Mitral regurgitation: primary and secondary

Overview and definition

Mitral regurgitation is systolic backflow from the left ventricle into the left atrium through leaflets that fail to coapt.^[33] The ESC/EACTS 2025 guideline frames the first decision: MR comes either from anatomical changes of the valve apparatus (primary) or from LV or LA dilatation and dysfunction (secondary).^[1] The 2020 ACC/AHA guideline puts it the same way: primary MR is a disease of the valve apparatus; secondary MR is a disease of the ventricle or atria.^[2] ACC/AHA 2020 also labels chronic primary MR "degenerative" and chronic secondary MR "functional".^[2]

Why does this matter at the bedside? Primary MR is a mechanical problem with a mechanical solution, and correcting it before irreversible change can be curative.^[2] In secondary MR the leak is one component of a myocardial disease, so restoring valve competence is not curative.^[2] ESC/EACTS 2025 asks for the two populations to be kept apart because natural history, prognosis and management differ.^[1]

Classification

^[1]

Per ESC/EACTS 2025, atrial secondary MR is most frequently defined by four key criteria, joined by "AND":^[1]

1. Preserved LVEF (50% or more) without regional wall motion abnormalities or leaflet tethering.
2. No or mild LV dilatation, given in brackets as: LV end-diastolic dimension below 56 mm in women and below 63 mm in men; indexed LV end-diastolic volume below 71 mL/m² in women or below 79 mL/m² in men. The guideline separates the two measures with a semicolon and does not say whether one or both are required.
3. Mitral annular dilatation, with an anteroposterior diameter above 35 mm.
4. An enlarged left atrium, LAVI above 34 mL/m².

^[1]

Clinical criteria, a history of AF and/or a diagnosis of HFpEF, are also useful. In advanced stages, late LV damage from continuing volume overload can blur the line between atrial and ventricular forms.^[1]

^{[1] [2]}

ACC/AHA 2020 stages of chronic primary MR

The ACC/AHA 2020 guideline grades chronic primary MR in four stages (its Table 17). Not every haemodynamic criterion will be present in every patient. Grading depends on data quality and integration of the parameters with other clinical evidence.^[2]

^[2]

Epidemiology and risk factors

^{[1] [23]}

MR affects more than 2% of the general population, and prevalence rises with age.^[33] In high-income countries the commonest cause of chronic primary MR is mitral valve prolapse. Younger patients tend to have Barlow's myxomatous degeneration of both leaflets, while older patients have fibroelastic deficiency with chordal rupture.^[2] Less common causes include endocarditis, connective tissue disorders, rheumatic disease, cleft mitral valve and radiation heart disease.^[2]

Dilated or ischaemic cardiomyopathy are the most frequent causes of severe ventricular secondary MR.^[1] Atrial secondary MR is due to annular dilation and is seen in patients with long-standing AF and/or HFpEF; age 65 or over, female sex, LA dilatation and diastolic dysfunction predispose to it.^[1] ESC/EACTS 2025 calls AF the main trigger of atrial secondary MR and TR.^[1]

Acute MR arises from endocarditis, chordal rupture or papillary muscle rupture after myocardial infarction.^[1] Papillary muscle rupture usually follows an inferior ST-elevation infarction.^[2]

Pathophysiology

Chronic primary MR is a volume-overload lesion. When progressive or severe, the regurgitant flow causes chronic volume overload of both the left atrium and the left ventricle.^[33][2] MR may beget MR: LV dilation stresses the apparatus, the leak may worsen, and the ventricle dilates further.^[2] Longstanding volume overload ends in irreversible LV dysfunction and a poorer prognosis.^[2]

Why a "normal" EF misleads in primary MR. The ventricle keeps ejecting late in systole into a low-impedance left atrium. ACC/AHA 2020 therefore uses a higher cut-off for normal LVEF in MR than in other heart disease.^[2] LVEF is load dependent and often overestimates LV function in MR. Global longitudinal strain may warn of decline before LVEF becomes abnormal.^[2]

