A 32-year-old woman from rural Bihar with a history of acute rheumatic fever (ARF) at age 10 presents with NYHA class III dyspnoea, haemoptysis, and atrial fibrillation. Transthoracic echocardiography shows a mitral valve area of 0.9 cm² with a mean transmitral gradient of 14 mmHg. At surgical pathology, the excised valve demonstrates the characteristic appearance shown in the diagram. The structure marked **A** represents the fish-mouth shaped stenotic mitral orifice. Which of the following best explains the pathophysiological consequence of this morphological change in the context of her clinical presentation?
A. Marked reduction in mitral valve area leading to increased transmitral pressure gradient, left atrial hypertension, and pulmonary venous congestion with secondary atrial fibrillation
B. Prolapse of the anterior mitral leaflet due to rupture of the chordae tendineae, resulting in acute mitral regurgitation and acute pulmonary oedema
C. Perforation of the mitral leaflets due to infective endocarditis, leading to acute haemodynamic decompensation
D. Rupture of the papillary muscles with subsequent acute mitral regurgitation and cardiogenic shock
Explanation
Why option 1 is right
The fish-mouth shaped stenotic mitral orifice (structure A) represents severe mitral stenosis resulting from rheumatic carditis. This morphological narrowing of the mitral valve orifice to <1 cm² creates a fixed obstruction to left ventricular filling, causing a marked increase in transmitral pressure gradient (14 mmHg in this case). The resulting left atrial hypertension is transmitted retrograde to the pulmonary vasculature, causing pulmonary venous congestion, pulmonary hypertension (65 mmHg systolic in this patient), and secondary atrial fibrillation—all of which are evident in this patient's clinical presentation. This is the defining pathophysiology of mitral stenosis as described in Robbins and Cotran.
Why each distractor is wrong
Option 2: Mitral valve prolapse with chordal rupture causes acute mitral regurgitation, not stenosis. The diagram shows a stenotic orifice with fused commissures and shortened chordae (structure C), not ruptured chordae. The clinical picture is chronic stenosis, not acute regurgitation.
Option 3: Papillary muscle rupture is a complication of acute myocardial infarction, not rheumatic heart disease. The pathology here shows fibrosis and calcification from healed rheumatic carditis, not acute necrosis. There is no history of MI.
Option 4: Infective endocarditis can cause valve perforation, but the histology explicitly confirms "diffuse fibrosis, neovascularisation and dystrophic calcification consistent with healed rheumatic carditis"—not acute infection. The clinical course (5-year progressive history) is also inconsistent with acute endocarditis.
High-YieldNEET PG
Rheumatic mitral stenosis creates a fish-mouth orifice due to commissural fusion and leaflet thickening; the resulting obstruction causes left atrial hypertension, pulmonary congestion, and secondary atrial fibrillation—the classic triad of mitral stenosis sequelae.
Robbins and Cotran Pathologic Basis of Disease, 10th ed., Ch. The Heart
Practice similar questions
Sign up free to access AI-powered MCQ practice with detailed explanations and adaptive learning.
