Abstract 127

The myocarditis that develops in acute rheumatic fever (ARF) is manifested by Aschoff bodies that are primarily made up of damaged collagen and certain other components of interstitial tissue with only a small numbers of damaged cardiac muscle cells. During ARF, many anti-heart antibodies like anti-myosin and anti-tropomyosin are found. The exact roles these antibodies play in rheumatic heart disease are not known. It has been speculated that their presence may indeed reflect myocardial injury. The cross-reactive streptococcal M6 protein has a strong homology to tropomyosin and myosin. Cardiac troponin I (cTnI) is a cytoskeleton protein that is associated with the actin filament and is responsible for calcium interaction with the contractile apparatus. It is a sensitive and a specific marker for myocardial injury. We measured cTnI to determine the nature of cardiac injury during ARF. METHODS: Sera of 9 patients who fulfilled the revised Jones criteria were obtained. Carditis was present in 4/9 patients. Sera of 9 patients with Scarlet fever (SF) served as age matched control. All 18 patients had either throat cultures positive for group A streptococcus or elevated antistreptolysin O titer. Sera were collected in mean of 1, 5, 12 weeks in ARF and 1, 3, 6 weeks in SF patients from the onset of illness. Serum levels of cTnI were measured by Microparticle Enzyme Immunoassay (Abbot, AxSYM, IL, USA). Normal values are ≤ 0.4 ng/ml for healthy and ≤ 2.3 ng/ml for non-acute myocardial infarct patients. RESULTS: All serum values were ≤ 0.4 ng/ml, except for one SF patient in the first week with 1.1 ng/ml. CONCLUSION: None of the ARF patients had elevated levels of cTnI. This may be because there is more endocardial involvement with valvulitis in ARF rather than myocardial injury.