Key result
Acute rheumatic fever was not associated with significant myocardial involvement, as left ventricular ejection fraction (P=0.09) and cardiac troponin I levels (P=0.45) did not differ by carditis status.
Why the study?
Do echocardiography and cardiac troponin I levels show evidence of rheumatic myocarditis in patients with acute rheumatic fever?
Cross-Sectional (n=95)
Do echocardiography and cardiac troponin I levels show evidence of rheumatic myocarditis in patients with acute rheumatic fever?
p-value: p=0.09
Echocardiography and cTnI levels do not support the existence of significant myocardial involvement (myocarditis) during acute rheumatic fever, suggesting congestive heart failure in this setting is driven by severe valve regurgitation.
Echocardiography and troponin I findings support valvular regurgitation over myocarditis as heart failure driver in acute rheumatic fever; hypothesis-generating and needs prospective confirmation.
AIMS: Revised guidelines for diagnosis of rheumatic fever indicate that rheumatic myocarditis may 'contribute' to the genesis of congestive heart failure. Our objective was to assess non-invasively the presence of non-clinical markers of myocardial involvement in acute rheumatic fever. METHODS: Echocardiography and assessment of cardiac troponin I (cTnI) blood levels were systematically performed in 95 consecutive patients with acute rheumatic fever, who were divided into three groups. Group 1: patients without carditis (n=22); group 2: patients with carditis and without congestive heart failure (n=59); group 3: patients with carditis and congestive heart failure (n=14). RESULTS: Left ventricular ejection fraction was normal in all patients and did not differ between groups (group 1: 0.72+/-0.08, group 2: 0.69+/-0.06, and group 3: 0.66+/-0.07, p=0.09). Left ventricular diameters tend to be larger in group 3, but all patients had severe mitral and/or aortic regurgitation. Mean cTnI was 0.077+/-0.017 ng/ml (normal <0.1 ng/ml), did not differ between groups (p=0.45), and only 13 patients (seven with pericardial effusion) had detectable levels (0.2-0.4 ng/ml). CONCLUSIONS: Our study neither detected cTnI elevations nor echocardiographic abnormalities suggesting significant myocardial involvement during rheumatic fever. Congestive heart failure was always associated to severe valve regurgitation.
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J Kamblock (2003) conducted a cross-sectional in Acute rheumatic fever (n=95). Carditis and congestive heart failure vs. No carditis was evaluated on Left ventricular ejection fraction and cardiac troponin I blood levels (p=0.09). Acute rheumatic fever was not associated with significant myocardial involvement, as left ventricular ejection fraction (P=0.09) and cardiac troponin I levels (P=0.45) did not differ by carditis status.
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