The surgical approach to mitral valve disease must be tailored to the underlying pathophysiologic etiology. The mitral valve can be repaired using a number of different strategies to address the underlying pathophysiology. When repair cannot be done with a reasonable expectation of durability, replacement is indicated either with a bioprosthetic or a mechanical valve.

Mitral stenosis is associated with rheumatic valve disease and, less frequently, malignant carcinoid and systemic lupus. Rheumatic mitral valve disease manifests as a progressive fibrotic process that affects the leaflets and subvalvular apparatus resulting in leaflet thickening, chordal shortening, and leaflet fusion. The normal mitral valve area is 4 to 6 cm². When this decreases to less than 2.5 cm², a pressure gradient develops across the valve resulting in elevated left atrial pressure. Left atrial pressure overload translates into left atrial enlargement, elevated pulmonary venous pressure and pulmonary edema, and in turn pulmonary hypertension as a direct result of pressure transmission and compensatory vasoconstriction, and ultimately to cor pulmonale. Chronic mitral stenosis ultimately results in decreased left ventricular function. Symptoms initially are brought on by exertion as flow across the valve increases, but as the disease progresses, symptoms are present at rest.

Mitral stenosis is a progressive process and when not amenable to repair, replacement is indicated.

Mitral regurgitation is caused by two broad etiologic categories: Structural (degenerative) and functional regurgitation. The Carpentier classification is a useful framework to evaluate the valve.

After careful review of the transesophageal echocardiogram, the mechanism of regurgitation is determined. When ischemic (functional) mitral regurgitation is present the valve is normal and ventricular distortion is the foremost contributor to valve dysfunction and regurgitation. If the left ventricular cause is not reversible by revascularization, then a valve operation is indicated. Both valve repair and replacement are viable options depending on the expectation of durability. If a structural cause is identified, repair should be undertaken to correct the valve and replacement considered if this is not possible. If a left internal mammary artery is not planned, there is a lateral wall motion abnormality or a complex mitral regurgitation jet, and mitral valve repair is less likely to be successful.

Mitral valve replacement is contraindicated in patients who are not surgical candidates based on evaluation of comorbidities or specific ability to tolerate open heart surgery. These patients may be candidates for interventional techniques (e.g., MitraClip) to palliate their mitral regurgitation or balloon valvuloplasty to palliate their mitral stenosis.

Before coming to the operating room, optimal medical management, including occasional in-patient optimization, is useful. Renal function should be maximized and nephrotoxic medications should be discontinued.

Coronary angiography is indicated for patients at risk of coronary artery disease or with evidence of ischemia, decreased systolic function, or with a strong family history of coronary artery disease. Generally, men older than 40 years of age and postmenopausal women warrant coronary evaluation. In patients deemed low risk, coronary artery computed tomography (CT) may be elected. The dominance of the left circumflex artery must be noted as this is important for suture placement.

Right heart catheterization may be performed in select patients preoperatively to assess right heart function and characterize pulmonary hypertension. Nitroprusside responsiveness can be assessed. In patients with pulmonary hypertension that is responsive, inhaled nitric oxide may be useful during weaning from cardiopulmonary bypass postoperatively.

The selection of the valve prosthesis is important. The guidelines set forth by the American Heart Association and American College of Cardiology follow. In light of advancing transcatheter valve technology and valve-in-valve replacement, tissue bioprostheses are favored in the seventh decade of life and beyond and in younger patients with
multiple comorbidities. Low-profile prostheses are indicated in patients with small left ventricles to avoid the struts causing significant left ventricular outflow tract obstruction.