^{[2] [12] [33] [1]}

Secondary MR starts outside the leaflets. ESC/EACTS 2025 describes a grossly normal valve made incompetent by altered LV and LA geometry, dyssynchrony, and imbalance between closing and tethering forces.^[1] In the ventricular form, the dilated LV displaces the papillary muscles. The leaflets are tethered and the annulus dilates, so the leaflets cannot coapt.^[2] Grayburn's framework adds that EROA depends on LV end-diastolic volume; this underpins the proportionate versus disproportionate idea used to compare COAPT with MITRA-FR.^[12]

Prolapse and arrhythmia. In a small subgroup, primary MR is associated with more ventricular arrhythmias, and sudden cardiac death has been reported in individual cases, especially with Barlow's disease. This arrhythmic burden is independent of MR severity and is linked to mitral annular disjunction.^[1]

Acute severe MR. A sudden volume load raises LA and pulmonary venous pressure, giving pulmonary congestion and hypoxia. Forward output falls at the same time.^[2]

Clinical presentation

Chronic primary MR. Symptoms are exertional dyspnoea, orthopnoea and declining exercise tolerance.^[2] Up to a quarter of patients with degenerative disease may have no symptoms despite severe regurgitation.^[28] Some patients may not recognise their symptoms, may deny them, or may limit their activity to stay asymptomatic.^[2] If intervention is delayed, the haemodynamic load can lead to LV remodelling, AF, pulmonary hypertension and heart failure.^[33]

Acute severe MR. Expect pulmonary congestion with low forward output.^[2] The diagnosis is often missed or delayed because the presentation differs so much from chronic MR.^[13] After infarction, sudden hypotension, recurrent chest pain, a new murmur, pulmonary congestion or raised JVP should raise suspicion of a mechanical complication.^[4]

Secondary MR. Secondary MR is common in heart failure, especially HFrEF.^[3] Decompensation of chronic HF may follow a new ischaemic event, an arrhythmia, infection or volume overload.^[1] Patients with atrial secondary MR are typically elderly with AF.^[1]

Differential diagnosis

^{[1] [2] [6] [4] [5] [37] [38]}

Clinical and bedside assessment

Chronic MR produces a holosystolic murmur best heard at the apex, radiating toward the left axilla.^[33] In acute severe MR, falling LV systolic pressure limits the gradient and confines the leak to early systole. The murmur may be short and unimpressive.^[2]

Separate HCM at the bedside: its classic murmur is a harsh crescendo-decrescendo systolic murmur, often from SAM with LVOT obstruction. Seek LVOT obstruction at rest and, when possible, with Valsalva or standing from a squat.^[6] When a patient with severe primary MR says they have no symptoms, a formal treadmill test can establish true exercise tolerance and can form a baseline.^[2]

Where on the chest wall a systolic murmur is heard is the most useful single finding. Use the third left parasternal space as the landmark.^[38] A broad apical murmur suggests significant MR (LR 6.8). A left lower sternal murmur points to significant TR (LR 8.4). An apical-base murmur points to raised aortic velocity (LR 9.7).^[38]

^{[37] [38]}

No single manoeuvre is 100% accurate, but a combination of manoeuvres can locate the origin of a systolic murmur accurately at the bedside.^[37] MR and VSD respond in parallel to every manoeuvre, so manoeuvres do not separate them.^[37] Examination cannot reliably tell severe aortic stenosis from less severe stenosis.^[38]

Investigations

^{[1] [2]}

Watch the measurement traps. In assessing primary MR, ESC/EACTS 2025 says colour-flow settings must be accurate to avoid overestimating MR.^[1] In secondary MR, 2D PISA underestimates the true ERO because the proximal convergence is crescentic in shape.^[2] A pulmonary capillary wedge v-wave can inform about MR severity but is neither sensitive nor specific.^[1] In primary MR, the ESC/EACTS 2025 text says genetic testing is not recommended in routine practice.^[1]

