Acute valvular disease with heart failure or chronic valvular disease account for most of the morbidity and mortality associated with rheumatic fever.[7] Revised guidelines for the diagnosis of rheumatic fever indicate that when rheumatic fever affects the heart, it usually involves the endocardium, myocardium, and pericardium to varying degrees. These guidelines also indicate that rheumatic myocarditis, although “uncommon” in the absence of severe valvular damage, “may contribute” to the genesis of heart failure during rheumatic fever.[8] However, the existence of a specific primary myocardial involvement contributing to the occurrence of heart failure during rheumatic fever is controversial and still needs further studies.

Out of the study population, 20 children (59%) showed evidence of carditis, and 14 children (41%) had ARF without evidence of carditis.

Table 1 shows the characteristics of the study population. From this table, we can see that there is no significant difference between the two groups of children (with and without carditis) regarding the age, sex, CRP, and ESR. The PR interval on ECG was prolonged in the group of patients with carditis (0.17 ± 0.03 s) compared to the group without carditis (0.10 ± 0.05 s). The difference was statistically significant. In addition, the resting pulse rate was significantly higher in the group of patients with carditis (109.3 ± 15.7 beats/min), compared to those without carditis (89.6 ± 19.4 beats/min).

The distribution of valvular lesions in children with carditis is shown in Table 2. Fifteen children had isolated mitral regurgitation (four children grade 1, seven children grade 2, and four children grade 3). Another three patients had both mitral and aortic regurgitation (grade 2). Isolated aortic regurgitation was present in two children (one child grade 1, and one child grade 2). Among the 20 children with carditis, heart failure was present in five children with mitral regurgitation.

Table 3 shows the cTnT level in both groups of children with ARF. The mean level of cTnT in patients with carditis is 0.051 ± 0.01 ng/mL, while the mean level of cTnT in patients without carditis is 0.039 ± 0.02 ng/mL. The difference is not significant (P > 0.05).

Table 4 shows the echocardiographic measurements in the two groups of children with ARF. We can see from this table that the left ventricular ejection fraction is 59.2 ± 7.3% in patients with carditis and 65.6 ± 6.4% in patients without carditis. The difference is not significant (P > 0.05). In addition, there was no significant difference between the two groups regarding the fractional shortening which was 31.8 ± 6.2% in the group of children with carditis and 37.5 ± 6.4% in the children without carditis (P > 0.05).

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.,[13] 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.[14] 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.[15] 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.,[4] 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.