Mitral stenosis is characterized by obstruction to LV inflow at the level of mitral valve due to structural abnormality of the mitral valve apparatus. The most common cause of mitral stenosis is rheumatic fever. Other, less common etiologies of mitral stenosis include malignant carcinoid disease, systemic lupus erythematosus, rheumatoid arthritis, mucopolysaccharidoses of the Hunter-Hurler phenotype, Fabry disease, Whipple disease, and methysergide therapy. Congenital mitral stenosis can also occur.
Symptoms of mitral stenosis usually manifest during the third or fourth decade of life and nearly half of patients do not recall a history of acute rheumatic fever. Patients are generally asymptomatic at rest during the early stage of the disease. However, factors that increase heart rate, such as fever, severe anemia, thyrotoxicosis, exercise, excitement, pregnancy, and atrial fibrillation, may result in dyspnea. Mitral facies (pinkish-purple patches on the cheeks) indicate chronic severe mitral stenosis leading to reduced cardiac output and vasoconstriction. Jugular vein distention may be seen.
Echocardiography is the most specific and sensitive method of diagnosing and quantifying the severity of mitral stenosis. With echocardiography, the size of the mitral valve orifice can be precisely quantified. Important information about the ventricular and atrial chamber sizes, presence of a left atrial thrombus, measurement of transvalvular gradient, and pulmonary arterial pressure can also be obtained. TEE provides better-quality images than TTE and is more accurate in assessing the anatomical features of the valve and the presence of left atrial appendage thrombus.
The goal of medical treatment for mitral stenosis is to reduce recurrence of rheumatic fever, provide prophylaxis for infective endocarditis, reduce symptoms of pulmonary congestion (eg, orthopnea, paroxysmal nocturnal dyspnea), control the ventricular rate if atrial fibrillation is present, and prevent thromboembolic complications.
In patients with mild mitral stenosis and recent-onset (< 6 mo) atrial fibrillation, conversion to sinus rhythm can be accomplished with pharmacologic agents or electrical cardioversion. In this circumstance, anticoagulation therapy should be given for at least 3 weeks before cardioversion. Alternatively, TEE can be performed before cardioversion to exclude the presence of left atrial thrombus. Patients who are successfully converted to sinus rhythm should receive long-term anticoagulation and antiarrhythmic drugs. Warfarin is indicated for anticoagulation. The novel anticoagulants dabigatran and rivaroxaban are approved for nonvalvular atrial fibrillation.
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Cite this: Yasmine S. Ali. Fast Five Quiz: Heart Valve Disease - Medscape - Apr 22, 2020.