An 11-year-old boy had a sore throat, no cough, tonsillar exudates, and 38.3deg C fever 3 weeks ago, and a throat culture was positive for group A b-hemolytic Streptococcus. On the follow-up examination, the child is afebrile. His pulse is 85/min, respirations are 18/min, and blood pressure is 90/50 mm Hg. On auscultation, a diastolic mitral murmur is audible, and there are diffuse rales over both lungs. Over the next 2 days, he has several episodes of atrial fibrillation accompanied by signs of acute left ventricular failure. Which of the following pathologic changes occurring in this child's heart is most likely to be the cause of the left ventricular failure?
This boy developed acute left ventricular failure, an uncommon but serious complication of acute rheumatic fever. Pancarditis with pericarditis, endocarditis, and myocarditis develop during the acute phase. Myocarditis led to dilation of the ventricle so severe that the mitral valve became incompetent. Rheumatic heart disease is now uncommon, and the number of children that require prophylactic antibiotic therapy to prevent just one case is >10,000. Chronic inflammatory conditions may produce reactive systemic amyloidosis, but this is unlikely to occur given the limited and episodic nature of the streptococcal infection that causes rheumatic heart disease. Fibrinous pericarditis can produce an audible friction rub, but it is not constrictive, and the amount of fluid and fibrin is not great, so no tamponade occurs. Myocardial necrosis associated with myocarditis is patchy, and the ventricle does not rupture to produce tamponade. Fibrosis and fusion of the mitral valve leaflets develop over weeks to months and indicate chronic rheumatic valvulitis. Verrucous vegetations are small and may produce a murmur, but they do not interfere greatly with valve function and do not tend to embolize.
Amyloidosis
Fibrinous pericarditis
Mitral valve fibrosis
Myocarditis
C.V.S