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Detection of cardiac damage is greatly facilitated by serial blood measurements of myocardial cell markers. In many hospitals creatine kinase MBmass concentration (CK MBmass) constitutes the biochemical criterion (WHO) for acute myocardial infarction (AMI). Cardiac troponin T (TnT) is an even more sensitive and specific marker for myocardial damage. With discriminator levels of 10.0 and 0.10 micrograms/l, respectively, serial measurements of both markers provide a useful diagnostic strategy for ischemic heart disease. This survey reviews representative cumulated time curves in individual patients covering the spectrum of myocardial damage, including unstable angina pectoris (UAP), non-Q-wave and Q-wave infarctions with and without early reperfusion, re-infarction, and subacute infarction. Increased TnT detects minor myocardial damage (MMD) in over 30% of patients with UAP, although CK MBmass remains below its discriminator. Subacute infarction is detected by the wide diagnostic time window of the serum TnT at a time when CK MBmass has already returned to normal. In a substudy of 502 suspected cases of AMI, the distributions of maximum serum TnT concentrations within each patient series demonstrated that TnT had a diagnostic sensitivity of 100% and a specificity of 99%. Median, 5th and 95th percentiles of maximum TnT values within the diagnostic subgroups showed that serum TnT was increased five-fold more than CK MBmass. Median values of Q-wave AMI were higher than in non-Q-wave AMI. A diagnostic strategy using TROPT, a rapid test specific for the cardiac isoform of TnT with a detection limit 0.10 microgram/l, is presented.
Detection of cardiac damage is greatly facilitated by serial blood measurements of myocardial cell markers. In many hospitals creatine kinase MBmass concentration (CK MBmass) constitutes the biochemical criterion (WHO) for acute myocardial infarction (AMI). Cardiac troponin T (TnT) is an even more sensitive and specific marker for myocardial damage. With discriminator levels of 10.0 and 0.10 micrograms/l, respectively, serial measurements of both markers provide a useful diagnostic strategy for ischemic heart disease. This survey reviews representative cumulated time curves in individual patients covering the spectrum of myocardial damage, including unstable angina pectoris (UAP), non-Q-wave and Q-wave infarctions with and without early reperfusion, re-infarction, and subacute infarction. Increased TnT detects minor myocardial damage (MMD) in over 30% of patients with UAP, although CK MBmass remains below its discriminator. Subacute infarction is detected by the wide diagnostic time window of the serum TnT at a time when CK MBmass has already returned to normal. In a substudy of 502 suspected cases of AMI, the distributions of maximum serum TnT concentrations within each patient series demonstrated that TnT had a diagnostic sensitivity of 100% and a specificity of 99%. Median, 5th and 95th percentiles of maximum TnT values within the diagnostic subgroups showed that serum TnT was increased five-fold more than CK MBmass. Median values of Q-wave AMI were higher than in non-Q-wave AMI. A diagnostic strategy using TROPT, a rapid test specific for the cardiac isoform of TnT with a detection limit 0.10 microgram/l, is presented.
The cardiac troponin T level is a powerful, independent risk marker in patients who present with acute myocardial ischemia. It allows further stratification of risk when combined with standard measures such as electrocardiography and the CK-MB level.
Metaanalysis is a method that incorporates the pooling of previously published results to produce more statistically significant results. We used metaanalysis to examine the role of a new cardiac marker, cardiac troponin T (cTnT), in patients with ischemic heart disease. Metaanalysis of six articles and one abstract on cTnT showed that this marker was just as sensitive as creatine kinase MB isoenzyme (CK-MB) for the retrospective diagnosis of acute myocardial infarction (AMI) 12-48 h after onset but less specific. Most of these articles showed that cTnT was increased in non-AMI patients with unstable angina pectoris. In a metaanalysis of four papers, two abstracts, a letter, and an unpublished manuscript, we examined the prognostic role of cTnT in non-AMI cardiac patients. For an unfavorable endpoint defined as cardiac death, AMI, or the need for coronary artery revascularization, the results demonstrated that abnormal concentrations of cTnT were associated with a higher risk for a poor outcome than were normal concentrations of cTnT. We also compared cTnT with CK-MB for risk stratification. Metaanalysis will become an increasingly important tool for evaluating new tests as they become available.
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