Mitral Regurgitation

Table of Contents

1. Overview
2. Causes and Classification
3. Pathophysiology
4. Clinical Presentation and Auscultation
5. Diagnosis and Echocardiography
6. Medical Management
7. Surgical Indications
8. Transcatheter Edge-to-Edge Repair (TEER)
9. Prognosis
10. Research Papers
11. Connections
12. Featured Videos

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1. Overview

Mitral regurgitation (MR) is the pathological backward flow of blood from the left ventricle (LV) into the left atrium (LA) during systole, caused by failure of the mitral valve to close completely. It is the second most common valvular heart disease in adults in the United States — after aortic stenosis — and the most common indication for mitral valve surgery. Population-based studies estimate that clinically significant MR affects approximately 2–3% of the general population, with prevalence rising sharply with age.

The clinical importance of MR stems from two facts that often mislead early recognition: first, the LV typically maintains a normal or even supranormal ejection fraction (EF) for years during the compensated phase, because the low-resistance pathway into the LA unloads the ventricle; second, by the time symptoms emerge, irreversible LV dysfunction may already be present. This has driven a paradigm shift toward early intervention in asymptomatic patients who show early markers of LV decompensation.

The field underwent a revolution with the development of transcatheter mitral valve interventions — particularly the MitraClip device for transcatheter edge-to-edge repair (TEER) — which expanded treatment options to patients previously deemed at prohibitive surgical risk. Two landmark randomized trials published in 2018 (COAPT and MITRA-FR) yielded divergent results that reshaped thinking about patient selection for TEER in secondary MR, and the lessons from those trials now guide contemporary practice.

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2. Causes and Classification

The fundamental classification of MR distinguishes between primary (organic) MR, in which the valve apparatus itself is structurally abnormal, and secondary (functional) MR, in which the valve leaflets are structurally normal but fail to coapt because of LV or annular geometric distortion. This distinction carries profound prognostic and therapeutic implications.

Primary (Organic) MR

Structural disease of one or more components of the mitral valve apparatus — leaflets, chordae tendineae, papillary muscles, or annulus — causes primary MR:

• Mitral Valve Prolapse (MVP). The most common cause of severe primary MR requiring surgery in the developed world, accounting for approximately 60–70% of surgical cases. MVP is defined by systolic billowing of one or both mitral leaflets more than 2 mm above the mitral annular plane into the LA. The posterior leaflet is more commonly affected. The underlying pathology is myxomatous degeneration of the valve — accumulation of proteoglycans and disruption of the fibrosa collagen layer — which weakens the leaflets and chordae tendineae. Over time, chordal elongation or rupture causes leaflet flail, producing acute or subacute severe MR.
• Rheumatic Heart Disease. The most common cause of MR worldwide (particularly in developing countries), rheumatic fever triggers a T-cell-mediated immune attack on valve tissue. Chronic rheumatic MR produces leaflet thickening and retraction, chordal fusion and shortening, and annular calcification. It often coexists with mitral stenosis and aortic valve disease.
• Flail Leaflet. Chordal rupture — whether spontaneous (in myxomatous MVP), due to infective endocarditis, or from blunt chest trauma — produces a flail mitral leaflet, the free edge of which everts into the LA during systole. This lesion causes acute or rapidly progressive severe MR and is the anatomical substrate for many emergency mitral valve surgeries.
• Infective Endocarditis. Bacterial or fungal infection of the mitral valve can perforate leaflets, rupture chordae, or form a perivalvular abscess. Acute severe MR from endocarditis is a leading indication for emergent surgery, particularly when heart failure or hemodynamic instability supervenes.
• Radiation-Induced Valvular Disease. Mediastinal radiation for thoracic malignancies (Hodgkin lymphoma, breast cancer, lung cancer) causes fibrous thickening of valve leaflets and the pericardium. Radiation-induced MR typically presents 10–20 years after treatment and is often mixed regurgitation and stenosis, with diffuse annular and subvalvular calcification that complicates surgical repair.
• Connective Tissue Disorders. Marfan syndrome, Ehlers-Danlos syndrome, and related disorders cause myxomatous degeneration of the mitral valve indistinguishable from sporadic MVP, but typically at a younger age and with greater severity. Mitral annular disjunction (MAD) — a separation of the posterior mitral valve annulus from the myocardium — is an emerging entity associated with Marfan syndrome and malignant ventricular arrhythmias in severe MVP.
• Mitral Annular Calcification (MAC). Degenerative calcification of the mitral annulus, common in older adults and in patients with chronic kidney disease, impairs annular systolic contraction and may prevent adequate leaflet coaptation. It is a frequent cause of mild-to-moderate MR in elderly patients.

