<article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" article-type="Research Article" dtd-version="1.0"><front><journal-meta><journal-id journal-id-type="pmc">iarjms</journal-id><journal-id journal-id-type="pubmed">IARJMS</journal-id><journal-id journal-id-type="publisher">IARJMS</journal-id><issn>2708-3594</issn></journal-meta><article-meta><article-id pub-id-type="doi">https://doi.org/10.47310/iarjms.2021.v02i02.033</article-id><title-group><article-title>Management of Acute Mycardial Infarction: The Present Scenario and Way Ahead</article-title></title-group><contrib-group><contrib contrib-type="author"><name><given-names>Aman</given-names><surname>Sharma</surname></name></contrib></contrib-group><contrib-group><contrib contrib-type="author"><name><given-names>Shilpa</given-names><surname>Sharma</surname></name></contrib></contrib-group><aff-id id="aff-a" /><abstract>The definition of MI requires cardiac myocyte necrosis with an increase and/or a decrease in plasma of cardiac troponin (cTn). At least one cTn measurement should be greater than the 99th percentile normal reference limit during: (1) symptoms of myocardial ischemia, (2) new (or presumably new) significant ECG ST-segment/T-wave changes or left bundle branch block, (3) the development of pathological electrocardiographic (ECG) Q waves, (4) new loss of viable myocardium or regional wall motion abnormality identified by an imaging procedure; or (5) identification of intracoronary thrombus by angiography or autopsy.</abstract></article-meta></front><body /><back /></article>