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Chronic primary mitral regurgitation: General management

Chronic primary mitral regurgitation: General management
Literature review current through: Jan 2024.
This topic last updated: Nov 06, 2023.

INTRODUCTION — Primary mitral regurgitation (MR) is caused by a primary abnormality of one or more components of the valve apparatus (leaflets, chordae tendineae, papillary muscles, annulus), in contrast to secondary MR, which is caused by alterations in left ventricular (LV) and/or atrial geometry and function (table 1). Identification of the cause and type (primary or secondary) of MR is required for appropriate management of MR as well as any associated conditions.

Mitral valve prolapse is the most common cause of chronic primary MR in resource-abundant countries. Rheumatic heart disease is a prominent cause of primary MR in resource-limited countries (particularly during the first two decades of life), but it is an uncommon cause of MR in resource-abundant countries. (See "Mitral valve prolapse: Clinical manifestations and diagnosis" and "Clinical manifestations and diagnosis of rheumatic heart disease", section on 'Mitral regurgitation'.)

Other causes of primary MR are discussed separately. (See "Clinical manifestations and diagnosis of chronic mitral regurgitation", section on 'Etiology'.)

This topic will discuss general management for patients with chronic primary MR. Indications for intervention are discussed separately. (See "Chronic primary mitral regurgitation: Indications for intervention".)

The pathophysiology, natural history, diagnosis, and evaluation of chronic MR, and the management of chronic secondary MR, are presented elsewhere. (See "Pathophysiology and natural history of chronic mitral regurgitation" and "Natural history of chronic mitral regurgitation caused by mitral valve prolapse and flail mitral leaflet" and "Clinical manifestations and diagnosis of chronic mitral regurgitation" and "Chronic secondary mitral regurgitation: General management and prognosis".)

MONITORING — Following initial evaluation of chronic primary MR, including staging and identification of its cause, serial monitoring and restaging is required as clinical findings evolve. Staging is based upon symptoms, valve anatomy, valve hemodynamics (severity of MR), and hemodynamic consequences of MR as reflected by left atrial size, LV size and function, and pulmonary artery pressure (table 2). MR severity should be formally quantified, as color Doppler appearance may be misleading. Concurrent valve disease, including tricuspid valve prolapse and tricuspid regurgitation, should also be monitored. (See "Etiology, clinical features, and evaluation of tricuspid regurgitation" and "Echocardiographic evaluation of the tricuspid valve".)

A goal of monitoring is to identify changes (which can occur with or without reported symptoms) for optimal timing of intervention.

We agree with the following recommendations for clinical and transthoracic echocardiographic (TTE) monitoring in asymptomatic patients with primary mitral valve disease and chronic MR in the 2020 American College of Cardiology/American Heart Association guidelines [1]:

Annual visits – Follow-up for patients with primary mitral valve disease and moderate to severe MR includes at least an annual history and physical examination. For individuals with mild MR, frequency of follow-up is based on the type and severity of mitral leaflet disease.

Echocardiography – Serial TTE is performed to assess the severity of valve disease, LV size, LV ejection fraction (LVEF), and LV end-systolic dimension. TTE interpretation should include careful comparison with prior TTE studies. The frequency of recommended follow-up varies with the severity of MR:

Mild MR – For patients with primary mitral valve disease and mild MR and no evidence of LV enlargement, LV dysfunction, or pulmonary hypertension, echocardiography every three to five years is appropriate.

Moderate MR – Patients with primary mitral valve disease and moderate MR should undergo echocardiography every one to two years.

Severe MR – Patients with severe MR should be seen every 6 to 12 months (sooner if symptoms occur) with a repeat TTE. The six-month interval is preferred if stability has not been documented, if there is evidence of progressive LV dilation, reduction in LV systolic function, or increase in pulmonary pressure, or if measurements are approaching values used in an indication for mitral valve surgery.

While LV systolic function is most commonly assessed by LVEF, global longitudinal strain may be a helpful adjunct in patients with asymptomatic severe MR, as strain is a more sensitive indicator of LV systolic dysfunction in patients with MR, although not yet included in guidelines for timing of intervention [1]. (See "Tests to evaluate left ventricular systolic function", section on 'Other measures'.)

In addition, TTE should be performed in patients with MR with a change in symptoms (eg, dyspnea or reduced exercise tolerance) or signs, or new onset of atrial fibrillation [1].

ADJUNCTIVE TESTING

Natriuretic peptide levels — Natriuretic peptide (B-type natriuretic peptide [BNP] or N-terminal pro-BNP [NT-proBNP]) level measurement is not routinely required but may be helpful in settings in which clinical data are conflicting or uncertain [1,2]. As an example, natriuretic peptide testing may be a helpful adjunct in asymptomatic patients with severe MR.

