperfusion injury medical therapy|medical therapy]] section<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>. Animal studies have shown that [[reperfusion injury]] may be responsible for about 50% of the total infarct size after an acute [[myocardial infarction]]. | ||
==Complications== | ==Complications== | ||
* [[Myocardial stunning]]: Delayed recovery, usually 2-3 days, of the viable myocardium after reperfusion is termed as "myocardial stunning". It is mainly due to the release of reactive oxygen species and intracellular calcium overload. | * [[Myocardial stunning]]: Delayed recovery, usually 2-3 days, of the viable myocardium after reperfusion is termed as "myocardial stunning". It is mainly due to the release of reactive oxygen species and intracellular calcium overload. | ||
Revision as of 20:52, 17 May 2012
|
Reperfusion injury Microchapters |
|
Treatment |
|---|
|
Reperfusion injury natural history On the Web |
|
American Roentgen Ray Society Images of Reperfusion injury natural history |
|
Risk calculators and risk factors for Reperfusion injury natural history |
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
Hypothetical assessment of reperfusion injury and change in its natural history with myocardial protective methods is presented in medical therapy section[1]. Animal studies have shown that reperfusion injury may be responsible for about 50% of the total infarct size after an acute myocardial infarction.
Complications
- Myocardial stunning: Delayed recovery, usually 2-3 days, of the viable myocardium after reperfusion is termed as "myocardial stunning". It is mainly due to the release of reactive oxygen species and intracellular calcium overload.
- Myocardial infarction: Irreversible myocyte cell death secondary to reduced oxygen delivery for more than 20-30 minutes, will lead to infarction. Reperfusion helps prevent complete loss of the involved area, however oxidative stress due to this may prevent complete resolution.
- Acute heart failure: Loss of myocardial contractility and systolic dysfunction associated with ischemia/reperfusion injury may lead to development of acute heart failure. Early reperfusion in the course of STEMI prevents myocardial necrosis and may lead to complete recovery of function.
- Ventricular arrhythmias: Reperfusion of the blocked coronary artery can also precipitate arrhythmias ranging from ventricular premature beats to life-threatening ventricular fibrillation.