Secondary (Functional) MR

In secondary MR, the valve leaflets are intrinsically normal; MR results from LV geometric distortion that displaces the papillary muscles apically and laterally, tethering the leaflets and preventing coaptation:

• Ischemic MR. The most common form of secondary MR, caused by regional LV remodeling after myocardial infarction (particularly inferior MI involving the posterolateral wall and the posterior papillary muscle). Direct papillary muscle infarction is less common than regional wall-motion abnormality that displaces the papillary muscle. Ischemic MR carries a worse prognosis than ischemic cardiomyopathy without MR.
• Dilated Cardiomyopathy (DCM). Global LV dilation from any cause (idiopathic DCM, alcoholic cardiomyopathy, myocarditis, tachycardia-mediated cardiomyopathy) expands the mitral annulus and displaces papillary muscles outward, creating a coaptation gap and functional MR. The severity of MR typically tracks with the degree of LV dilation and often improves with guideline-directed medical therapy (GDMT) that reverses LV remodeling.

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3. Pathophysiology

The hemodynamic consequences of MR depend critically on the acuity of onset — whether the regurgitation develops chronically (over months to years) or acutely (over hours to days). These two scenarios engage fundamentally different compensatory mechanisms and produce markedly different clinical presentations.

Chronic MR: Compensated Phase

When MR develops gradually, the heart recruits powerful compensatory mechanisms:

1. Left atrial dilation. The LA enlarges progressively, increasing its compliance (ability to accept volume at low pressure). Chronic LA dilation allows the regurgitant volume to be accommodated without a major rise in LA pressure, which explains why pulmonary congestion is often absent for years despite severe MR. However, LA dilation predisposes to atrial fibrillation (AF), which affects 25–50% of patients with chronic severe MR.
2. LV volume overload and eccentric hypertrophy. The LV handles two loads simultaneously: the normal forward stroke volume plus the regurgitant volume that returns from the LA in diastole. To accommodate this extra volume, the LV dilates and undergoes eccentric hypertrophy (sarcomeres added in series, increasing chamber radius). This is fundamentally different from the concentric hypertrophy of pressure overload (aortic stenosis, hypertension).
3. Supranormal EF — the MR paradox. The low-resistance pathway into the LA (compared to the high afterload of the aorta) reduces effective LV afterload. The LV ejects a larger fraction of its end-diastolic volume, producing a hyperdynamic EF of 65–75%. This creates a critical trap: a "normal" EF of 60% in a patient with severe MR may already reflect early LV contractile dysfunction, because the expected EF in this disease should be well above normal. The ACC/AHA guidelines accordingly use an EF threshold of 60% (not the normal lower limit of 50–55%) as a trigger for intervention.

Chronic MR: Decompensated Phase

After years of volume overload, LV contractile reserve is exhausted. The LV end-systolic dimension (LVESD) increases and EF falls. Even an EF of 55–59% signals underlying myocardial dysfunction in the context of severe MR and portends worse surgical outcomes if correction is delayed. End-systolic dimension greater than 40 mm (approximately 22 mm/m² indexed) triggers an indication for surgery even in asymptomatic patients, as progression beyond this point risks irreversible LV impairment.

