disease and the coronary arteries were not affected. On day 24 of the illness, however, mitral regurgitation with an audible murmur occured suddenly, resulting in the rapid development of severe heart failure. Doppler echocardiography demonstrated prolapse of the posterior leaflet of the mitral valve, which before operation was attributed to rupture of the papillary muscle in the setting of recurrent myocarditis. Rupture of the chordae tendineae was confirmed at the time of operation; however, there was no evidence of valvulitis. The valve was successfully repaired by mitral valvuloplasty with total circular annuloplasty. Results of this case suggest that initial mild mitral regurgitation may be attributable to papillary muscle dysfunction caused by recurrent myocarditis. Severe mitral regurgitation, however, may be caused by chordal rupture that occurs because of functional impairment of the valve apparatus. This is the first report of mitral regurgitation resulting from ruptured chordae tendineae in a patient with Kawasaki disease. Evaluation of similar patients will be necessary to investigate in greater detail mechanisms responsible for chordal rupture. R E F E R E N C E S 1. Takahashi M. Myocarditis in Kawasaki syndrome: a minor villian? Circulation 1989;79:1398-400. 2. Suzuki A, Kamiya T, Tsuchiya K, et al. Tricuspid and mitral regurgitation detected by color flow Doppler in the acute phase of Kawasaki disease. Am J Cardiol 1988;61:386-90. 3. Akagi T, Kato H, Inoue O, Sato N, Imamura K. Valvular heart disease in Kawasaki syndrome: incidence and natural history. Am Heart J 1990;120:366-72. 4. Konishi Y, Tastuta N, Miki S, et al. Mitral insufficiency secondary to mucocutaneous lymph node syndrome: a case report of successful surgical treatment. Jpn Circ J 1978;42: 901-9. 5. Gidding SS, Shulman ST, Ilbawi M, Crussi F, Duffy CE. Mucocutaneous lymph node syndrome (Kawasaki disease): delayed aortic and mitral insufficiency secondary to active valvulitis. J Am Coll Cardiol 1986;7:894-7.