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Technical Briefs |
Department of Laboratory Medicine and Pathology, Hennepin County Medical Center and University of Minnesota School of Medicine, Minneapolis, MN;
aaddress correspondence to this author at: Hennepin County Medical Center, Clinical Laboratories P4, 701 Park Ave., Minneapolis, MN 55415; fax 612-904-4229, e-mail fred.apple@co.hennepin.mn.us
| The first 300 words of the full text of this article appear below. |
Cardiac troponin monitoring for detection of myocardial injury has been designated the new standard for differentiating the diagnosis of unstable angina and non-ST-elevation myocardial infarction (NSTEMI) in acute coronary syndrome patients (1)(2)(3)(4). Increased cardiac troponin I (cTnI) or T (cTnT) in the clinical setting of ischemia is defined as an acute MI and has been endorsed by the European Society of Cardiology, American College of Cardiology, the American Heart Association, the IFCC, and the Epidemiology World Council (1)(2)(3)(4)(5)(6). One of the challenges that confronts cardiac troponin monitoring encompasses the clinical setting of myocardial reinfarction within a short time period after an initial MI. Because cardiac troponins can remain increased in the circulation for up to 5 (cTnI) or 10 days (cTnT) after an acute MI, in theory, the role for monitoring cardiac troponins during reinfarction has been questioned. The European Society of Cardiology/American College of Cardiology consensus document notes that in the clinical setting of a reinfarction, creatine kinase MB (CKMB) may be more useful for monitoring for MI because CKMB remains increased for only 2–4 days after an acute MI (1)(2)(3)(4). There are only two case reports in the literature, both from a previous report from our laboratory, that readdressed the role of cardiac troponin monitoring in reinfarction (7).
The purpose of this study was to compare the patterns of increases and decreases in cTnI and CKMB mass in a series of nine MI patients who experienced an in-hospital myocardial reinfarction (MI extension) within 4 days of the initial MI event. Over a period of 16 months (September 1999 through February 2001), nine MI patients were identified who experienced
The following articles in journals at HighWire Press have cited this article:
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  A. K. Saenger and A. S. Jaffe Requiem for a Heavyweight: The Demise of Creatine Kinase-MB Circulation, November 18, 2008; 118(21): 2200 - 2206. [Full Text] [PDF]
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 F. S. Apple, S. W. Smith, L. A. Pearce, R. Ler, and M. M. Murakami Use of the Centaur TnI-Ultra Assay for Detection of Myocardial Infarction and Adverse Events in Patients Presenting With Symptoms Suggestive of Acute Coronary Syndrome Clin. Chem., April 1, 2008; 54(4): 723 - 728. [Abstract] [Full Text] [PDF]
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 K. Thygesen, J. S. Alpert, H. D. White, and on behalf of the Joint ESC/ACCF/AHA/WHF Task Force Universal Definition of Myocardial Infarction J. Am. Coll. Cardiol., November 27, 2007; 50(22): 2173 - 2195. [Full Text] [PDF]
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K. Thygesen, J. S. Alpert, H. D. White, on behalf of the Joint ESC/ACCF/AHA/WHF Task Force, TASK FORCE MEMBERS: Chairpersons: Kristian Thygese, Biomarker Group: Allan S. Jaffe, Coordinator (USA), ECG Group: Bernard Chaitman, Co-ordinator (USA), P, Imaging Group: Richard Underwood, Coordinator (UK), Intervention Group: Jean-Pierre Bassand, Co-ordina, Clinical Investigation Group: Paul W. Armstrong, C, et al. Universal Definition of Myocardial Infarction Circulation, November 27, 2007; 116(22): 2634 - 2653. [Full Text] [PDF]
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 Task Force Members, K. Thygesen, J. S. Alpert, H. D. White, Biomarker Group, A. S. Jaffe, F. S. Apple, M. Galvani, H. A. Katus, L. K. Newby, et al. Universal definition of myocardial infarction: Kristian Thygesen, Joseph S. Alpert and Harvey D. White on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction Eur. Heart J., October 2, 2007; 28(20): 2525 - 2538. [Full Text] [PDF]
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NACB WRITING GROUP MEMBERS, D. A. Morrow, C. P. Cannon, R. L. Jesse, L. K. Newby, J. Ravkilde, A. B. Storrow, A. H.B. Wu, and R. H. Christenson National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical Characteristics and Utilization of Biochemical Markers in Acute Coronary Syndromes Circulation, April 3, 2007; 115(13): e356 - e375. [Full Text] [PDF]
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NACB WRITING GROUP MEMBERS, D. A. Morrow, C. P. Cannon, R. L. Jesse, L. K. Newby, J. Ravkilde, A. B. Storrow, A. H.B. Wu, R. H. Christenson, NACB COMMITTEE MEMBERS, et al. National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical Characteristics and Utilization of Biochemical Markers in Acute Coronary Syndromes Clin. Chem., April 1, 2007; 53(4): 552 - 574. [Full Text] [PDF]
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A. S. Jaffe, L. Babuin, and F. S. Apple Reply J. Am. Coll. Cardiol., December 5, 2006; 48(11): 2358 - 2359. [Full Text] [PDF]
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A. S. Jaffe Chasing Troponin: How Low Can You Go if You Can See the Rise? J. Am. Coll. Cardiol., November 7, 2006; 48(9): 1763 - 1764. [Full Text] [PDF]
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A. S. Jaffe, L. Babuin, and F. S. Apple Biomarkers in Acute Cardiac Disease: The Present and the Future J. Am. Coll. Cardiol., July 4, 2006; 48(1): 1 - 11. [Abstract] [Full Text] [PDF]
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 L. Babuin and A. S. Jaffe Troponin: the biomarker of choice for the detection of cardiac injury Can. Med. Assoc. J., November 8, 2005; 173(10): 1191 - 1202. [Abstract] [Full Text] [PDF]
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C. Cavallini, S. Savonitto, and D. Ardissino Impact of the elevation of biochemical markers of myocardial damage on long-term mortality after percutaneous coronary intervention: results of the CK-MB and PCI study: reply Eur. Heart J., October 2, 2005; 26(20): 2206 - 2207. [Full Text] [PDF]
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