Abstract

Introduction

Myocardial infarction is a syndrome arising from injury to the myocardial tissues due to imbalance in the perfusion and demand with the major cause being coronary atherosclerosis with a superimposed coronary thrombus. When a myocardial injury occurs, various enzymes are being released in to the blood after two hours and they are detectable in the blood by various assays. Cardiac troponin T, troponin I,  creatine kinase MB (CK-MB) are all important biomarkers of myocardial injury  and when elevated, signify myocardial damage with good sensitivity and specificity^[1,2]. CK-MB has a lot of false positive values as they can be elevated in conditions associated with skeletal muscle injury. Troponin T and I are more specific than CK-MB for cardiac injury. CK-MB starts decreasing by 12 hours and at 24 hours, the sensitivity of Troponin is very high^[3]. Troponins can detect very small degrees of myocardial damage. Troponin T has practical advantages over CK-MB in the assessment of left ventricular ejection fraction. Troponin T starts to rise by 3-12 hours and peaks at 12 hours from the onset of pain. However the plateau phase lasts up to 48 hours. Thus, there is a large time window for the peak value. So unlike CK-MB, multiple measurements are not needed in determining the peak value. Also its concentration is unaffected by thrombolysis after the first 12 hours. Thus its measurement directly correlates with the infarct size which is inversely proportional to the ejection fraction.