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    Abstract
   Introduction
   Methods
   Results
   Discussion
   Conclusions
   Acknowledgments
    References

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Table of Contents   
BRIEF COMMUNICATION  
Year : 2011  |  Volume : 4  |  Issue : 2  |  Page : 156-158
Can troponin T levels be useful in the diagnosis of rheumatic carditis?


1 Department of Pediatric Cardiology, Akdeniz University School of Medicine, Arapsuyu, Antalya, Turkey
2 Department of Pediatrics, Akdeniz University School of Medicine, Arapsuyu, Antalya, Turkey
3 Department of Biochemistry, Akdeniz University School of Medicine, Arapsuyu, Antalya, Turkey

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Date of Web Publication8-Sep-2011
 

   Abstract 

Objective: Acute rheumatic fever (ARF) is an endemic disease observed in children of developing countries. The purpose of this study was to test if it was possible to identify myocardial involvement in cases with rheumatic carditis by the measurement of serum cardiac TnT.
Methods: 30 patients diagnosed as ARF underwent echocardiography and their cardiac troponin T (cTnT) serum levels were measured. Patients were divided into group 1: Arthritis alone, group 2: carditis, and group 3 carditis with congestive heart failure (CHF).
Results: cTnT serum levels were normal in all except one patient with in group 3. Two patients in carditis (group 2) and three patients in CHF (group 3) had dilation in left ventricular end diastolic diameter.
Conclusions: Normal cTnT levels in our patient group suggests that inflammation rather than myocardial necrosis is predominant in ARF carditis.

Keywords: Acute rheumatic fever, rheumatic heart disease, Troponin-T

How to cite this article:
Ertug MH, Yilmaz GG, Akçurin G, Kardelen F, Kocabas A, Gumuslu S, Genç SK. Can troponin T levels be useful in the diagnosis of rheumatic carditis?. Ann Pediatr Card 2011;4:156-8

How to cite this URL:
Ertug MH, Yilmaz GG, Akçurin G, Kardelen F, Kocabas A, Gumuslu S, Genç SK. Can troponin T levels be useful in the diagnosis of rheumatic carditis?. Ann Pediatr Card [serial online] 2011 [cited 2019 Jul 19];4:156-8. Available from: http://www.annalspc.com/text.asp?2011/4/2/156/84657



   Introduction Top


Clinically significant abnormalities in acute rheumatic heart disease (RHD) are due to valvular problems rather than myocardial and pericardial involvement. Studies have shown that Troponin I (TnI) and TnT are significant indicators for identifying myocardial injury in hypoxic myocardial injury and viral myocarditis. [1],[2],[3],[4] Clinically significant abnormalities in ARF are supposed to result from valvular rather than myocardial involvement. However, there are limited number of studies to determine TnI and TnT levels. We hypothesized that cTnT levels may elucidate myocardial involvement in rheumatic carditis patients.


   Methods Top


Patient population

Thirty patients who were admitted to the pediatric cardiology department of Akdeniz University Medical School, with their first ARF attack, according to the modified Jones criteria, were enrolled to this prospective study. Thirteen (43.3%) of them were male and 17 (56.7%) female with ages between 5 and 18 years (mean: 10.64 ± 3.16 years). Three patients (10%) had arthritis, 14 (46.7%) carditis, and 13 carditis with CHF. The patients had had no treatment before recruitment to the study. After detailed history and physical examination, blood samples were drawn for evaluating acute phase reactants and cTnT levels. ECG and echocardiographic evaluation were carried out in all patients.

Echocardiography

Echocardiography was performed with GE Vivid 7 machine, Norway, via 3, 5 and 7 MHz transducers. The two-dimensional, M-mode and Doppler ECHO were used to evaluate left ventricular end-diastolic and end-systolic diameters and volumes, systolic functions and valvular regurgitations. For the measurement of valvular regurgitation, modified Perry criteria for aortic valve and modified Helmcke [5] criteria for mitral valve were used. Echocardiographic evaluations were performed by the same experienced echocardiographer in all patients.

Cardiac TnT levels

Serum samples were examined to measure of cTnT level, by Elecsys 2010 analyzer using Troponin T STAT kit in compliance with the electrochemiluminessance immunoassay method according to the manufacturer's recommendations. Measurement span was 0.01-25 ng/ml.

Statistical analysis

First, identifying statistics were assigned to variables. Mean and standard deviations were calculated for time-varying variables and percentages were calculated for categoric variables.