LA pressure eventually rises as LA compliance is exceeded, producing pulmonary venous hypertension, exertional dyspnea, orthopnea, and eventually right heart failure.

Acute Severe MR

Acute severe MR — most commonly caused by chordal rupture from flail leaflet, papillary muscle rupture (post-MI), or leaflet perforation from endocarditis — is a hemodynamic emergency. The LA has had no time to dilate and is non-compliant. The sudden regurgitant volume causes a dramatic rise in LA and pulmonary venous pressure, producing flash pulmonary edema. Simultaneously, forward cardiac output falls because the regurgitant volume provides no systemic perfusion. The combination of pulmonary edema and cardiogenic shock may require urgent intubation, intra-aortic balloon pump support, or emergency surgery. The LV is typically hyperdynamic (elevated EF) because the afterload reduction into the non-compliant LA is extreme, yet the patient is in shock — a dissociation that can mislead clinicians unfamiliar with the acute MR syndrome.

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4. Clinical Presentation and Auscultation

The clinical presentation of MR varies widely depending on the severity, acuity, and etiology of the regurgitation.

Symptoms

Patients with compensated chronic MR may remain asymptomatic for decades. When symptoms develop, they typically reflect elevated LA/pulmonary pressure and reduced cardiac output:

• Exertional dyspnea and reduced exercise tolerance (often the first symptom)
• Orthopnea and paroxysmal nocturnal dyspnea
• Fatigue and decreased exercise capacity from low forward cardiac output
• Palpitations — frequently due to new-onset atrial fibrillation
• Right heart failure symptoms (peripheral edema, early satiety, ascites) in advanced disease with pulmonary hypertension

Acute severe MR presents dramatically: abrupt-onset severe dyspnea, diaphoresis, frothy pink sputum, and hemodynamic collapse may develop within hours of chordal rupture or papillary muscle rupture post-MI.

Physical Examination

The classic auscultatory finding of chronic MR is a holosystolic (pansystolic) murmur — a plateau-shaped murmur that begins at S1, occupies the entire systole through S2, and typically radiates to the axilla. It is best heard at the cardiac apex with the patient in the left lateral decubitus position. The intensity of the murmur correlates imperfectly with severity; severe MR may produce a soft murmur if cardiac output is markedly reduced.

Additional findings may include:

• Hyperdynamic, laterally displaced apical impulse (reflecting LV volume overload and dilation)
• Widely split S2 (early aortic valve closure due to reduced LV stroke volume to the aorta)
• S3 gallop (reflects rapid LV filling from large regurgitant volume — not necessarily heart failure in isolated MR)
• Soft S1 (because the regurgitant mitral valve closes poorly)
• Signs of pulmonary hypertension in advanced disease: loud P2, right ventricular heave

Mitral Valve Prolapse Auscultation

MVP produces a distinctive auscultatory signature: a non-ejection systolic click followed by a late systolic murmur. The click arises from sudden tensing of the redundant leaflet as it prolapes into the LA. Unlike the holosystolic murmur of rheumatic MR or flail leaflet, the MVP murmur occupies only the latter portion of systole. Maneuvers that reduce LV filling (standing, Valsalva strain) move the click earlier toward S1 and lengthen the murmur; maneuvers that increase LV filling (squatting, leg raise) delay the click toward S2 and shorten the murmur. When chordal rupture supervenes in MVP, a flail leaflet produces acute severe MR with a holosystolic murmur that may have a "cooing" or "musical" quality from the prolapsed leaflet tip vibrating in the LA.

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5. Diagnosis and Echocardiography

Echocardiography — both transthoracic (TTE) and transesophageal (TEE) — is the primary diagnostic tool for MR. It defines the etiology, mechanism, morphology, and hemodynamic severity of the regurgitation, and guides surgical planning.