Studies suggest that serum BNP may have prognostic value in patients with chronic primary MR [3]. As an example, a report evaluated 124 patients with chronic MR, 94 with mitral valve prolapse; almost all patients were asymptomatic or had only a mild limitation in physical activity and the mean LVEF was 69 percent [4]. Serum BNP values ≥31 pg/mL predicted lower five-year survival (72 versus 96 percent). BNP was independently predictive of mortality with adjustment for age, sex, functional class, MR severity, and LVEF. Thus, BNP level reflected the clinical consequences of MR rather than the severity of MR. Similarly, a study of 135 asymptomatic patients with moderate to severe primary MR and preserved LVEF found that BNP was an independent predictor of cardiac events [5]. Observational studies have also suggested that patients with MR with elevated BNP or NT-proBNP levels may face increased risk of adverse outcomes following mitral valve surgery [6,7].

Transesophageal echocardiography — Transesophageal echocardiography (TEE) is not indicated for follow-up of most patients. TEE is indicated when noninvasive imaging fails to determine the severity or cause of MR [1]. TEE also has a role in preoperative and intraoperative evaluation for mitral valve surgery to assess valve anatomy and help guide repair.

Exercise testing — Hemodynamic exercise testing (with Doppler echocardiography, cardiac catheterization, or cardiopulmonary exercise testing) is not required for monitoring of most patients with chronic primary MR but may be helpful in certain settings [1]:

If it is unclear whether there is any exercise limitation by clinical history, exercise stress testing may add objective evidence about symptoms and a change in exercise tolerance.

For patients with symptoms that are greater than expected for the degree of MR at rest or for patients with borderline echocardiographic findings [8], exercise echocardiography including measurement of MR severity and pulmonary artery pressure during exercise may be helpful. Results of exercise echocardiography may have prognostic value in asymptomatic patients with moderate or severe chronic primary MR [9-11].

Cardiovascular magnetic resonance imaging — Cardiovascular magnetic resonance imaging is not routinely indicated for monitoring of MR but is indicated when echocardiography is not adequate to assess MR severity or left and right ventricular volumes and function [1]. (See "Clinical utility of cardiovascular magnetic resonance imaging", section on 'Regurgitant valve disease'.)

Coronary angiography — Many patients requiring surgery for chronic primary MR also have significant coronary artery disease. The prevalence of coronary artery disease (CAD) was assessed by a study of 722 patients (67 percent men, mean age 61 years) with primary MR who did not have a history of myocardial infarction, ischemic electrocardiographic changes, or angina [12]. Routine coronary angiography identified obstructive (≥50 percent) coronary lesions in one or more major vessels in 19 percent of patients.

Coronary angiography is recommended for hemodynamically stable patients who are planning to undergo valve surgery and have or are suspected of having CAD [1,2]. Individuals with coronary risk factors include men >40 years of age and postmenopausal women. For patients with low to intermediate pretest probability of CAD, contrast-enhanced coronary computed tomographic angiography is an option to exclude the presence of significant obstructive CAD [1,2]. (See "Cardiac imaging with computed tomography and magnetic resonance in the adult".)

Obstructive coronary lesions are generally revascularized at the time of mitral valve surgery, since concurrent bypass surgery typically adds little morbidity or mortality to the procedure. (See "Chronic primary mitral regurgitation: Choice of intervention", section on 'Concurrent procedures'.)

GENERAL MANAGEMENT — There is a limited role for medical management in patients with chronic primary MR, since valve intervention is required to address the primary process. The approach to management presented here is in general agreement with 2020 American College of Cardiology/American Heart Association (ACC/AHA) valve guidelines and 2021 European Society of Cardiology valve guidelines [1,2].

No routine vasodilator therapy — Given lack of evidence of efficacy, vasodilators are not indicated for use in normotensive asymptomatic patients with chronic primary MR and normal systolic function [1,2].

Treatment of heart failure — Symptomatic patients with chronic primary MR (stage D) and LVEF <60 percent who are awaiting valve surgery or who are not candidates for valve surgery are treated with standard evidence-based medical therapy for heart failure with reduced ejection fraction (HFrEF), which is also suggested for patients with heart failure with mildly reduced ejection fraction (HFmrEF; LVEF 41 to 49 percent). (See "Overview of the management of heart failure with reduced ejection fraction in adults" and "Primary pharmacologic therapy for heart failure with reduced ejection fraction" and "Secondary pharmacologic therapy for heart failure with reduced ejection fraction" and "Treatment and prognosis of heart failure with mildly reduced ejection fraction" and "Treatment and prognosis of heart failure with mildly reduced ejection fraction", section on 'Therapy for mildly reduced ejection fraction'.)