Assess secondary MR after medical therapy is optimised, with the patient euvolaemic and normotensive.^[1][3]

Management: acute severe MR

In acute heart failure caused by valve disease, untreated decompensation leads to cardiogenic shock.^[29] ESC/EACTS 2025 notes that, apart from papillary muscle rupture, acute primary MR rarely leads to cardiogenic shock.^[1]

1. Image now. Echocardiography is immediate when a mechanical complication is suspected.^[4] After infarction with sudden haemodynamic instability, a hyperdynamic LV on TTE and no other cause for the deterioration, TOE can be especially helpful in detecting papillary muscle or chordal rupture.^[2]
2. Unload the ventricle. Vasodilators lower aortic impedance, steering flow forward and reducing the leak. ACC/AHA 2020 says this is usually done by infusing an easily titratable agent such as sodium nitroprusside or nicardipine; doses per local formulary and specialist guidance.^[2] ESC/EACTS 2025 says nitroprusside has been used as a bridge to intervention in acute severe primary MR without signs of hypotension.^[1] Vasodilator use is often limited by systemic hypotension.^[2]
3. Treat congestion and output. In acute primary MR, the ESC/EACTS 2025 text (not a recommendation-table row) says inotropes and diuretics are usually indicated to reduce filling pressure; an intra-aortic balloon pump further reduces afterload in exceptional cases.^[1] Counterpulsation raises forward output and lowers regurgitant volume.^[2]
4. Bridge the unstable patient. A percutaneous circulatory assist device may stabilise the patient before the procedure.^[2] ESC 2023 ACS says IABP should be considered while awaiting surgery for mechanical complications.^[4]
5. Fix the valve urgently. The ESC/EACTS 2025 text, rather than a recommendation-table row, says urgent surgery or transcatheter treatment is indicated for acute severe primary MR.^[1] Papillary muscle rupture and endocarditis generally need surgical valve replacement. Acute degenerative chordal rupture can be repaired surgically, or treated with TEER in high-risk patients.^[1]

^{[1] [2] [4]}

ESC 2023 ACS: surgery is currently regarded as the treatment of choice for mechanical complications of ACS; percutaneous strategies are occasionally used in selected patients with a prohibitive risk profile or contraindications to surgery.^[4] For acute ventricular secondary MR, particularly after infarction, ESC/EACTS 2025 notes increasing evidence for M-TEER, with lower mortality than surgery or medical treatment in propensity-matched analyses.^[1]

Management: chronic primary MR

The decision on mode of intervention, or conservative care, belongs to the Heart Team. It weighs clinical and anatomical features, procedural risk and patient preference.^[1]

^{[1] [2]}

Surgery

ESC/EACTS 2025 recommends MV repair as the surgical technique for severe primary MR when the result is expected to be durable (I B). Its text calls surgical repair, including annuloplasty, the treatment of choice in operable patients when an optimal and durable result is expected. According to contemporary data, repair can be performed with a low mortality risk (1.2%) in appropriately selected patients.^[1] Compared with replacement, repair has been associated with lower peri-operative mortality and better long-term survival and function.^[1] If repair is not feasible, replace the valve and preserve the subvalvular apparatus.^[1]

ACC/AHA 2020 makes repair the procedure of choice for isolated severe primary MR limited to less than half the posterior leaflet; replacement is inappropriate unless repair has been attempted and failed. Repair there is associated with operative mortality below 1%, about 95% freedom from reoperation and over 80% freedom from recurrent moderate or severe (grade 3 or more) MR at 15 to 20 years.^[2] Complex anterior or bileaflet repairs give about 80% freedom from reoperation and 60% freedom from recurrent moderate or severe MR at 15 to 20 years.^[2] A poor repair is worse than a replacement.^[2]

