Originally published 30 January 2021. Revised October 2026.

Update note: This post has been reorganised and checked against the 2020 ACC/AHA and 2021 ESC/EACTS guidance. The main changes: the surgical thresholds in the original were muddled and have been corrected, primary and secondary MR are now separated, the acute presentation is described more accurately (the murmur can be soft), and the medical-management line now says what is and is not supported.

Mitral regurgitation (MR) is the retrograde flow of blood from the left ventricle (LV) into the left atrium (LA) through the mitral valve (MV). It is often heard as a holosystolic murmur at the apex, radiating to the left axilla. StatPearls describes it as affecting more than 2% of the population, with prevalence rising with age.¹

Causes: primary and secondary

• Primary (degenerative) MR is a problem of the valve itself. Myxomatous degeneration causing mitral valve prolapse is the most common cause. Others include congenital abnormalities, rheumatic disease, papillary muscle rupture and leaflet perforation. In developing countries, rheumatic heart disease is the commonest cause of mitral valve disease requiring admission.
• Secondary (functional) MR occurs when the valve is structurally normal but the LV is not. LV dilatation or remodelling, ischaemic or non-ischaemic, displaces the papillary muscles and the leaflets fail to meet. Atrial fibrillation and hypertrophic cardiomyopathy can also cause it.

Based on acuity, MR can be acute or chronic. Acute MR has a specific set of causes: rupture of the chordae or papillary muscle (from trauma or STEMI), or infective endocarditis (IE) causing leaflet perforation or chordal rupture.²

Presentation

• Chronic MR: slow LV volume overload, dilatation and hypertrophy. Patients are often well until the LV decompensates, when fatigue and dyspnoea appear. Examination shows cardiomegaly and a holosystolic precordial murmur radiating to the axilla.
• Acute MR: sudden clinical and haemodynamic decompensation, with acute pulmonary oedema. The murmur can be holosystolic, early systolic or barely audible, because the left atrial and left ventricular pressures equalise rapidly. A quiet murmur does not exclude severe acute MR.²

Differential diagnosis

• Tricuspid regurgitation (TR): also a holosystolic murmur, but heard at the lower left sternal edge and typically louder on inspiration. Look for large V waves in the jugular venous pulse, a pulsatile liver and right heart failure.
• Ventricular septal defect (VSD): also holosystolic, but loudest at the lower left sternal edge, often with a thrill, and it does not radiate to the axilla.
• Mitral valve prolapse: a mid-systolic click followed by a late systolic murmur. It is also a cause of MR.
• Papillary muscle dysfunction: ischaemic, or from hypertrophic cardiomyopathy (HOCM).
• Aortic stenosis: an ejection systolic murmur, crescendo-decrescendo in shape, which can be mistaken for MR when it radiates to the apex.

About the images: both figures are original schematic drawings, not recordings. Intensity and timing are illustrative.

Management

Acute MR needs emergency care, usually with critical care support. Most cases need urgent surgical or percutaneous intervention, and urgent revascularisation is the treatment of choice when acute ischaemia has caused papillary muscle dysfunction or rupture.²

Chronic MR: no drug has a guideline recommendation for treating the valve lesion itself. ACE inhibitors and ARBs have been used in asymptomatic patients, but their role is discouraged because the evidence is limited. Beta-blockers show little or no benefit in primary MR, but may improve survival in secondary MR. Diuretics help with congestion. Vasodilators may worsen MR in hypertrophic cardiomyopathy or mitral valve prolapse.¹

Surgery for primary MR. Surveillance and timely intervention are the key factors for outcomes, and observational data suggest that early surgery gives better survival than conservative management in patients with a flail leaflet. Both the ACC/AHA and ESC/EACTS guidelines give a Class I recommendation for surgery in:

• symptomatic patients with severe chronic primary MR, and
• asymptomatic patients with severe MR when the LV ejection fraction (LVEF) is below 60% and/or the LV end-systolic diameter (LVESD) is 40 mm or more. LVESD is the width of the LV cavity at the end of systole, measured on echo. It rises as the LV starts to fail and can no longer empty properly, and in MR the ejection fraction can look normal while this is happening, because the regurgitant volume flows into the low-pressure left atrium.

A reasonable summary is: do not wait for the LV to fail. Refer asymptomatic patients with severe primary MR to an experienced valve centre before LV function falls. Guidelines also support surgery when severe MR is found at the time of other cardiac surgery, and some count new atrial fibrillation or resting pulmonary hypertension as additional triggers for referral. Check the current guideline text for the exact criteria.

Repair or replacement. Valve repair is generally preferred over replacement, depending on the anatomy, the leaflets involved and the chance of a successful repair. In asymptomatic patients with a high likelihood of repair, repair rates above 95% and operative mortality below 1% have been reported.² If atrial fibrillation is present at surgery, a surgical maze procedure is recommended.

Transcatheter edge-to-edge repair (TEER) is for selected symptomatic patients with primary MR who have favourable anatomy and a high or prohibitive surgical risk. It is rated Class IIa by ACC/AHA and Class IIb by ESC/EACTS. In secondary MR, TEER may be offered to highly selected patients with severe symptoms despite optimal medical therapy. The 2020 ACC/AHA criteria are LVEF 20% to 50%, LV end-diastolic diameter of 70 mm or less and pulmonary artery systolic pressure of 70 mmHg or less.

Secondary MR is treated through its cause first: guideline-directed medical therapy for heart failure, revascularisation where appropriate and evaluation for cardiac resynchronisation therapy.

Severity (for reading an echo report)

Severe MR is generally defined as an effective regurgitant orifice area of 0.4 cm² or more, a regurgitant volume of 60 mL or more and a regurgitant fraction of 50% or more. A vena contracta above 7 mm is consistent with severe MR.¹

References

1. Douedi S, Douedi H. Mitral Regurgitation. [Updated 2020 Aug 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK553135/.
2. Chaudhari SS, Chokkalingam Mani B. Mitral Valve Insufficiency. [Updated 2020 May 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557898/.
3. Ibrahim, Bassem Sobhi.”Right ventricular failure.” e-Journal of Cardiology Practice 14(32); Dec 12, 2016.
4. American College of Cardiology. Valvular heart disease guideline comparison: key points (ACC/AHA 2020 and ESC/EACTS 2021). https://www.acc.org/latest-in-cardiology/ten-points-to-remember/2023/08/17/14/47/acc-aha-and-esc-eacts-guidelines
5. Cleveland Clinic. Perspectives on the 2020 ACC/AHA guideline for valvular heart disease: focus on the mitral valve. https://consultqd.clevelandclinic.org/perspectives-on-the-2020-acc-aha-guideline-for-valvular-heart-disease-focus-on-the-mitral-valve