History

Symptoms of mitral regurgitation (MR) may be subtle as its progression may be insidious and patients may self-limit their physical activity.^{[11, 12]}

Acute mitral regurgitation

When associated with coronary artery disease and acute myocardial infarction (typically, inferior myocardial infarction, which may lead to papillary muscle dysfunction), significant acute MR is accompanied by symptoms of impaired LV function, such as dyspnea, fatigue, and orthopnea. In these cases, pulmonary edema is often the initial manifestation because of rapid volume overload on the left atrium and the pulmonary venous system.

Chronic mitral regurgitation

Chronic MR often results from a primary defect of the mitral valve apparatus with subsequent progressive enlargement of the left atrium and ventricle. In this state, patients may remain asymptomatic for years. Patients may have normal exercise tolerance until systolic dysfunction of the LV develops, at which point they may experience symptoms of a reduced forward cardiac output (ie, fatigue, dyspnea on exertion, or shortness of breath). With time, patients may feel chest palpitations if atrial fibrillation develops as a result of chronic atrial dilatation.

Patients with LV enlargement and more severe disease eventually progress to symptomatic congestive heart failure with pulmonary congestion and edema. At this stage of LV dilatation, the myocardial dysfunction often becomes irreversible.

Physical Examination

On palpation, a brisk carotid upstroke and hyperdynamic cardiac impulse may be noted, and a prominent left ventricular (LV) filling wave may be present.

On auscultation, S₁ may be diminished in acute mitral regurgitation (MR) and chronic severe MR with defective valve leaflets, and wide splitting of S₂ may occur due to early closure of the aortic valve. S₃ may be present due to LV dysfunction or as a result of increased blood flow across the mitral valve. P₂ may be accentuated if pulmonary hypertension is present.

If murmurs are present, note and characterize the following features:

Quality: Usually high-pitched, blowing
Location: Usually best heard over the apex; usually radiates to the left axilla or subscapular region: posterior leaflet dysfunction causes murmur to radiate to the sternum or aortic area, and anterior leaflet dysfunction causes murmur to radiate to the back or top of the head
Duration: Usually holosystolic, may be confined to early systole in acute MR, may be confined to late systole in MVP or papillary muscle dysfunction (S₁ will probably be normal in these cases since initial closure of mitral valve cusps is unimpeded, and a midsystolic click preceding murmur is suggestive of MVP)
Intensity: Little correlation exists between intensity of murmur and severity of MR; intensity may be diminished in severe MR caused by LV dysfunction, acute myocardial infarction, or periprosthetic valve regurgitation

Differential Diagnoses

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Media Gallery

Transthoracic echocardiogram demonstrating severe mitral regurgitation with heavily calcified mitral valve and prolapse of the posterior leaflet into the left atrium.
Transesophageal echocardiogram demonstrating prolapse of both mitral valve leaflets during systole.
Transthoracic echocardiogram demonstrating bioprosthetic mitral valve dehiscence with paravalvular regurgitation.

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Table 1. Stages of Progression of Chronic Mitral Regurgitation

Table 1. Stages of Progression of Chronic Mitral Regurgitation

Stage	Valve Anatomy	Valve Hemodynamics*	Hemodynamic Consequences	Symptoms
A: Primary MR	Mild MV prolapse with normal coaptation Mild valve thickening and leaflet restriction	No MR jet or small central jet area < 20% LA Small vena contracta < 0.3 cm	None	None
A: Secondary MR	Normal valve leaflets, chords and annulus in patient with CAD or cardiomyopathy	No MR jet or small central jet area < 20% LA Small vena contracta < 0.3 cm	Normal or mildly dilated LV with infarction or ischemia regional wall motion abnormalities Primary myocardial disease with LV dilation and systolic dysfunction	Symptoms of coronary ischemia or HF that respond to revascularization and medical therapy
B: Primary MR	Severe MV prolapse with normal coaptation Rheumatic valve changes, leaflet restriction, and loss of central coaptation Prior IE	Central jet MR area 20-40% LA or late systolic eccentric jet MR Vena contracts < 0.7 cm Regurgitant volume < 60 mL Regurgitant fraction < 50% ERO < 0.40 cm ² Angiographic grade 1-2+	Mild LA enlargement No LV enlargement Normal Pulmonary pressure	None
B: Secondary MR	Regional wall motion abnormalities with mild tethering of mitral leaflet Annular dilation with mild loss of central coaptation of the mitral leaflets	Regurgitant volume < 30 mL Regurgitant fraction < 50% ERO < 0.20 cm ^2†	Regional wall motion abnormalities with reduced LV systolic function LV dilation and systolic dysfunction	Symptoms of coronary ischemia or HF that respond to revascularization and medical therapy
C: Primary MR	Severe MV prolapse with loss of coaptation or flail leaflet Rheumatic valve changes, leaflet restriction, and loss of central coaptation Prior IE Thickening of leaflets with radiation heart disease	Central jet MR area >40% LA or holosystolic eccentric jet MR Vena contracta ≥0.7 cm Regurgitant volume ≥60 mL Regurgitant fraction ≥50% ERO ≥0.40 cm ² Angiographic grade 3-4+	Moderate to severe LA enlargement LV enlargement Pulmonary hypertension may be present Stage C1: LVEF >60% and LVESD < 40 mm Stage C2: LVEF ≤60% and LVESD ≥40 mm	None
C: Secondary MR	Regional wall motion abnormalities and/or LV dilation with severe tethering of mitral leaflet Annular dilation with severe loss of central coaptation of the mitral leaflets	Regurgitant volume ≥30 mL Regurgitant fraction ≥50% ERO ≥0.20 cm ^2†	Regional wall motion abnormalities with reduced LV systolic function LV dilation and systolic dysfunction	Symptoms of coronary ischemia or HF that respond to revascularization and medical therapy
D: Primary MR	Severe MV prolapse with loss of coaptation or flail leaflet Rheumatic valve changes, leaflet restriction, and loss of central coaptation Prior IE Thickening of leaflets with radiation heart disease	Central jet MR area >40% LA or holosystolic eccentric jet MR Vena contracta ≥0.7 cm Regurgitant volume ≥60 mL Regurgitant fraction ≥50% ERO ≥0.40 cm ² Angiographic grade 3-4+	Moderate or severe LA enlargement LV enlargement Pulmonary hypertension present	Decreased exercise tolerance Exertional dyspnea
D: Secondary MR	Regional wall motion abnormalities and/or LV dilation with severe tethering of mitral leaflet Annular dilation with severe loss of central coaptation of the mitral leaflets	Regurgitant volume ≥30 mL Regurgitant fraction ≥50% ERO ≥0.20 cm ^2†	Regional wall motion abnormalities with reduced LV systolic function LV dilation and systolic dysfunction	HF symptoms due to MR persist after revascularization and medical therapy Decreased exercise tolerance Exertional dyspnea
*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.

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Author

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.

Coauthor(s)

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.

Specialty Editor Board

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 College of Physicians, American Heart Association, American Thoracic Society

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

Chief Editor

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.

Acknowledgements

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 Clinical Presentation

History

Acute mitral regurgitation

Chronic mitral regurgitation

Physical Examination

References

Tables

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