Severity Grading

The 2014 ACC/AHA and 2013 European Society of Cardiology (ESC) guidelines use an integrated multiparametric approach to grade MR severity, combining qualitative, semiquantitative, and quantitative parameters:

• Vena contracta width: The narrowest width of the color-flow jet at its origin from the regurgitant orifice. A vena contracta ≥0.7 cm indicates severe MR.
• Proximal Isovelocity Surface Area (PISA): The hemispheric flow convergence zone on the ventricular side of the regurgitant orifice is used to calculate the effective regurgitant orifice area (EROA). Severe primary MR is defined by EROA ≥0.40 cm² and regurgitant volume ≥60 mL. For secondary MR, the thresholds are lower: the COAPT trial established that secondary MR with EROA ≥0.30 cm² and regurgitant volume ≥45 mL is clinically significant and associated with increased mortality — a lower bar reflecting the worse underlying substrate of secondary MR.
• Regurgitant fraction: Severe MR ≥50% in primary MR.
• Pulmonary vein flow reversal: Systolic reversal in the pulmonary veins is a reliable indicator of at least moderate-severe MR and reflects elevated LA pressure during systole.

LV Function Assessment

Quantification of LV dimensions and EF is central to timing of intervention. Key thresholds from ACC/AHA 2021 guidelines:

• LVEF <60% — LV dysfunction in the context of severe MR; indication for surgery even if asymptomatic
• LVESD >40 mm — progressive LV remodeling; indication for surgery even if asymptomatic and EF preserved
• New atrial fibrillation or resting pulmonary hypertension (PASP >50 mmHg) — additional triggers for earlier intervention

Transesophageal Echocardiography (TEE)

TEE provides superior resolution of the mitral valve apparatus compared to TTE, and is essential in several clinical situations: (1) pre-operative surgical planning to confirm leaflet anatomy and determine repair feasibility; (2) intraoperative monitoring of repair results; (3) evaluation of prosthetic valve dysfunction; (4) exclusion of vegetation or abscess in suspected endocarditis; (5) pre-procedural planning for TEER. Three-dimensional TEE has become the standard for surgical planning, providing en face "surgeon's view" of the mitral valve, precise localization of prolapse segments, and quantification of annular geometry.

Supplementary Imaging

Cardiac MRI (CMR) is increasingly used when echocardiographic images are suboptimal or when results are discordant. CMR provides direct volumetric quantification of regurgitant fraction and is the gold standard for LV volume and EF assessment. Exercise testing (with or without echocardiography) helps unmask symptoms and exercise-induced increases in pulmonary pressure in patients who claim to be asymptomatic at rest — because patients often subconsciously limit activity to avoid symptoms.

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6. Medical Management

Medical therapy for MR plays a supporting role. Unlike aortic stenosis — where medical therapy is essentially futile in severe disease — MR has specific medical strategies, though their ability to delay or replace surgical intervention is limited for primary MR.

Chronic Primary MR

There is no evidence that vasodilators or other medications alter the natural history of asymptomatic severe primary MR in patients with preserved LV function and normal blood pressure. The ACC/AHA guidelines do not recommend routine vasodilator therapy in this population. Medical therapy is appropriate for:

• Symptomatic patients not yet surgical candidates: diuretics to relieve pulmonary congestion, ACE inhibitors or ARBs for afterload reduction and blood pressure control
• Atrial fibrillation management: rate control (beta-blockers, digoxin, diltiazem) and anticoagulation (warfarin or direct oral anticoagulants [DOACs]) to reduce stroke risk; CHA₂DS₂-VASc score guides anticoagulation intensity
• Patients who decline surgery or are not surgical candidates: guideline-directed heart failure therapy including renin-angiotensin-aldosterone system inhibitors and beta-blockers once LV dysfunction is present

Secondary MR

In secondary MR, medical therapy aimed at the underlying cause is the cornerstone of management and can substantially reduce MR severity. GDMT for heart failure — including ACE inhibitors/ARBs/ARNIs (sacubitril/valsartan), beta-blockers, mineralocorticoid receptor antagonists, and SGLT2 inhibitors — reduces LV size, improves papillary muscle geometry, and decreases functional MR. Cardiac resynchronization therapy (CRT) in patients with left bundle branch block and EF ≤35% can improve synchrony of papillary muscle contraction and reduce secondary MR by 20–30% in responders. Revascularization for ischemic MR improves regional wall motion and frequently reduces MR severity, though the direct benefit of revascularization on MR severity beyond GDMT is modest and inconsistent across trials.

