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Otto et al 2020 ACC/AHA Guideline for the Management of Valvular Heart Disease

Circulation. 2021;143:e72–e227. DOI: 10.1161/CIR.0000000000000923 February 2, 2021 e119 CLINICAL STATEMENTS AND GUIDELINES

for PMBC or surgical commissurotomy. Second, the presence of severe mitral annular calcification can be quite challenging for the surgeon because of technically difficult in securely attaching the prosthetic valve and placement of the prosthetic valve may result in narrowing of the orifice.17–22 Finally, patients with calcification are often elderly and debilitated, have multiple comorbidities, and are at high surgical risk.1–3 For these reasons, intervention should be delayed until symptoms are severely limiting and cannot be managed with diuresis and heart rate control. Catheter-based therapies for these high–surgical risk patients are being developed and evaluated.23

7 MITRAL REGURGITATION

7.1 Acute MR

Acute MR may be caused by disruption of different parts of the mitral valve apparatus. IE may cause leaflet perforation or chordal rupture. Spontaneous chordal rupture may occur in patients with myxomatous mitral valve disease. Rupture of the papillary muscle occurs in patients who have an acute ST-segment–elevation myocardial infarction, usually associated with an inferior infarction. The acute volume overload on the LV and LA results in pulmonary congestion and low forward cardiac output.1–4 Diagnosis of the presence and etiology of acute MR, along with urgent intervention, may be lifesaving.

7.1.1 Diagnosis of Acute MR

In patients with acute MR, TTE is the initial imaging modality of choice to evaluate LV function, RV function, pulmonary artery pressure, and mechanism of MR. The patient with severe acute MR, which might occur from chordal rupture, usually experiences acute hemodynamic decompensation. The sudden volume overload increases LA and pulmonary venous pressures, leading to pulmonary congestion and hypoxia, whereas decreased blood delivery to the tissues with a concomitant decrease in LV systolic pressure limits the pressure gradient, driving MR to early systole. Thus, the murmur may be short and unimpressive, as may be the color jet of MR by TTE. In the presence of sudden acute and hemodynamic instability after myocardial infarction, with hyperdynamic LV function by TTE and no other cause for the deterioration, TEE can be especially helpful in detecting papillary muscle or chordal rupture or valvular vegetations and annular abscesses that may further accentuate the need for a more urgent surgical approach.1

7.1.2 Medical Therapy

Vasodilator therapy improves hemodynamic compensation in acute MR. The premise for use of vasodilators in acute MR is a reduction in impedance of aortic flow, thereby preferentially guiding flow away from the LV-to-LA pathway, decreasing MR while simultaneously increasing forward output to the LV-to-aortic pathway.1,2 This is usually accomplished by infusion of an easily titratable agent, such as sodium nitroprusside or nicardipine. Use of vasodilators is often limited by systemic hypotension that is exacerbated when peripheral resistance is decreased. Intra-aortic balloon counterpulsation can be helpful to treat acute severe MR. By lowering systolic aortic pressure, intra-aortic balloon counterpulsation decreases LV afterload, increasing forward output while decreasing regurgitant volume. Simultaneously, intra-aortic balloon counterpulsation increases diastolic and mean aortic pressures, thereby supporting the systemic circulation. The use of a percutaneous circulatory assist device may stabilize a patient with acute hemodynamic compromise before the procedure.

7.1.3 Intervention

Prompt mitral valve surgery, preferably mitral repair if possible, is lifesaving in the symptomatic patient with acute severe primary MR. The severity of acute primary MR is variable, and some patients with more moderate amounts of MR may develop compensation as LV dilation allows for lower filling pressure and increased forward cardiac output. However, most patients with acute severe MR require surgical correction for reestablishment of normal hemodynamics and for relief of symptoms.1–5 This is especially true for a complete papillary muscle rupture that causes very severe MR, which is poorly tolerated.

7.2 Chronic Primary MR

7.2.1 Stages of Chronic Primary MR

In assessing the patient with chronic MR, it is important to distinguish between chronic primary (degenerative) MR and chronic secondary (functional) MR, as these 2 conditions have more differences than similarities. Primary MR is a disease of the mitral valve apparatus, and secondary MR is a disease of the ventricle or atria. In chronic primary MR, the pathology of ≥1 of the components of the valve (leaflets, chordae tendineae, papillary muscles, annulus) causes valve incompetence, with systolic regurgitation of blood from the LV to the LA (Table 17). The most common cause of chronic primary MR in high-income countries is mitral valve prolapse, which has a wide spectrum of etiology and presentation. Younger populations present with severe myxomatous degeneration with gross redundancy of both anterior and posterior leaflets and the chordal apparatus (Barlow’s valve). A subset of these patients will present with ventricular arrhythmias, mitral annular disjunction, and LV dilation. Alternatively, older populations present with fibroelastic deficiency disease, in which lack of connective tissue leads to chordal rupture. The differentiation between these 2 etiologies may have implications for operative intervention. Other

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