Myocardial dysfunction in rheumatic carditis--does it really exist?

Acute rheumatic fever (ARF) continues to affect millions of children in developing countries. Aim of the present study was to evaluate the role of myocardial dysfunction in the genesis of heart failure in patients with rheumatic carditis. There are limited studies on this subject.

In this prospective study, 108 consecutive patients of ARF were evaluated by echocardiography and assay of cardiac troponin I blood levels. The patients were divided into three groups. Group A (n = 30): patients with no evidence of carditis; Group B (n = 45): patients with first attack of carditis; and group C (n = 33): patients with recurrent attacks of carditis. Left ventricular dimensions tended to be larger in Group B and C patients. Left ventricular ejection fraction did not differ between the groups (Group A: 63 +/- 8.1%, Group B: 58 +/- 7.9%, Group C: 61.2 +/- 9%, p = ns). Heart failure was present in 37.7% patients of Group B, and in 60.6% patients of Group C (p = < 0.05). Ejection fraction was normal in majority of heart failure patients (75.7%). It was reduced in 29.4% of patients in Group B and in 20% of Group C patients with heart failure (p = ns). All patients with low ejection fraction had hemodynamically significant regurgitant valvular lesions. Mean cardiac troponin I values, an index of myocardial damage, did not differ between the three groups (Group A: 0.062 +/- 0.027 ng/ml, Group B: 0.068 +/- 0.019 ng/ml, Group C: 0.071 +/- 0.031 ng/ml, p = ns).

The present study did not demonstrate any echocardiographic abnormalities or cardiac troponin I elevation suggesting significant myocardial involvement during acute rheumatic fever. This lends credence to the view that myocardial involvement does not play any significant role in the genesis of heart failure in patients with rheumatic carditis.