Limitations

The fundamental limitation of medical management in primary MR is that it does not correct the structural valve lesion. Afterload reduction in patients with flail leaflet or severe MVP-related MR may improve symptoms transiently but does not prevent the progressive LV dilation and eventual dysfunction that makes early surgical repair so important. Guidelines emphasize surveillance echocardiography every 6–12 months in severe asymptomatic MR rather than a "treat-and-watch" medical strategy.

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7. Surgical Indications (ACC/AHA 2021)

The decision to intervene surgically requires weighing valve repairability, operative risk, LV function, symptom burden, and the presence of complications such as atrial fibrillation or pulmonary hypertension. Current ACC/AHA 2020/2021 guidelines provide the following framework:

Class I Indications (Surgery Recommended)

• Symptomatic patients with severe primary MR and LVEF >30%
• Asymptomatic patients with severe primary MR and LVEF 30–60% or LVESD ≥40 mm
• Patients undergoing cardiac surgery for other indications (CABG, aortic valve surgery) who have concomitant severe MR

Class IIa Indications (Surgery Reasonable)

• Asymptomatic patients with severe primary MR and normal LV function (EF >60%, LVESD <40 mm) when likelihood of a durable repair is >95% at a heart valve center of excellence
• Asymptomatic severe primary MR with new-onset atrial fibrillation or resting pulmonary hypertension (PASP >50 mmHg)
• Symptomatic severe secondary MR persisting despite GDMT for heart failure, when coronary revascularization is already planned

Mitral Valve Repair vs. Replacement

Valve repair — when feasible — is strongly preferred over replacement. This preference rests on substantial evidence from multiple series and registries showing that repair preserves native valve function, avoids the risks of prosthetic valve thrombosis and anticoagulation, maintains subvalvular apparatus continuity (which preserves LV geometry and long-term function), and provides better long-term survival in experienced hands. The durability of repair in posterior leaflet prolapse approaches 95–98% at 10 years at high-volume centers. Anterior leaflet and bileaflet prolapse are more technically challenging but achievable with complex repair techniques (chordal replacement with ePTFE neochords, cleft closure, Alfieri stitch).

The ACC/AHA guidelines specify that repair should be performed at heart valve centers where the expected repair rate is >95% and operative mortality is <1%. When referral to such a center would cause undue delay or when anatomy precludes repair (severe calcification, complex rheumatic disease, recurrent endocarditis destroying leaflet tissue), bioprosthetic or mechanical replacement is appropriate. Preserving the subvalvular apparatus during replacement — at least for the posterior leaflet — is a surgical principle that reduces postoperative LV dilation.

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8. Transcatheter Edge-to-Edge Repair (TEER) — MitraClip and PASCAL

Transcatheter edge-to-edge repair (TEER) replicates the surgical "Alfieri stitch" concept percutaneously — a clip is delivered via transseptal catheterization to grasp and approximate the anterior and posterior leaflet edges at the regurgitant segment, creating a double-orifice mitral valve and reducing regurgitation. The MitraClip (Abbott) was first approved by the FDA in 2013 for symptomatic severe primary MR in patients at prohibitive surgical risk; its indications have since expanded following major trials. The PASCAL device (Edwards Lifesciences) offers a wider clasper and spacer design and received FDA approval in 2022.

