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Detection of Cardiac Troponin I Early after Onset of Chest Pain in Six Patients

Departments of
¹ Physiology, Queen’s University, Kingston, Ontario, K7L 3N6 Canada;
² Department of Emergency Medicine, Queen’s University, Kingston, Ontario, K7L 3N6 Canada;
³ Department of Pathology,, Queen’s University, Kingston, Ontario, K7L 3N6 Canada;
⁴ Biochemistry, Queen’s University, Kingston, Ontario, K7L 3N6 Canada

^aauthor for correspondence: Fax 613-533-6880, e-mail JVE1@post.queensu.ca)

Patients presenting to the emergency departments (ED) with symptoms of acute coronary syndrome (ACS) and with a nondiagnostic electrocardiogram (ECG) pose a management challenge (1). Cardiac troponins [(cTns), tropinin I (cTnI) and tropinin T [cTnT)], creatine kinase (CK), and CK-MB are frequently used in the assessment of ACS. cTns are superior in their analytical specificity and diagnostic sensitivity and specificity for myocardial injury (2)(3). Findings from both animal and clinical studies show that cTnI is released into the blood in various cardiac conditions, including angina, acute myocardial infarction (1)(4)(5), congestive heart failure (6), and myocarditis (7). Because cTns in serum represent myocardial damage and increased risk of future adverse outcomes (8), improving the detection of serum cTns has implications for better diagnosis of myocardial damage and better risk stratification for patients with ACS.

With current clinical assays, cTns are detectable in the circulation 4–6 h after the onset of pain in acute myocardial infarction, peaking within 12–24 h and remaining increased for a few days (9). However, a recently developed Western blot method, WB-DSA (10), detected minute amounts of cTnI in serum of patients undergoing bypass surgery within 10 min after reperfusion (11), suggesting increased detection of TnI by the WB-DSA method. Although WB-DSA does not permit analysis of troponin’s quaternary structure, it does allow accurate assessment of the chemical status of individual troponin subunits, such as the extent and pattern of cTnI degradation. cTnI is specifically degraded in ischemic/reperfused injured rat myocardium (4)(12), and TnI degradation products are detected in myocardium of patients undergoing coronary artery bypass surgery. Because ACS represents a spectrum of cardiac pathophysiology, unique patterns of cTnI degradation . . . [Full Text of this Article]

Patient 1.

Patient 2.

Patient 3.

Patient 4.

Patient 5.

Patient 6.

Patients 7–10.

Acknowledgments

References

The following articles in journals at HighWire Press have cited this article:

				S. Eriksson, M. Junikka, P. Laitinen, K. Majamaa-Voltti, H. Alfthan, and K. Pettersson Negative Interference in Cardiac Troponin I Immunoassays from a Frequently Occurring Serum and Plasma Component Clin. Chem., July 1, 2003; 49(7): 1095 - 1104. [Abstract] [Full Text] [PDF]

				R. Labugger, J. A. Simpson, M. Quick, H. A. Brown, C. E. Collier, I. Neverova, and J. E. Van Eyk Strategy for Analysis of Cardiac Troponins in Biological Samples with a Combination of Affinity Chromatography and Mass Spectrometry Clin. Chem., June 1, 2003; 49(6): 873 - 879. [Abstract] [Full Text] [PDF]