Mitral Regurgitation

Updated: Dec 08, 2021
  • Author: Ivan Hanson, MD; Chief Editor: Terrence X O'Brien, MD, MS, FACC  more...
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Practice Essentials

Mitral regurgitation (MR) is defined as an abnormal reversal of blood flow from the left ventricle (LV) to the left atrium (LA). It is caused by disruption in any part of the mitral valve (MV) apparatus. The most common etiologies of MR include MV prolapse (MVP), rheumatic heart disease, infective endocarditis, annular calcification, cardiomyopathy, and ischemic heart disease. See the video below.

Transthoracic echocardiogram demonstrating severe mitral regurgitation with heavily calcified mitral valve and prolapse of the posterior leaflet into the left atrium.

Signs and symptoms

When associated with coronary artery disease (CAD) and acute myocardial infarction (MI), significant acute MR is accompanied by the following symptoms:

  • Dyspnea

  • Fatigue

  • Orthopnea

  • Pulmonary edema (often the initial manifestation)

The following may be noted with chronic MR:

  • Some patients may remain asymptomatic for years

  • Patients may have normal exercise tolerance until systolic LV dysfunction develops, at which point they may experience symptoms of a reduced forward cardiac output

  • Patients may feel chest palpitations if AF develops as a result of chronic atrial dilatation

  • Patients with LV enlargement and more severe disease eventually progress to symptomatic congestive heart failure (CHF) with pulmonary congestion and edema

Palpation may reveal the following:

  • Brisk carotid upstroke and hyperdynamic cardiac impulse

  • Prominent LV filling wave

Auscultation may reveal the following:

  • Diminished S1 in acute MR and chronic severe MR with defective valve leaflets

  • Wide splitting of S2 as a result of early closure of the aortic valve

  • S3 as a result of LV dysfunction or increased blood flow across the MV

  • Accentuated P2 if pulmonary hypertension is present

  • Characteristic holosystolic murmur (or mid-systolic if etiology of MR is mitral valve prolapse)

See Presentation for more detail.


The following findings may be noted on chest radiography:

  • Evidence of LV enlargement due to volume overload (particularly in chronic MR), though pulmonary congestion may not be observed until heart failure has developed

  • Evidence of LA enlargement in the anteroposterior view

European Society of Cardiology (ESC)/European Association for Cardio-Thoracic Surgery (EACTS) echocardiographic criteria [1] for the definition of severe MR are as follows:

  • Flail leaflet/ruptured papillary muscle/large coaptation defect

  • Very large color flow central jet or eccentric jet adhering, swirling, and reaching the posterior wall of the LA

  • Dense/triangular continuous-wave signal of regurgitant jet

  • Large flow convergence zone

American College of Cardiology (ACC)/American Heart Association (AHA) class I indications for transthoracic echocardiography (TTE) are as follows:

  • Baseline evaluation for LV size and function, right ventricular (RV) and LA size, pulmonary artery pressure, and severity of MR

  • Determining the etiology of MR

  • Annual or semiannual surveillance of LV ejection fraction (LVEF) and end-systolic dimension in asymptomatic patients with moderate-to-severe MR

  • Evaluation of the MV apparatus and LV function after a change in signs or symptoms

  • Evaluation of LV size and function and mitral valve hemodynamics in the initial evaluation after MV replacement or repair

ACC/AHA class I indications for serial TTE are as follows:

  • Asymptomatic patients with mild MR and no evidence of LV enlargement, LV dysfunction, or pulmonary hypertension – Yearly observation; serial TTE is not indicated

  • Patients with moderate MR – Yearly TTE

  • Asymptomatic patients with severe MR – TTE and clinical evaluation every 6-12 months to assess symptoms and development of LV dysfunction

ACC/AHA class I indications for transesophageal echocardiography (TEE) are as follows:

  • Assessment of etiology of severe MR in patients for whom surgery is recommended to determine the feasibility of MV repair

  • Evaluation of mitral valve and associated structures when TTE is nondiagnostic

Other tests include the following:

  • Electrocardiography (ECG)

  • Brain natriuretic peptide (BNP) assessment

  • Cardiac catheterization

See Workup for more detail.