Medical therapy for symptomatic MR with LVEF <60 percent is largely based on evidence in patients with HFrEF or HFmrEF [1]. Although LVEF values in the range of 50 to 60 percent are considered to be in a low-normal range in the general population without MR, patients with chronic primary MR and a low-normal LVEF have depressed LV intrinsic contractility, which is associated with suboptimal outcomes after otherwise successful corrective mitral surgery [13,14]. Scant evidence is available on HF therapy in patients with primary MR. Limited evidence on beta blocker therapy in patients with MR suggests a possible benefit. A preliminary trial randomly assigned 38 asymptomatic adults with moderate to severe MR to placebo or beta-1 blockade (with extended-release metoprolol) for two years [15]. LVEF and LV early diastolic filling rate improved with beta blocker therapy. A retrospective study of 895 patients with severe MR and normal LVEF found that beta blocker use was associated with a lower mortality rate [16], but this finding is not sufficient to establish the efficacy of beta blocker therapy.

Intervention — Management of primary MR is directed towards optimal timing of intervention with surgical mitral valve repair or replacement, as discussed separately. Transcatheter mitral valve repair is an option for selected severely symptomatic patients who are not surgical candidates. (See "Chronic primary mitral regurgitation: Indications for intervention".)

Endocarditis prophylaxis — Antibiotic prophylaxis is not indicated for patients with native mitral valve disease (in the absence of history of infective endocarditis) undergoing dental or oral procedures [1,2]. (See "Prevention of endocarditis: Antibiotic prophylaxis and other measures" and "Mitral valve prolapse: Overview of complications and their management", section on 'Infective endocarditis'.)

Exercise — Exercise has a variable effect on the regurgitant fraction in patients with chronic MR [17]. The reduction in systemic vascular resistance may result in no change or a mild reduction in the regurgitant fraction. On the other hand, an elevation in blood pressure or heart rate can lead to an increase in regurgitant volume and pulmonary capillary pressure.

We agree with the following recommendations for athletes with MR modified from the 2015 AHA/ACC scientific statement for competitive athletes with valvular heart disease [17] (figure 1):

Athletes with MR should be evaluated annually by physical examination, echocardiography, and exercise stress testing to determine whether sport participation can continue.

Exercise testing to at least the level of activity achieved in competition and training is useful to confirm asymptomatic status in patients with MR.

Estimation of pulmonary artery systolic pressure during exercise by Doppler echocardiography can be helpful, particularly in athletes with significant MR. This evaluation is used to determine whether sport participation can continue.

Athletes in sinus rhythm with mild to moderate MR, normal LV function, and normal pulmonary artery pressure can participate in all competitive sports.

It is reasonable for athletes with moderate MR in sinus rhythm with normal LV systolic function at rest (stage B) and mild LV enlargement (compatible with that resulting solely from athletic training; LV end-diastolic dimension [LVEDD] <60 mm or <35.3 mm/m2 in males or <40 mm/m2 in females) to participate in all competitive sports.

Athletes with asymptomatic severe MR in sinus rhythm with normal LV systolic function at rest and mild LV enlargement (compatible with that resulting solely from athletic training; LVEDD <60 mm or <35.3 mm/m2 in males or <40 mm/m2 in females [stage C1]) can participate in low-intensity and some moderate-intensity sports (classes IA, IIA, and IB).

Athletes with MR and definite LV enlargement (LVEDD ≥65 mm or ≥35.3 mm/m2 in males or ≥40 mm/m2 in females), pulmonary hypertension, or any degree of LV systolic dysfunction at rest (LVEF ≤60 percent or LVEDD ≥40 mm [stage C2]) should not participate in any competitive sports, with the possible exception of low-intensity class IA sports.

Athletes with a history of atrial fibrillation who are receiving long-term anticoagulation should not engage in sports involving risk of bodily contact (table 3).

Exercise following mitral valve replacement or repair is discussed separately. (See "Overview of the management of patients with prosthetic heart valves", section on 'Exercise recommendations'.)

CAUSE-SPECIFIC MANAGEMENT — Additional management considerations vary depending upon the cause of primary MR.

Management for mitral valve prolapse — Management of mitral valve prolapse includes assessment and management of concurrent tricuspid valve prolapse and arrhythmic risk, as discussed separately. (See "Mitral valve prolapse: Overview of complications and their management".)

Management of rheumatic heart disease — Management of rheumatic heart disease is discussed separately. For patients with rheumatic heart disease, long-term prophylaxis against rheumatic fever is recommended according to standard guidelines. (See "Acute rheumatic fever: Treatment and prevention", section on 'Secondary prevention (antibiotic prophylaxis)'.)