   Results Top


Erythrocyte sedimentation rates (ESR) were between 27 and 120 mm/hour (mean 81.3 mm/hour) and C reactive protein (CRP) levels were between 0.4-24.2 mg/dL (mean 7.2 mg/dL). There was no difference between the three groups in terms of ESR or CRP. Anti-Streptolysin O (ASO) values, were ranging from 160 to 2096 (mean 1193.3 IU/mL), were positive in all patients except one in the arthritis group. ECG showed prolonged PR interval in 6 patients and sinus tachycardia in 16 patients (13 of whom were in the CHF group). Among the patients with carditis, 25 (83.3%) had mitral insufficiency (11 cases with isolated mitral insufficiency), 16 (53.4%) had aortic insufficiency (2 cases with isolated aortic insufficiency), 14 (46.7%) had both mitral and aortic insufficiency. None of the patients showed any indication of myocarditis. Left ventricular end diastolic diameters were between 37 and 61 mm and exceeded age appropriate sizes in 5 (16.6%) patients suggesting dilation. Left ventricular end diastolic diameter in this patient was 61 mm, showing the highest dilation among all patients. Left atrial dimensions (LAD) were between 19 and 54 mm and aortic dimensions (AD) were between 18 and 32.5 mm. LAD/AD ratios ranged from 0.86 to 1.99. Nine (30%) patients had high ratios according to their age.

Troponin levels

Troponin levels were normal in all the patients except one patient in group 3 with CHF, He had cardiac TnT level of 0.096 ng/mL (positive), all the others had troponin levels <0.01 ng/mL (negative).


   Discussion Top


ARF is a systemic inflammatory disease that follows infection with some strains of group A streptococci (GAS). An immune response against streptococcal antigens triggers events in inflammatory response against heart, joints and brain. [6] RHD, which is among major symptoms of ARF, is the most common acquired cardiac disease for all age groups in the world. [7] CHF is rare in patients with acute rheumatic carditis without hemodynamically significant regurgitation. [8],[9],[10]

The carditis of ARF is considered to be pancarditis. However, myocarditis may be difficult to diagnose because its clinical presentation is not typical in all cases. Despite clinical and pathological evidence of myocardial inflammation, the significance of myocarditis in the prognosis of ARF remains contoversial. There are several studies with different results about the existence of cardiac troponins as indicators of myocarditis in ARF. [11],[12],[13],[14],[15],[16],[17] In our study, none of 30 patients showed high cTnT level, except for one in the CHF group.

Mishra et al., [18] by using ECHO and cardiac TnI, argued that there was no serious myocardial involvement in ARF cases, and myocardial injury had no serious contribution to CHF development. It is stated that CHF is related to the degree of valvular involvement rather than myocardial injury.

Most studies about myocarditis in ARF is have measured TnI. But TnT is known to be more sensitive and specific in indicating myocardial injury. In a study involving 46 cases, Alehan [19] showed that there was no significant difference between carditis and arthritis groups in terms of CK-MB or Ccardiac TnT concentrations, and cardiac TnT level did not increase in carditis cases with no accompanying heart insufficiency. Low levels of cardiac TnT was considered to be related to the lack of myocyte injury in rheumatic carditis. Although, raised levels are not always seen in myocarditis. [11]


   Conclusions Top


Cardiac TnT levels are normal in patients with ARF. This may suggest that CHF in ARF is due to serious valvular regurgitation rather than myocardial necrosis.


   Acknowledgments Top


This study is funded by Akdeniz University Research Projects Coordination Unit; 2006.04.0103.008 project number.

 
   References Top

1.Williams RV, MinichLL, Shaddy RE, Veasy LG, Tani LY. Evidence for lack of myocardial injury in children with acute rheumatic carditis. Cardiol Young 2002;12:519-23.  Back to cited text no. 1
    
2.Lipshultz SE, Rifai N, Sallan SE, Lipsitz SR, Dalton V, Sacks DB, et al. Predictive value of cardiac troponin T in pediatric patients at risk for myocardial ýnjury. Circulation 1997;96:2641-8.  Back to cited text no. 2
    
3.Alehan D, Ayabakan C, Celiker A. Cardiac Troponin T and myocardial ýnjury during routine cardiac catheterisation in children. Int J Cardiol 2003;87:223-30.  Back to cited text no. 3
    
