CONCLUSION
Although it is important not to miss an ACS, it is equally important for physicians and other health care providers to determine the underlying cause of troponin elevation. It may not be related to ACS but to a condition that is causing myocardial strain, loss of cell integrity, and cell death. Proper clinical investigations through good history taking, physical examination, and diagnostic testing will assist in determining a reason for an isolated elevation of troponins in the bloodstream.
This review has highlighted some common scenarios that need to be considered when troponins are elevated. Diagnosing the underlying cause of troponin elevation helps in patients’ treatments, affects quality of life, and avoids pitfalls and additional medical care costs. Troponin elevation is thus not an automatic diagnosis of ACS but an injury to cardiac cell from many causes, including ACS. By broadening our knowledge on conditions that cause elevated troponins and considering the different mechanisms by which cardiac troponin elevations can occur, we will improve the care of patients when confronted with elevated troponin.
REFERENCES
1. Thygesen K, Alpert JS, White HD; Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction. Universal definition of myocardial infarction. Eur Heart J. 2007;28(20):2525-2538.
2. Kelley WE, Januzzi JL, Christenson RH. Increases of cardiac troponin in conditions other than acute coronary syndrome and heart failure. Clin Chem. 2009;55(12):2098-2112.
3. Thygesen K, Alpert JS, White HD, et al. Universal definition of myocardial infarction. Circulation. 2007;116(22):2634-2653.
4. Hansen MS, Nogareda GJ, Hutchison SJ. Frequency of and inappropriate treatment of misdiagnosis of acute aortic dissection. Am J Cardiol.2007;99(6):852-856.
5. von Kodolitsch Y, Nienaber CA, Dieckmann C, et al. Chest radiography for the diagnosis of acute aortic syndrome. Am J Med. 2004;116(2): 73-77.
6. Nunes JP, Mota Garcia JM, Farinha RM, et al. Cardiac troponin I in aortic valve disease. Int J Cardiol.2003;89(2-3):281-285.
7. Arlati S, Brenna S, Prencipe L, et al. Myocardial necrosis in ICU patients with acute non-cardiac disease: A prospective study. Intensive Care Med.2000;26(1):31-37.
8. Zellweger MJ, Schaer BA, Cron TA, Pfisterer ME, Osswald S. Elevated troponin levels in absence of coronary artery disease after supraventricular tachycardia. Swiss Med Wkly. 2003;133(31-32):439-441.
9. Bakshi TK, Choo MK, Edwards CC, Scott AG, Hart HH, Armstrong GP. Causes of elevated troponin I with a normal coronary angiogram. Intern Med J. 2002;32(11):520-525.
10. Fruchter O, Yigla M. Cardiac troponin-I predicts long-term mortality in chronic obstructive pulmonary disease. COPD. 2009;6(3):155-161.
11. Troøyen M, Indredavik B, Rossvoll O, Slørdahl SA. Myocardial injury in acute stroke assessed by troponin I. Tidsskr Nor Laegeforen. 2001;121(4):421-425.
12. Tung P, Kopelnik A, Banki N, et al. Predictors of neurocardiogenic injury after subarachnoid hemorrhage. Stroke. 2004;35(2):548-551.
13. Erauzkin, G. The value of troponin T as a marker of ischemic heart disease in renal insufficiency. Nefrologia. 2008;28(suppl 6):113-118.
14. Ooi DS, Isotalo PA, Veinot JP. Correlation of antemortem serum creatine kinase, creatine kinase-MB, troponin I, and troponin T with cardiac pathology. Clin Chem. 2000;46(3):338-344.
15. Antman EM, Grudzien C, Mitchell RN, Sacks DB. Detection of unsuspected myocardial necrosis by rapid bedside assay for cardiac troponin T. Am Heart J. 1997;133(5):596-598.
16. Diris JHC, Hackeng CM, Kooman JP, Pinto YM, Hermens WT, van Dieijen-Visser MP. Impaired renal clearance explains elevated troponin T fragments in hemodialysis patients. Circulation. 2004;109(1):23-25.
17. Buhaescu I, Izzedine H, Covic A. Cardiac troponins in renal failure—time for an optimistic consensus? Int J Clin Pract. 2005;59(11):1317-1325.
18. Choy, JB, Armstrong, PW, Ulan, RA, et al. Do cardiac troponins provide prognostic insight on hemodialysis patients? Can J Cardiol. 2003;19(8):907-911.
19. Parrillo JE. Pathogenetic mechanisms of septic shock. N Engl J Med. 1993;328(20):1471-1477.
20. Ammann P, Fehr T, Minder EI, Gunter C, Bertel O. Elevation of troponin I in sepsis and septic shock. Intensive Care Med. 2001;27(6):965-969.
21. Andresen M, Regueira T. Myocardial dysfunction in sepsis. Rev Med Chil. 2010;138(7):888-896.
22. Logeart D, Beyne P, Cusson C, et al. Evidence of cardiac myolysis in severe nonischemic heart failure and the potential role of increased wall strain. Am Heart J. 2001;141(2):247-253.
23. Sato Y, Yamada T, Taniguchi R, et al. Persistently increased serum concentrations of cardiac troponin T in patients with idiopathic dilated cardiomyopathy are predictive of adverse outcomes. Circulation.2001;103(3):369-374.
24. Alpert JS, Thygesen K, Antman E, Bassand JP. Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol.2000;36(3):959-969.