Comparable detection of acute myocardial infarction by creatine kinase MB isoenzyme and cardiac troponin I

Abstract

Although measurement of cardiac troponin I (cTnI) is, in some situations, more specific for detection of cardiac injury than is measurement of the MB isoenzyme of creatine kinase (MBCK), its sensitivity and specificity relative to MBCK for detection of myocardial infarction has not been established. Accordingly, we studied prospectively 199 consecutive patients admitted to the coronary care unit. Values of MBCK and cTnI mass were determined in all samples. Of the 188 patients admitted with a suspicion of acute myocardial ischemia, 89 were diagnosed as having an acute myocardial infarction on the basis of the patterns of MBCK values. Eighty-six of these patients also had increased cTnI (concordance, 96.6%); three did not. Of the patients diagnosed as without infarction, five with unstable angina and symptoms in the day(s) prior to admission had increased cTnI, for a cTnI specificity of 94.9%. Receiver operating characteristic curve analysis indicated that cTnI and MBCK had statistically indistinguishable diagnostic accuracies for the detection of acute myocardial infarction.

Correlation of Serum Cardiac Troponin I and Myocardial Damage in Cattle with Monensin Toxicosis

“…In human cardiomyocytes, approximately 6-8% of total cellular cardiac troponin is cytosolically dissolved and thus unbound in cytoplasm. 21 Early after myocardial cell injury, affecting cell membrane permeability, parts of this free pool are liberated into the blood stream, but the majority of cTnI is retained intracellularly because of structural linkage to the contractile apparatus. Thus, release of cTnI may occur monophasically, with only minor increase after reversible myocyte injury, or bi-or polyphasically with more severe injury of the myocardium affecting the structurally bound portion of cTnI.…”

Perioperative catecholamine changes in cardiac risk patients

“…Post-operative ischaemia seems to correlate with adverse outcome, and prolonged subendocardial ischaemia rather than acute coronary artery occlusion precedes cardiac complications [1,6]. Cardiac troponins (TNs) -troponin T (TNT) and troponin I (TNI) -have been established as a sensitive marker for detection of major and minor myocardial cell injury, avoiding the high incidence of false-positive results by the use of creatine kinase (CK)-MB [7][8][9][10][11][12]. Metzler et al [13] found that in cardiac risk patients undergoing non-cardiac surgery high postoperative levels of TNT and TNI were correlated with post-operative cardiac complications, whereas patients with no or only slightly increased concentrations of both troponins had a good outcome.…”

Serum cardiac troponin I concentrations decrease following treatment of primary immune‐mediated haemolytic anaemia

“…A wide range of biomarkers have been used to assess cardiac myocyte damage, including aspartate dehydrogenase, creatinine kinase, lactate dehydrogenase, myoglobin and cardiac troponin (cTn) (Adams et al 1993, Spratt et al 2005, Jaffe et al 2006. Cardiac troponin I (cTnI) is exclusively found in the myocardium and is a sensitive and specific marker of myocyte damage (Adams et al 1993(Adams et al , 1994. Serum cTnI concentrations have been measured in many species to non-invasively assess myocardial damage (Apple et al 2008, Mikaelian et al 2010.…”

“…The median time between the pre-and post-diagnosis samples in this study was 4 weeks, which provided sufficient time to examine the relationship between changes in HCT and serum cTnI concentrations. After an acute cardiac injury the cytosolic pool, which is about 2 to 4% of total cTnI (Adams et al 1994), is released, causing an early peak in serum cTnI concentrations. The peak in cTnI concentrations in canine models of acute myocardial infarction has been reported to occur 10 to 16 hours post infarction (Cummins & Cummins 1987).…”