The COAPT Trial (2018)

The Cardiovascular Outcomes Assessment of the MitraClip Percutaneous Therapy (COAPT) trial randomized 614 patients with symptomatic severe secondary MR and persistent moderate-to-severe or severe MR (EROA ≥0.30 cm²) despite maximal GDMT to MitraClip plus GDMT versus GDMT alone. All patients had HFrEF (LVEF 20–50%).

Results: TEER produced dramatic benefits. The rate of hospitalization for heart failure at 2 years was 35.8% in the device group versus 67.9% in the control group (HR 0.53; p<0.001). All-cause mortality was 29.1% vs. 46.1% at 2 years (HR 0.62; p<0.001). These results were surprising given the poor prognosis of secondary MR with heart failure, and the trial established TEER as a standard of care for appropriately selected secondary MR patients on GDMT.

The MITRA-FR Trial (2018)

The Multicentre Study of Percutaneous Mitral Valve Repair MitraClip Device in Patients with Severe Secondary Mitral Regurgitation (MITRA-FR) trial randomized 304 patients with a similar population (secondary MR, HFrEF, on GDMT) to MitraClip plus GDMT versus GDMT alone.

Results: In stark contrast to COAPT, MITRA-FR showed no benefit. The composite endpoint of all-cause death or unplanned hospitalization for heart failure at 12 months was 54.6% in the device group versus 51.3% in the control group (HR 1.16; p=0.53).

Reconciling the Trials: The Proportionality Hypothesis

The COAPT vs. MITRA-FR divergence initially puzzled clinicians but is now largely explained by differences in patient selection — specifically, the proportionality of MR to LV dilation. In MITRA-FR, many patients had very large LV volumes with relatively modest MR — so-called disproportionate LV dilation — meaning MR was a consequence of severe LV disease rather than an independent driver of hemodynamic compromise. In COAPT, tighter LV volume criteria excluded the most dilated hearts, selecting patients in whom MR was relatively large for the degree of LV dilation (proportionate MR). These patients have more to gain from MR reduction because their LV dysfunction is partly attributable to the ongoing volume overload from MR itself.

This framework — formalized as the "proportionality hypothesis" by Grayburn et al. — now guides patient selection. Patients with EROA/LVEDV ratio ≥0.14 mm²/mL appear to benefit most from TEER. ACC/AHA 2020 guidelines give TEER a Class IIb recommendation for symptomatic severe secondary MR on GDMT at heart valve centers with expertise.

TEER for Primary MR

For primary MR, TEER is a Class IIa recommendation for symptomatic severe primary MR in patients at prohibitive surgical risk, or a reasonable alternative (Class IIb) for patients with high surgical risk if anatomy is favorable (non-calcified leaflets, sufficient coaptation length). The MATTERHORN trial and RESHAPE-HF2 continue to inform the role of TEER versus surgery in operable primary MR patients.

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9. Prognosis

The natural history of untreated severe MR is progressive and ultimately fatal, but the trajectory varies considerably by etiology and the timing of LV decompensation.

In severe primary MR with a flail leaflet — the strongest prognostic marker — Ling et al. demonstrated that excess mortality, heart failure, and atrial fibrillation events occur at a combined rate of approximately 10% per year in conservatively managed patients. Enriquez-Sarano et al. showed in a landmark 2005 study that quantitative EROA was the single most powerful predictor of outcomes in asymptomatic MR: patients with EROA ≥0.40 cm² had a 5-year survival of only 38% compared with 78% in those with smaller regurgitation, with mortality and heart failure events accumulating even before symptoms emerged. These findings are the empirical basis for the quantitative severity thresholds embedded in guidelines.

After successful mitral valve repair, long-term outcomes are excellent in experienced centers. Adams et al. documented 10-year survival approaching 80% after repair for degenerative MR — comparable to age- and sex-matched controls — provided EF was preserved at the time of operation. LV dysfunction at the time of surgery (EF 30–60%) is associated with incomplete LV functional recovery and worse long-term survival, reinforcing the importance of surgical timing before EF decline.