Medical therapy includes the following:

  • Afterload-reducing agents and diuretics in MR with symptoms or LV dysfunction

  • Beta blockers and biventricular pacing for primary treatment of LV dysfunction in functional MR

  • Consideration of intra-aortic balloon counterpulsation in acute MR with hemodynamic compromise

  • In the presence of AF, beta blockers, calcium channel blockers, digitalis, or a combination

  • Consideration of anticoagulation for patients who develop AF or have had MV replacement surgery

  • Prophylactic antibiotics before any dental procedure involving manipulation of gingival tissue, the periapical region of a tooth, or perforation of oral mucosa in patients with a prosthetic heart valve, previous infectious endocarditis, some forms of congenital heart disease, or valvulopathy in a cardiac transplant recipient

  • Consideration of inotropic agents in chronic severely symptomatic MR; consultation with a cardiothoracic surgeon

ACC/AHA indications for MV surgery are as follows:

  • Repair is preferred to replacement in most patients with moderate-to-severe (3+) or severe (4+) chronic MR who require surgery; patients should be referred to experienced surgical centers (class I)

  • Surgery is indicated for symptomatic patients with acute severe MR (class I)

  • Symptomatic chronic severe MR – Surgery is recommended for New York Heart Association (NYHA) functional class II-IV symptoms without severe LV dysfunction; chronic severe MR due to a primary abnormality of the MV apparatus and NYHA functional class III-IV symptoms and mild-to-moderate LV dysfunction in whom MV repair is highly likely (class IIa)

  • Asymptomatic chronic severe MR – Surgery is recommended for those with mild-to-moderate LV dysfunction (class I); repair is reasonable in experienced centers for those with preserved LV function in whom the likelihood of successful repair without residual MR is >90% (class IIa); surgery is reasonable for those with preserved LV function, new-onset AF, or pulmonary artery hypertension (class IIa)

ESC/EACTS indications for MV surgery in severe primary MR are as follows:

  • Repair is preferred to replacement when it is expected to be durable (class I)

  • Surgery is indicated in asymptomatic patients with LVEF >30% and end-systolic dimension < 55 mm (class I)

  • Surgery is indicated for asymptomatic patients with LV end-systolic dimension ≥45 mm and/or LVEF ≤60% (class I)

  • Surgery should be considered in asymptomatic patients with preserved LV function and new-onset AF or pulmonary hypertension (class IIa)

  • Surgery should be considered in asymptomatic patients with preserved LV function and a high likelihood of durable repair, low surgical risk and flail leaflet, and LV end-systolic dimension ≥40 mm (class IIa)

  • Surgery should be considered in patients with severe LV dysfunction refractory to medical therapy with a high likelihood of durable repair and low comorbidity (class IIa)

  • Surgery may be considered in patients with severe LV dysfunction refractory to medical therapy with low likelihood of durable repair and low comorbidity (class IIb)

  • Surgery may be considered in asymptomatic patients with preserved LV function, high likelihood of durable repair, low surgical risk, and either LA dilatation and sinus rhythm or pulmonary hypertension on exercise

Surgical MV repair remains the criterion standard intervention for severe MR; however, percutaneous double-orifice repair is a viable alternative for patients at high risk. In addition, in October 2013, the FDA approved the MitraClip valve repair system for patients with symptomatic degenerative MR with a prohibitive risk for mitral-valve surgery. [2, 3]

See Treatment and Medication for more detail.



Mitral regurgitation (MR), the most frequent valvular heart disease, [4, 5, 6] is defined as an abnormal reversal of blood flow from the left ventricle to the left atrium. It is caused by disruption in any part of the mitral valve apparatus, which comprises the mitral annulus, the leaflets (a large anterior [aortic] leaflet and a small posterior [mural] leaflet), the chordae tendineae, and the papillary muscles (anteromedial and posterolateral). The most common etiologies of MR include mitral valve prolapse (MVP), rheumatic heart disease, infective endocarditis, annular calcification, cardiomyopathy and ischemic heart disease. The pathophysiology, clinical manifestations and management of MR differ with the chronicity of the disease and the etiology.

