A male aged 35 years with a history of cyanosis from early childhood was referred for evaluation of low grade fever and worsening breathlessness on exertion. There was no history of a recent dental or surgical procedure. General physical examination revealed a moderately nourished individual with central cyanosis and grade IV clubbing. The jugular venous pulse was elevated. The pulse was regular with a rate of 100 beats per minute and a collapsing character. The blood pressure was 120/60 mmHg. On precordial examination the first heart sound was palpable. Auscultation revealed a loud first heart sound, single second heart sound and an apical opening snap. Additional findings included ejection systolic and early diastolic murmurs at the left sternal border and a mid-diastolic murmur with pre-systolic accentuation at the apex. The lungs were clear. Abdominal examination revealed a tender enlarged liver. There was no enlarged spleen. Pulse oximetry showed a room air oxygen saturation of 78%. Chest X-ray revealed enlarged heart, pulmonary oligemia and no evidence of pulmonary venous hypertension. Electrocardiogram revealed sinus rhythm, normal PR interval, right axis deviation, left atrial enlargement and right ventricular hypertrophy. An echocardiogram revealed a large malaligned ventricular septal defect with 60% aortic override. The aortic valve was trileaflet with a vegetation on the right coronary cusp. The mitral valve was thickened. Diastolic doming of the anterior leaflet, fixed posterior mitral leaflet with paradoxical motion and two well-formed papillary muscles were noted. There was no aortic stenosis and grade II aortic regurgitation was noted in addition to severe infundibular and annular stenosis with confluent branch pulmonary arteries. Non calcific severe mitral stenosis with commissural fusion and thickening of the sub-valvular apparatus was noted. The mitral valve area was 1.1 cm2. There was no mitral regurgitation. The peak and mean gradients across the valve were 36 and 21 mmHg respectively and the echocardiographic mitral valve score was 6/16. Blood cultures revealed Streptococcus viridans as the infecting organism. The serum antistreptolysin O titers were within reference range, C-reactive protein was positive and erythrocyte sedimentation rate was elevated. A final diagnosis of TF, subacute bacterial endocarditis of the aortic valve and severe mitral stenosis, probably of rheumatic etiology, was considered. Endocarditis with aortic regurgitation added to the hemodynamic burden and the patient succumbed to infective complications during the course of stabilization.