ROLE OF INFLAMMATION IN ACUTE MYOCARDIAL INFARCTION
Vadivelan Ramachandran*, Sudeep Sugumar, Vikash Sundharam
The important therapeutic goals of current cardiology are to project approaches to reduce myocardial necrosis and improving cardiac restoration following myocardial infarction. Myocardial infarction (MI) refers to partial (regional) myocardial necrosis, typically endocardium-based, inferior to occlusion of an epicardial artery. In dissimilarity, concentric subendocardial necrosis may affect from global ischemia and reperfusion in cases of long cardiac arrest with resuscitation. Zones of myocardial infarction may be subepicardial if there is occlusion of slighter vessels by thromboemboli creating from coronary thrombi. Myocardial necrosis encourages match initiation and free radical group, generating a cytokine cascade initiated by Tumour Necrosis Factor (TNF)-α release. Despite this potential damage, substantial evidence proposes that reperfusion improves cardiac repair cultivating patient survival; this outcome may be in part associated to the inflammatory response.
Keywords: Acute Myocardial Infarction, Atherosclerosis, Inflammation, Inflammatory Markers, Reactive Oxygen Species.
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