For patient education resources, see Heart Health Center as well as Mitral Valve Prolapse.



Mitral regurgitation (MR) can be caused by organic disease (eg, rheumatic fever, ruptured chordae tendineae, myxomatous degeneration, leaflet perforation) or a functional abnormality (ie, a normal valve may regurgitate [leak] because of mitral annular dilatation, focal myocardial dysfunction, or both). Congenital MR is rare but is commonly associated with myxomatous mitral valve disease. Alternatively, it can be associated with cleft of the mitral valve, as occurs in persons with Down syndrome, or an ostium primum atrial septal defect.

Acute mitral regurgitation

Acute MR is characterized by an increase in preload and a decrease in afterload causing an increase in end-diastolic volume (EDV) and a decrease in end-systolic volume (ESV). This leads to an increase in total stroke volume (TSV) to supranormal levels. However, forward stroke volume (FSV) is diminished because much of the TSV regurgitates as the regurgitant stroke volume (RSV). This, in turn, results in an increase in left atrial pressure (LAP). According to the Laplace principle, which states that ventricular wall stress is proportional to both ventricular pressure and radius, LV wall stress in the acute phase is markedly decreased since both of these parameters are reduced.

Chronic compensated mitral regurgitation

In chronic compensated MR, the left atrium (LA) and ventricle have sufficient time to dilate and accommodate the regurgitant volume. Thus LA pressure is often normal or only minimally elevated. Because of the left ventricular dilatation via the process of eccentric hypertrophy, TSV and FSV are maintained. Wall stress may be normal to slightly increased as the radius of the LV cavity increases but the end-diastolic LV pressure remains normal. As the LV progressively enlarges, the mitral annulus may stretch and prevent the mitral valve leaflets from coapting properly during systole, thus worsening the MR and LV dilatation.

Chronic decompensated mitral regurgitation

In the chronic decompensated phase, cardiac dysfunction has developed, impairing both TSV and FSV (although ejection fraction still may be normal). This results in a higher ESV and EDV, which in turn causes a elevation of LV and LA pressure, ultimately leading to pulmonary edema and, if left untreated, cardiogenic shock.



Acute mitral regurgitation

Causes of acute mitral regurgitation (MR) include coronary artery disease, infectious endocarditis, chordae tendineae rupture (as with myxomatous valve disease), valvular surgery, and other conditions.

Coronary artery disease (ischemia or acute myocardial infarction) may result in papillary muscle dysfunction or rupture; it does not cause chordae tendineae dysfunction or rupture as they are not vascularized. The posteromedial papillary muscle is supplied by the terminal branch of the posterior descending artery and is more vulnerable to ischemic insult than the anterolateral papillary muscle, which is usually supplied by both the left anterior descending and circumflex arteries. Transient ischemia may result in transient MR associated with angina. Myocardial infarction or severe prolonged ischemia produces irreversible papillary muscle dysfunction and scarring.

Infectious endocarditis features include the following:

  • Abscess formation

  • Vegetations

  • Rupture of chordae tendineae

  • Leaflet perforation

Following valvular surgery, acute MR may occur as a result of trauma, percutaneous valvuloplasty, or suture interruption.

