A 62-year-old man with past medical history significant for childhood rheumatic fever presents with chronic dyspnea that has progressed over the past 6 months. He can now only walk 2 to 3 blocks before becoming short of breath. An echocardiogram shows normal left ventricular function, a moderately calcified mitral valve with thickening of the leaflets, and subvalvular apparatus (Figure 22-1). The mean gradient across the mitral valve is 15 mm Hg. What should be done next?

Mitral stenosis (MS) is a narrowing of the mitral valve (MV) orifice, resulting in impairment of left ventricle filling in diastole. Worldwide, it is most commonly caused by rheumatic heart disease. Other causes include severe calcification of the mitral annulus, infective endocarditis, systemic lupus erythematosus, rheumatoid arthritis, and carcinoid heart disease. The incidence of rheumatic heart disease has steeply declined during the past 4 decades in the United States, but it still remains a major cause of cardiovascular disease in the developing countries. It is estimated that 15.6 million people suffer from rheumatic heart disease worldwide, with approximately 282,000 new cases and 233,000 related deaths each year.¹

The treatment for MS is often mitral commissurotomy, resulting in a reduction in the obstruction, a decrease in left atrial pressure, and improvement in patient symptoms. Surgical mitral commissurotomy was first performed in the 1920s and was accepted as an effective clinical procedure for treating severe MS in symptomatic patients. Percutaneous balloon mitral valvuloplasty (PBMV) has replaced surgical mitral commissurotomy as the preferred treatment of rheumatic MS in appropriate patients.²

The MV apparatus consists of the mitral annulus, 2 leaflets, chordae tendineae, and papillary muscles. The 2 leaflets of the MV are referred to as the anterior and posterior leaflets or aortic and mural leaflets, respectively. The mural (posterior) leaflet is narrow and has indentations or clefts that form 3 scallops. Carpentier’s nomenclature³ describes the most lateral segment as P1, the central segment as P2, and the most medial segment as P3. The aortic (anterior) leaflet is larger and also divided into 3 regions labeled A1, A2, and A3 corresponding to the adjacent regions of the mural leaflet.

The mitral annulus is a fibrous junctional zone separating the left atrium and left ventricle that gives attachment to the MV. It is a pliable oval structure that undergoes both translational change (height from base to apex) and contraction during the cardiac cycle. The anterior region of the annulus is mostly fibrous and less prone to dilatation, while the remaining two thirds of the annulus is mainly muscular. The posterior region is often more prone to dilatation and calcification.

Chordae tendineae are fan-shaped, chord-like structures running from the papillary muscles to the leaflets. Primary chords attach to the free edge of the rough zone of both leaflets, while secondary chords attach to the ventricular surface in the region of the rough zone. The tertiary chords are found only in the mural (posterior) leaflet and attach directly to the ventricular wall.

The 2 papillary muscle bundles are generally described as anterolateral and posteromedial. The anterolateral papillary muscle attaches to the border of the lateral and inferolateral walls of the left ventricle, and the posteromedial papillary muscles attach to the inferior wall of the left ventricle. In the majority of adults, the papillary muscles can have up to 3 heads.⁴

The American Heart Association (AHA)/American College of Cardiology (ACC) classification of MS is based on symptoms and is divided into 4 stages. Stage A includes patients with mild valve doming during diastole and considered at risk of MS. Stage B is more advanced (progressive) rheumatic valve changes such as commissural fusion and moderate diastolic doming of the MV leaflets. Stage C is asymptomatic severe MS, defined by an MV area (MVA) of 1.5 cm² or less (normal valve area, 4-5 cm²). Stage D is symptomatic severe MS.⁵

Classification of MS severity by echocardiography criteria is determined by MVA, mean MV gradient, and associated severity of pulmonary hypertension (Table 22-1).⁶

The normal MV orifice is 4 to 5 cm². In early diastole, there is a negligible gradient between left atrium and left ventricle, which equalizes quickly so that pressure in the 2 chambers is equal for most of the filling.⁷ In MS, there is obstruction to flow of blood from left atrium to left ventricle, resulting in pressure gradient between the 2 chambers. This pressure results in increasing left atrial pressure that can eventually lead to left atrial enlargement and pulmonary hypertension. When pulmonary hypertension develops, surgical risk is increased. PBMV can produce excellent early hemodynamic improvement and is associated with a lower rate of residual stenosis requiring less repeat interventions.⁸ In these patients, immediate procedural result is the main determinant of long-term outcome. Although MVA might decrease over time after successful PBMV, the mitral regurgitation tends to remains unchanged.⁹ ACC/AHA indications for MV intervention for rheumatic MS are based on severity of MS, presence of symptoms, surgical and percutaneous procedure risk, and pulmonary artery pressures (Table 22-2).¹⁰