4.Gupta M, Lent RW, Kaplan EL, Zabriskie JB. Serum Cardiac Troponin I in acute rheumatic fever. Am J Cardiol 2002;89:779-82.  Back to cited text no. 4
    
5.Helmcke F, Nanda NC, Hsiung MC, Soto B, Adey CK, Goyal RG, et al. Color Doppler assesment of mitral regurgitation using orthogonal planes. Circulation 1987;75:175-83.  Back to cited text no. 5
    
6.Sallakci N, Akcurin G, Köksoy S, Kardelen F, Uguz A, Coskun M, et al. TNF-alpha G-308A polymorphism is associated with rheumatic fever and correlates with increased TNF-alpha production. J Autoimmun 2005;25:150-4.  Back to cited text no. 6
    
7.Lloyd Y, Tani MD. Rheumatic Fever and Rheumatic Heart Disease. In: Allen HD, Driscoll DJ, Shaddy RE, Feltes TF, editors. Moss and Adams' Heart Disease in Infants, Children, and Adolescents: Including the Fetus and Young Adults. 7 th ed. Philedelphia: Lipincott Williams and Wilkins; 2008. p. 1257-75.  Back to cited text no. 7
    
8.Fyler DC. Rheumatic Fever. In: Fyler DC, editor. Nadas' Pediatric Cardiology. 2 nd ed. Philadelphia: Hanley and Belfus Inc; 1992. p. 305.  Back to cited text no. 8
    
9.Kamblock J, Payot L, Lung B, Costes P, Gillet T, Le Goanvic C, et al. Does rheumatic myocarditis really exist? Systematic study with echocardiograpy and cardiac troponin I blood levels. Eur Heart J 2003;24:855-62.  Back to cited text no. 9
    
10.Essop MR, Wisenbaugh T, Sareli P. Evidence against a myocardial factor as the cause of left ventricular dilation in active rheumatic carditis. J Am Coll Cardiol 1993;22:826-9.  Back to cited text no. 10
    
11.Soonswang J, Durongpisitkul K, Nana A, Laohaprasittiporn D, Kangkagate C, Punlee K, et al. Cardiac troponin T: A marker in the diagnosis of acute myocarditis in children. Pediatr Cardiol 2005;26:45-9.  Back to cited text no. 11
    
12.Freedman SB, Haladyn JK, Floh A, Kirsch JA, Taylor G, Thull-Freedman J. Pediatric myocarditis: Emergency department clinical findings and diagnostic evaluation. Pediatrics 2007;120:1278-85.  Back to cited text no. 12
    
13.Lauer B, Nýederau C, Kuhl U, Schannwell M, Pauschýnger M, Strauber BE, et al. Cardiac Troponin T in patients with clinically suspected myocarditis. J Am Coll Cardiol 1997;30:1354-9.  Back to cited text no. 13
    
14.Kamblock J. Serum cardiac troponin I in acute rheumatic fever. Am J Cardiol 2002;90:1277-8.  Back to cited text no. 14
    
15.Smith SC, Landenson LH, Mason JW, Jaffe AS. Elevations of cardiac troponin I associated with myocarditis. Experimental and clinical correlates. Circulation 1997;95:163-8.  Back to cited text no. 15
    
16.Franz WM, RemppisA, Kandolf R, Kubler W, Katus HA. Serum Troponin T: Diagnostic marker for acute myocarditis. Clin Chem 1996;42:340-1.  Back to cited text no. 16
    
17.Soonswang J, Durongpisitkul K, Nana A, Laohaprasittiporn D, Kangkagate C, Punlee K, et al. Cardiac Troponin T: A marker in the diagnosis of acute myocarditis in children. Pediatr Cardiol 2005;26:45-9.  Back to cited text no. 17
    
18.Mishra TK, Mohanty NK, Mishra SK, Rath PK. Myocardial dysfunction in rheumatic carditis- does it really exist? J Assoc Physicians India 2007;55:276-80.  Back to cited text no. 18
    
19.Alehan D, Ayabakan C, Hallioglu O. Role of serum cardiac troponin T in the diagnosis of acute rheumatic fever and rheumatic carditis. Heart 2004;90:689-90.  Back to cited text no. 19
    

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Correspondence Address:
Firat Kardelen
Department of Pediatric Cardiologys, Akdeniz University School of Medicine, 07070, Arapsuyu, Antalya
Turkey
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0974-2069.84657

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