AS AN INDEPENDENT PREDICTOR OF CARDIAC DYSFUNCTION AFTER SUPRAVENTRICULAR TACHYCARDIA IN CHILDREN WITH STRUCTURAL NORMAL HEART ?

Introduction Elevated cardiac troponin gives excellent accuracy in the identification of myocardial damage in children, but it can also be elevated in a series of other diseases. Case report We showed two children aged thirteen years with a high serum troponin-I after an acute episode of supraventricular tachycardia. We analyzed troponin-I levels in correlated with the maximum heart rate, duration of tachycardia and systolic left ventricular function (ejection fraction and fractional shortening). Conclusion Abnormal troponin level can be seen in children presenting with sustained supraventricular tachycardia and normal heart. Caution is advised in the diagnosis cardiac dysfunction in children with supraventricular tachycardia and elevated troponin levels.


Introduction
Cardiac troponin as marker of myocardial necrosis is now commonly used in clinical practice in adults with coronary artery diseases.In children, it is a sensitive and specific biomarker consistent with cardiac damage (within severe acute and chronic heart failure, congenital heart disease or myocarditis, cardioversion, cateter ablation or trauma of myocardium, endoyocardial biopsy, drug-and toxin-induced cardiac toxicity) [1][2][3] .
Up to now, was not researched supraventricular tachycardia (SVT) -induced elevations in cTnI in children with normal heart.The aim of our study was to determine the prognostic value of troponin assays in children presenting to the emergency department with tachycardia.We assessed the test characteristics for positive cTnI (defined as > 0.04 µg/L, the manufacturer's upper limit of normal) in correctly identifying children who had SVT.

Case 1
A 13 years and 6 months-old female child was admitted to our hospital because of chest pain and palpitation after a heavy meal.The symptoms lasted for at least 8 hours and were relieved when she arrived at the hospital.She had no personal or family history about congenital heart anomaly, or other diseases (complete blood count, sedimentation, Creactive protein, procalcitonin, glycaemia, electrolytes, transaminase, urea, creatinine, thyroid hormones and native chest X-ray were within normal ranges).

Her electrocardiogram (ECG) at admision to intensive care unit (ICU) showed
Atrioventricular Reentry Tachycardia (AVRT); ST segment depression 1,5-2 mm in leads V5-6 and Max HR=217 per minute.Figure 1 shows intermittent preexcitation in the Wolff-Parkinson-White syndrome, that was determined later.The echocardiogram showed no abnormal changes (EF and FS showed in Table 1).After attempt vagal maneuvers, she was treated with Adenosine and then continued with oral therapy -tablets Presolol (2x25mg 5 days and then 50+25mg to control).3) and no abnormal changes in echocardiogram (Table I).She received the same medicine as the first case.The level of cTnI was 0,377 µg/l at admission and fourth day later the value was up to 0,038 µg/l (Table I, Figure 2).Also, ProBNP was clearly elevated in the serum (1617 pg/ml) and the value was up to 286 pg/ml.During 24-hour ambulatory electrocardiogram monitoring 6 supraventricular extrasystoles were found.Also, ECG (without attack of SVT) and load test were normal.

Discussion
Cardiac troponin T and I in serum is commonly used as standard biomarker for the diagnosis of acute coronary syndrome or myocardial infarction.In adult patients with SVT, most authors posed the question are troponin levels useful for evaluating the presence of coronary artery disease [14][15][16][17][18][19][20][21][22][23][24] ?Published reports (limited case series: 1-7 patients ages 18-72)   illustrate that troponins can be released because of tachycardia alone in the absence of myodepressive factors, inflammatory mediators, or coronary artery disease [20][21][22][23][24] .The current literature on this topic shows that 12 to 48% of adult patients will have elevated troponins after SVT.Schmitz G et al. 14 in their research find troponin elevation in patients with SVT with normal coronary angiography and is thought to be due to cardiac stretch, poor diastolic perfusion, and/or coronary artery vasospasm.
In children SVT is a common and generally benign arrhythmia.Causes of SVT include: lung disease, abnormal heart structure or an abnormal extra electrical pathway of the heart and use of certain medications (in the asthmatic status diastolic hypotension and tachycardia are dose-dependent side effects of high-dose albuterol) 25,26 .The severity of SVT can vary greatly.It can last for < 30 sec.(nonsustained SVT) and cause little or no symptoms or it can last for hours (sustained SVT) and cause palpitations, chest pain, shortness of breath and even fainting in rare cases.
Left ventricular dysfunction can showed persisted symptoms or abnormal electrocardiograms after conversion to normal sinus rhythm.While you treat the children's heart rate, you wonder if a troponin level would be useful in evaluating the presence of cardiac dysfunction.Our case was series of two hemodynamically stable patients with various troponin elevation in proportion to the duration of tachycardia.Therefore the troponin rise in our series was a direct result of sustained SVT.
There has not been enough research to date to support the routine use of troponin in the evaluation of SVT in children.Routine testing can result in false positives findings (shortness of breath persistent, infection, chronic anemia, hemolysis and other reasons).
Consequently, in children with various duration tachycardias, the use of troponin testing would be the best performed selectively based on presenting symptoms and risk factors for cardiac dysfunction.