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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 e123 CLINICAL STATEMENTS AND GUIDELINES

patient with what appears to be less than severe MR suggests a noncardiac cause for the symptoms. Hemodynamic evaluation can be especially helpful in patients with concomitant lung disease. Normal LA (or pulmonary artery wedge) pressure and a large transpulmonary gradient suggest pulmonary hypertension that is attributable to lung disease rather than mitral valve disease. Left ventriculography may also be of diagnostic benefit. Whereas echocardiographic-Doppler interrogation of the mitral valve measures flow velocity, ventriculography uses the density of contrast to determine the amount of blood flow from the LV to the LA. Although only semiquantitative, a carefully performed ventriculogram can help in quantifying MR severity. Additional hemodynamic interventions, such as exercise or leg raising, may be helpful when the resting information is equivocal.

7.2.2.5 Diagnostic Testing: Exercise Testing

Recommendation for Diagnostic Testing: Exercise Testing for Chronic Primary MR Referenced studies that support the recommendation are summarized in Online Data Supplement 28. COR LOE Recommendation

2a B-NR 1.  In patients with primary MR (Stages B and C) and symptoms that might be attributable to MR, hemodynamic exercise testing using Doppler echocardiography or cardiac catheterization or cardiopulmonary exercise testing is reasonable.1–4

Synopsis

In a subset of apparently asymptomatic patients with severe primary MR, exercise testing with hemodynamics can provide additional diagnostic and prognostic information.

Recommendation-Specific Supportive Text

1.	 The onset of symptoms represents a key development in severe MR. However, some patients may not recognize their symptoms, may deny them, or may alter their lifestyle to remain asymptomatic. A formal treadmill exercise test can establish true exercise tolerance and can also form the baseline for future symptom assessment. Additional information about a cardiac or noncardiac limitation can be obtained from oxygen consumption measurements during exercise. When patients do complain of symptoms, they usually complain of dyspnea with exertion, yet noninvasive evaluation is usually made at rest. Exercise echocardiography or exercise invasive hemodynamics may add additional prognostic value beyond conventional exercise treadmill testing in patients with asymptomatic moderate or severe chronic primary MR.1–4 MR may worsen during exercise, or filling pressures may become markedly abnormal, helping to demonstrate MR as the cause of the patient’s dyspnea.1–4 7.2.3 Medical Therapy

Recommendations for Medical Therapy for Chronic Primary MR Referenced studies that support the recommendations are summarized in Online Data Supplement 29. COR LOE Recommendations

2a B-NR 1.  In symptomatic or asymptomatic patients with severe primary MR and LV systolic dysfunction (Stages C2 and D) in whom surgery is not possible or must be delayed, GDMT for systolic dysfunction is reasonable.1–3

3: No Benefit B-NR 2.  In asymptomatic patients with primary MR and normal LV systolic function (Stages B and C1), vasodilator therapy is not indicated if the patient is normotensive.4–8

Synopsis

In patients with primary MR, there is no convincing evidence that vasodilator therapy reduces MR severity. However, GDMT for LV systolic dysfunction or systemic hypertension should be implemented as in any patient with these conditions.

Recommendation-Specific Supportive Text

1.	 Patients with MR and LV dysfunction experience myocardial damage and HF. With onset of LV systolic dysfunction, surgery is usually indicated. However, in those patients in whom surgery (or transcatheter repair) is not performed or will be delayed, medical therapy for systolic dysfunction may be helpful to treat the LV dysfunction alone. Although data specific to patients with MR with LV dysfunction are sparse, treatment of such patients would consist of the standard regimen for HF, including beta-adrenergic blockade, ACE inhibitors or ARBs, and possibly aldosterone antagonists.1–3 Perhaps the best data exist for the use of beta blockers,1 which reverse LV dysfunction in experimental MR.2 Patients who are receiving beta blockers may have better surgical outcomes and delayed onset of LV dysfunction as compared with those not taking these medications.3 ACE inhibition has not been effective in experimental MR with LV dysfunction. Because aldosterone antagonism is thought to work in part by inhibiting fibrosis, its role in MR, where little fibrosis occurs, is unclear. 2.	 Because vasodilator therapy appears to be effective in acute severe symptomatic MR, it seems reasonable to attempt afterload reduction in chronic asymptomatic MR with normal LV function in an effort to forestall the need for surgery. However, the results from the limited number of trials addressing this therapy have been disappointing, demonstrating little or no clinically important benefit.4–8 Conversely, because vasodilators decrease LV size and mitral closing force, they may increase

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