Other causes of acute MR include the following:

  • Tumors (most commonly atrial myxoma)

  • Myxomatous degeneration (mitral valve prolapse, Ehlers-Danlos syndrome, Marfan syndrome)

  • Ruptured chordae tendineae (trauma, mitral valve prolapse, endocarditis, spontaneous)

  • Systemic lupus erythematosus (Libman-Sacks lesion)

  • Acute rheumatic fever (Carey Coombs murmur)

  • Acute global left ventricular dysfunction

  • Prosthetic mitral valve dysfunction

Chronic mitral regurgitation

Causes of chronic MR include the following:

  • Rheumatic heart disease

  • Systemic lupus erythematosus

  • Scleroderma

  • Myxomatous degeneration (mitral valve prolapse, Ehlers-Danlos syndrome, Marfan syndrome)

  • Calcification of mitral valve annulus

  • Infective endocarditis (can affect normal, abnormal, or prosthetic mitral valves)

  • Ruptured chordae tendineae (trauma, mitral valve prolapse, endocarditis, spontaneous)

  • Functional MR (dilation of mitral valve annulus, anormal tethering of leaflets due to enlargement of LV cavity and stretch of papillary muscles and chordae [dilated cardiomyopathies, aneurysmal dilation of the left ventricle])

  • Hypertrophic cardiomyopathy

  • Systolic anterior motion of the mitral valve

  • Perivalvular prosthetic leak

  • Congenital (mitral valve clefts, mitral valve fenestrations, parachute mitral valve abnormality)

  • Drug-related (ergotamine, methysergide, pergolide, anorexiant medications)



United States data

Acute and chronic mitral regurgitation (MR) affect approximately 5 in 10,000 people. Mitral valve disease is the second most common valvular lesion, preceded only by aortic stenosis. Myxomatous degeneration has replaced rheumatic heart disease as the leading cause of mitral valvular abnormalities. Mitral valve prolapse has been estimated to be present in 4% of the normal population. With the aid of color Doppler echocardiography, mild MR can be detected in as many as 20% of middle-aged and older adults. MR is independently associated with female sex, lower body mass index, advanced age, renal dysfunction, prior myocardial infarction, prior mitral stenosis, and prior mitral valve prolapse. It is not related to dyslipidemia or diabetes.

International data

In areas other than the Western world, rheumatic heart disease is the leading cause of MR.



There appears to be an association between recurrent mitral regurgitation (MR) after mitral valve (MV) repair in patients with degenerative MR and increased mortality and adverse LV remodeling. [7] Independent risk factors for recurrent MR after mitral valve repair include MV repair performed before 2000, preoperative atrial fibrillation, high LV end-diastolic dimension (LVEDD), prolapse of the isolated anterior leaflet or multiple segments, and absence of ring annuloplasty. LVEDD and repair without artificial chordae implantation appear to be predictors of MR progression. [7]

Outcomes for asymptomatic chronic severe degenerative MR are as follows:

  • Mortality ranges from 50-73% at 5 years.

  • Mortality in patients with preserved LV function ranges from 27-45%.

  • Sudden death may be as common as 1-8% per year in patients with a flail leaflet.

In a study of patients with low ejection fraction (EF) (regardless of ischemic or nonischemic etiology), the presence of functional MR is associated with a 2-fold greater risk of all-cause mortality and hospitalization at 1-5 years. [8]

Mitral valve surgery operative mortality includes the following:

  • Isolated mitral valve repair surgery carries a 2% mortality.

  • Mitral valve replacement surgery: 4% mortality for patients younger than 50 years; 17% mortality for patients older than 80 years.

Tribouilloy et al found that, in patients with organic MR due to flail leaflets, left ventricular end-systolic diameter (LVESD) is independently associated with increased mortality. Analysis of results in 739 patients showed that LVESD ≥ 40 mm independently predicted overall mortality (hazard ratio [HR] 1.95; 95% confidence interval [CI], 1.01-3.83) and cardiac mortality (HR 3.09; 95% CI, 1.35-7.09) under conservative management. Mortality risk increased linearly with LVESD >40 mm (HR 1.15; 95% CI, 1.04-1.27 per 1-mm increment). Tribouilloy et al conclude that these findings support prompt surgical rescue in patients with LVESD ≥40 mm but also suggest that operating on patients before LVESD reaches 40 mm will best preserve survival. [9]

Magne et al found that exercise pulmonary hypertension can be predicted using resting comprehensive echocardiography in asymptomatic patients with degenerative MR. [10]