Mitral Regurgitation

Mitral Regurgitation

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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.

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) echographic 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 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.

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.

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.

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

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)

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.

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]

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O’Riordan M. FDA approves MitraClip for degenerative MR. October 25, 2013. Medscape [serial online]. Available at http://www.medscape.com/viewarticle/813216. Accessed: October 28, 2013.

Abbott. Abbott’s first-in-class MitraClip device now available for U.S. patients [press release]. October 25, 2013. Available at http://www.abbott.com/press-release/abbotts-firstinclass-mitraclip-device-now-available-for-us-patients.htm. Accessed: October 28, 2013.

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[Guideline] O’Gara PT, Grayburn PA, Badhwar V, et al. 2017 ACC expert consensus decision pathway on the management of mitral regurgitation: a report of the American College of Cardiology Task Force on Expert Consensus Decision Pathways. J Am Coll Cardiol. 2017 Nov 7. 70 (19):2421-49. [Medline]. [Full Text].

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Thourani VH, Weintraub WS, Guyton RA, et al. Outcomes and long-term survival for patients undergoing mitral valve repair versus replacement: effect of age and concomitant coronary artery bypass grafting. Circulation. 2003 Jul 22. 108(3):298-304. [Medline].

Vahanian A, Iung B. Mitral regurgitation: Timing of surgery or interventional treatment. Herz. 2015 Dec 10. [Medline].

Rosenhek R, Rader F, Klaar U, et al. Outcome of watchful waiting in asymptomatic severe mitral regurgitation. Circulation. 2006 May 9. 113(18):2238-44. [Medline].

O’Riordan M. Early surgery bests “watchful waiting” in severe MR patients without symptoms. Medscape Medical News. Accessed August 19, 2013. Available at http://www.medscape.com/viewarticle/809403.

Suri RM, Vanoverschelde JL, Grigioni F, et al. Association between early surgical intervention vs watchful waiting and outcomes for mitral regurgitation due to flail mitral valve leaflets. JAMA. 2013 Aug 14. 310(6):609-16. [Medline].

Otto CM. Surgery for mitral regurgitation: sooner or later?. JAMA. 2013 Aug 14. 310(6):587-8. [Medline].

[Guideline] Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2007 Oct 9. 116(15):1736-54. [Medline]. [Full Text].

O’Riordan M. Repair and surgery fare equally well in ischemic MR. Heartwire. November 18, 2013. [Full Text].

Barbieri A, Bursi F, Grigioni F, et al. Prognostic and therapeutic implications of pulmonary hypertension complicating degenerative mitral regurgitation due to flail leaflet: A Multicenter Long-term International Study. Eur Heart J. 2011 Mar. 32(6):751-759. [Medline].

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Stage

Valve Anatomy

Valve Hemodynamics*

Hemodynamic Consequences

Symptoms

A:

Primary MR

A:

Secondary MR

B:

Primary MR

B:

Secondary MR

C:

Primary MR

C:

Secondary MR

D:

Primary MR

D:

Secondary MR

*Several criteria are provided but not all criteria for each category will be present. Severity of mild, moderate, or serve is dependent on data quality and integration with other clinical evidence.

In secondary MR, true ERO is underestimated due to the crescentic shape of the proximal convergence

CAD = coronary heart disease; ERO = effective regurgitation orifice; HF = heart failure; IE = infective endocarditis; LA = left atrium; LV = left ventricular; LVEF = left ventricular ejection factor; LVESD = left ventricular end-systolic dimension; MR = mitral regurgitation; MV = mitral valve; TTE = transthoracic echocardiography.

Ivan Hanson, MD Assistant Professor of Medicine, Oakland University William Beaumont School of Medicine

Ivan Hanson, MD is a member of the following medical societies: American College of Cardiology, American Society of Echocardiography

Disclosure: Nothing to disclose.

Luis C Afonso, MD Assistant Professor, Department of Internal Medicine-Cardiology, Program Director of Cardiology Fellowship Program, Wayne State University; Director of Echocardiography Laboratory, Harper University Hospital

Luis C Afonso, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, American Society of Echocardiography

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Ronald J Oudiz, MD, FACP, FACC, FCCP Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; Director, Liu Center for Pulmonary Hypertension, Division of Cardiology, LA Biomedical Research Institute at Harbor-UCLA Medical Center

Ronald J Oudiz, MD, FACP, FACC, FCCP is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American Thoracic Society, American College of Physicians, American Heart Association

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Actelion, Bayer, Gilead, Lung Biotechnology, United Therapeutics<br/>Received research grant from: Actelion, Bayer, Gilead, Ikaria, Lung Biotechnology, Pfizer, Reata, United Therapeutics<br/>Received income in an amount equal to or greater than $250 from: Actelion, Bayer, Gilead, Lung Biotechnology, Medtronic, Reata, United Therapeutics.

Terrence X O’Brien, MD, MS, FACC Professor of Medicine/Cardiology, Director, Clinical Cardiovascular Research, Medical University of South Carolina College of Medicine; Director, Echocardiography Laboratory, Veterans Affairs Medical Center of Charleston

Terrence X O’Brien, MD, MS, FACC is a member of the following medical societies: American College of Cardiology, American Heart Association, American Society of Echocardiography, Heart Failure Society of America, South Carolina Medical Association

Disclosure: Nothing to disclose.

Martin Gerard Keane, MD, FACC, FAHA Professor, Cardiovascular Medicine, Department of Medicine, Temple University School of Medicine

Martin Gerard Keane, MD, FACC, FAHA is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Heart Association, American Society of Echocardiography, Pennsylvania Medical Society, Phi Beta Kappa

Disclosure: Nothing to disclose.

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Shivkumar H Jha, MD; Jatin Dave, MD, MPH; Kishorkumar Desai, MD; and Abraham G Kocheril, MD, FACC, FACP to the development and writing of this article.

Mitral Regurgitation

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