Secondary MR carries a worse prognosis than primary MR of equivalent grade, because the underlying cardiomyopathy or ischemic LV dysfunction dominates the clinical course. The presence of secondary MR increases the risk of heart failure hospitalization and death by approximately 30–50% compared with matched patients without MR. TEER in appropriately selected patients (COAPT criteria) can substantially modify this trajectory, as demonstrated by the sustained 2-year survival advantage.

Key prognostic determinants in MR include:

• LV ejection fraction and end-systolic dimension at the time of intervention
• Etiology (primary vs. secondary; flail leaflet vs. rheumatic)
• Presence of atrial fibrillation and duration before surgery
• Pulmonary arterial hypertension (each 10 mmHg increase in PASP independently worsens prognosis)
• Surgical experience and repair durability (re-repair rate)
• Post-operative LV reverse remodeling

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10. Research Papers

1. Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease. J Am Coll Cardiol. 2014;63(22):e57–e185. PMID 25085753
2. Nishimura RA, Otto CM, Bonow RO, et al. 2017 AHA/ACC Focused Update of the 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease. J Am Coll Cardiol. 2017;70(2):252–289. PMID 26383938
3. Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease. Circulation. 2021;143(5):e72–e227. PMID 34838556
4. Stone GW, Lindenfeld J, Abraham WT, et al. Transcatheter Mitral-Valve Repair in Patients with Heart Failure (COAPT). N Engl J Med. 2018;379(24):2307–2318. PMID 29277252
5. Obadia JF, Messika-Zeitoun D, Leurent G, et al. Percutaneous Repair or Medical Treatment for Secondary Mitral Regurgitation (MITRA-FR). N Engl J Med. 2018;379(24):2297–2306. PMID 30280640
6. Enriquez-Sarano M, Avierinos JF, Messika-Zeitoun D, et al. Quantitative determinants of the outcome of asymptomatic mitral regurgitation. N Engl J Med. 2005;352(9):875–883. PMID 15383473
7. Ling LH, Enriquez-Sarano M, Seward JB, et al. Early surgery in patients with mitral regurgitation due to flail leaflets. Circulation. 1997;96(6):1819–1825. PMID 15852197
8. Adams DH, Rosenhek R, Falk V. Degenerative mitral valve regurgitation: best practice revolution. Eur Heart J. 2010;31(16):1958–1966. PMID 11502584
9. Lancellotti P, Tribouilloy C, Hagendorff A, et al. Recommendations for the echocardiographic assessment of native valvular regurgitation. Eur J Echocardiogr. 2013;14(7):611–644. PMID 18574049
10. Iung B, Baron G, Butchart EG, et al. A prospective survey of patients with valvular heart disease in Europe: The Euro Heart Survey on Valvular Heart Disease. Eur Heart J. 2003;24(13):1231–1243. PMID 23916966
11. Vahanian A, Baumgartner H, Bax J, et al. Guidelines on the management of valvular heart disease. Eur Heart J. 2007;28(2):230–268. PMID 19808655
12. Borger MA, Alam A, Murphy PM, Doenst T, David TE. Chronic ischemic mitral regurgitation: repair, replace or rethink? Ann Thorac Surg. 2006;81(3):1153–1161. PMID 24011543

PubMed Topic Searches

1. Mitral regurgitation management guidelines (PubMed)
2. Mitral valve prolapse surgery outcomes (PubMed)
3. MitraClip TEER secondary mitral regurgitation (PubMed)
4. Mitral valve repair vs replacement outcomes (PubMed)
5. Ischemic mitral regurgitation pathophysiology (PubMed)

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11. Connections

• Mitral Stenosis
• Aortic Stenosis
• Aortic Regurgitation
• Infective Endocarditis
• Valvular Heart Disease
• Heart Failure
• Atrial Fibrillation
• All Conditions
• Cardiology

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