T-cells that are responsive to the streptococcal M-protein infiltrate the valve through the valvular endothelium, activated by the binding of antistreptococcal carbohydrates with release or tumor necrosis factor (TNF) and interleukins.[5] A study reported that the increased expression of Th17 cell-associated cytokines might play an important role in the pathogenesis and development of rheumatic heart disease.[6] The acute involvement of the heart in rheumatic fever gives rise to pancarditis, with inflammation of the myocardium, pericardium, and endocardium. Carditis occurs in approximately 40-50% of patients on the first attack; however, the severity of acute carditis has been questioned.[7] Pericarditis occurs in 5-10% of patients with rheumatic fever; isolated myocarditis is rare.