Despite pathologic evidence of myocardial inflammation, the significance of myocarditis in children with acute rheumatic carditis remains controversial.[11
] The guidelines for the diagnosis of rheumatic fever indicated that rheumatic myocarditis, although uncommon, in the absence of severe valvular damage may have contributed to the genesis of heart failure during rheumatic fever.[8
In this study, we could not find any biochemical alteration or echocardiographic measurements change suggestive of significant hemodynamic effects due to myocardial involvement. No statistically significant difference was found in the level of cTnT between patients with and without rheumatic carditis. Furthermore, all patients showed cTnT level within the normal range even in those with heart failure. Cardiac troponin T is considered as one of the new “gold markers” of ischemic myocardial injury and has been detected as a sensitive and specific marker of even subclinical myocardial injury. It is also used in the diagnosis and monitoring of nonischemic myocardial injury, like myocarditis.[12
In addition, the echocardiographic study failed to show any significant difference in the left ventricular ejection and shortening fractions between children with and without rheumatic carditis whether or not they had congestive heart failure. Our results are in agreement with Tavli et al
] who showed that the level of cTnI is not elevated in acute rheumatic fever in children with and without carditis. In addition, they failed to show any echocardiographic signs of myocardial involvement in their study on rheumatic fever in children. Alehan et al
] also demonstrated that serum cTnT concentration does not increase above normal limits in rheumatic carditis with or without heart failure, also they could not find any significant change in function due to myocarditis using echocardiography. Kamblock et al
] examined a large series of children with ARF (95 children), they neither detected cTnI elevations nor echocardiographic abnormalities suggesting significant hemodynamic changes due to myocardial involvement during rheumatic fever, in patients with carditis even if they had congestive heart failure. Congestive heart failure was always related to severe valve regurgitation not to myocarditis. The same results were shown by Williams et al
] who demonstrated that serum cTnI was not elevated in patients with acute rheumatic fever. They stated that the fact that levels of cardiac troponin I are not elevated in the serum of children with acute rheumatic carditis suggesting that there is minimal myocyte necrosis in this setting.
The low cTnT values, especially in the presence of active carditis, dispute significant ischemic myocyte injury.[16
] Myocardial necrosis is not prominent despite intensive inflammation in ARF.[17
] ARF is mainly a disease of connective tissue, and endocarditis is the prominent factor.[18
] This may explain the normal concentrations of cTnT found in patients with ARF carditis. Aschoff nodules are the histological hallmark of rheumatic fever, and have been identified in left atrial appendages and ventricular myocardium of patients with rheumatic fever and rheumatic heart disease.[19
] However, the presence of Aschoff nodules in the ventricular myocardium does not signify that they play a role in the genesis of congestive heart failure during the acute stage of the disease.[8
We can conclude that this study did not demonstrate an elevated cTnT level suggesting clinically relevant myocardial involvement during acute rheumatic fever even in patients with severe carditis and congestive heart failure. In addition, we failed to show significant difference in echocardiographic measurements between patients with and without carditis. These findings substantiate the view that myocardial involvement during acute rheumatic fever has no significant hemodynamic effects and does not play a role in the development of heart failure in patients with rheumatic carditis. Heart failure is related mainly to the extent of valvular lesions rather than the myocardial involvement.
However, among study limitations are rather small number of studied population. Further studies are needed to confirm that myocardial involvement during acute rheumatic fever is not relevant in the development of heart failure in patients with rheumatic fever.