CONCURRENT CONDITIONS — Patients with primary MR frequently have concurrent conditions that require treatment.

Treatment of hypertension — General recommendations for cardiovascular risk assessment and modification apply to patients with primary MR, including identification and management of hypertension, if present. Patients with chronic primary MR and concomitant hypertension should receive standard antihypertensive therapy to reduce the morbidity and mortality associated with hypertension [1]. (See "Atherosclerotic cardiovascular disease risk assessment for primary prevention in adults: Our approach".)

Conditions requiring concurrent intervention — Some conditions that occur commonly in patients with primary MR may require intervention at the time of mitral valve intervention. These include coronary artery disease, atrial fibrillation, and concurrent valve disease (eg, tricuspid regurgitation). These issues are discussed separately. (See "Surgical procedures for severe chronic mitral regurgitation" and "Management and prognosis of tricuspid regurgitation" and "Atrial fibrillation: Surgical ablation".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cardiac valve disease".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topic (see "Patient education: Mitral regurgitation (The Basics)")

Beyond the Basics topic (see "Patient education: Mitral regurgitation (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Definition – Primary mitral regurgitation (MR) is caused by a primary abnormality of one or more components of the valve apparatus (leaflets, chordae tendineae, papillary muscles, annulus). Mitral valve prolapse is the most common cause of chronic primary MR in resource-abundant countries. Rheumatic heart disease is a prominent cause of primary MR in resource-limited countries (particularly during the first two decades of life), but it is an uncommon cause of MR in resource-abundant countries. (See "Mitral valve prolapse: Clinical manifestations and diagnosis" and "Clinical manifestations and diagnosis of rheumatic heart disease", section on 'Mitral regurgitation'.)

Monitoring – Patients with significant mitral valve disease and chronic primary MR require routine clinical and echocardiographic monitoring. Valve disease stage is based upon symptoms, valve anatomy, valve hemodynamics (severity of MR), and hemodynamic consequences of MR as reflected by left atrial size, left ventricular (LV) size and function, and pulmonary artery pressure (table 2). MR severity should be quantified when possible because color Doppler appearance often is misleading. The frequency of transthoracic echocardiographic (TTE) monitoring in patients with MR varies depending upon clinical findings and the severity of MR. (See 'Monitoring' above.)

Adjunctive testing – When the severity of MR is uncertain by TTE, transesophageal echocardiography or cardiovascular magnetic resonance imaging may be helpful. (See 'Adjunctive testing' above.)

Treatment of heart failure – Symptomatic patients with chronic primary MR (stage D) and LV ejection fraction (LVEF) <60 percent who are awaiting valve surgery or who are not candidates for valve surgery are treated with standard evidence-based medical therapy for heart failure with reduced ejection fraction (HFrEF). (See "Overview of the management of heart failure with reduced ejection fraction in adults" and "Primary pharmacologic therapy for heart failure with reduced ejection fraction" and "Secondary pharmacologic therapy for heart failure with reduced ejection fraction" and "Treatment and prognosis of heart failure with mildly reduced ejection fraction", section on 'Therapy for mildly reduced ejection fraction'.)

Endocarditis prophylaxis – Antibiotic prophylaxis is not indicated for patients with mitral valve disease (in the absence of prosthetic valve replacement or history of infective endocarditis). This is discussed separately. (See "Prevention of endocarditis: Antibiotic prophylaxis and other measures".)

Cause-specific management – Patients with mitral valve prolapse require assessment for concurrent tricuspid valve disease and arrhythmic risk. Patients with rheumatic heart disease are treated with prophylaxis against rheumatic fever. (See "Mitral valve prolapse: Overview of complications and their management" and "Management and prevention of rheumatic heart disease", section on 'Secondary prevention'.)

Concurrent conditions – Patients with mitral valve prolapse commonly have concurrent conditions such as hypertension, coronary artery disease, and atrial fibrillation that require treatment. (See 'Concurrent conditions' above.)

Intervention - Indications for mitral valve intervention (surgical repair or replacement or transcatheter repair) and the timing and optimal choice of intervention are discussed separately. (See "Chronic primary mitral regurgitation: Indications for intervention".)

ACKNOWLEDGMENTS

The UpToDate editorial staff acknowledges Sorin Pislaru, MD, PhD, who contributed to earlier versions of this topic review.

The UpToDate editorial staff also acknowledges William H Gaasch, MD (deceased), who contributed to earlier versions of this topic.

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  2. Vahanian A, Beyersdorf F, Praz F, et al. 2021 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J 2022; 43:561.
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References

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