Volume matters: hospital mortality is on average 50% lower in the highest-volume hospitals performing 50 repairs per year.^[2] ESC/EACTS 2025 says repair of calcified or rheumatic valves is challenging and should be attempted in experienced Heart Valve Centres.^[1] In an RCT cited by ESC/EACTS 2025, mini-thoracotomy was associated with shorter hospital stay and improved physical activity in the first 6 weeks, a difference gone by 12 weeks. A national registry showed less clear benefit. Minimally invasive MV surgery may be considered at experienced centres to reduce length of stay and accelerate recovery (IIb B).^[1] In the UK RCT, repair rates were about 96% with either approach.^[21][1]

Transcatheter options

ACC/AHA 2020 found surgery superior to TEER, so TEER is for severely symptomatic patients at high or prohibitive surgical risk.^[2] ESC/EACTS 2025 says TEER should be considered in symptomatic patients with severe primary MR who are anatomically suitable and at high surgical risk according to the Heart Team (IIa B). In 2021 the corresponding row was IIb B. Residual MR and mean transmitral gradient track outcome after TEER.^[1]

• EVEREST II: the authors suggest that, in patients undergoing de novo MV surgery or surgery after MitraClip, anterior leaflet pathology is strongly associated with valve replacement; the clip had a repair rate similar to surgery through 1 year but imparted a risk of replacement of a potentially repairable valve.^[9]
• TVT registry: 19,088 degenerative MR patients (median age 82); MR success in 88.9%; success, compared with an unsuccessful procedure, was linked to lower 1-year mortality (adjusted HR 0.49).^[20]
• CLASP IID: PASCAL was noninferior to MitraClip in prohibitive-risk degenerative MR; 6-month MR 2+ or less 97.9% vs 95.7%.^[22]
• TMVI: very effective in abolishing MR in selected high-risk patients, particularly those with anatomy complex for TEER, but limited by availability, screening failure, LVOT obstruction and valve thrombosis. ESC/EACTS 2025 notes limited data for primary MR and for mid-term prosthesis durability.^[1]

Medical therapy

ESC/EACTS 2025 finds no evidence for prophylactic afterload reduction in chronic primary MR without signs of LV dysfunction or criteria for intervention. Patients with impaired LV function should receive GDMT per heart failure guidelines.^[1] ACC/AHA 2020 adds that vasodilators may increase prolapse and worsen MR. Hypertension still needs treatment because higher LV systolic pressure worsens the leak.^[2]

Evidence for acting early

• Early surgery cohort (Circulation 2025): 1063 asymptomatic patients with severe degenerative MR and preserved LV function, median follow-up 12 years. Cardiovascular death was 1.5% with early surgery vs 10.4% with conventional care (HR 0.17); no operative deaths; repair in 97%.^[31]
• Lancet review: repair improves outcome compared with replacement, and reduces mortality of severe organic MR by about 70%.^[7]
• Flail leaflets: ACC/AHA 2020: in excellent hands, patients with severe MR from flail leaflets who undergo early operation have less HF and lower mortality than with watchful waiting.^[2] In the MIDA flail-leaflet registry, over a median follow-up of 3.9 years, linearised yearly event rates under non-surgical management were 5.4% for AF, 8.0% for HF and 2.6% for death.^[34] In a 1996 study of flail-leaflet MR first diagnosed in 1980–1989, medically treated patients had 6.3% yearly mortality.^[35]

^{[1] [3] [2]}

Management: ventricular secondary MR

^{[1] [3] [39]}

The two ESC documents differ in level of evidence (A versus B1). Their population wording also differs: ESC/EACTS 2025 says impaired LVEF (below 50%) and ventricular SMR, and ESC HF 2026 says HFrEF and secondary MR.^[1][3] ACC/AHA 2020 states that mitral TEER is indicated to improve symptoms and prolong life in a select subset with chronic severe secondary MR, LV systolic dysfunction and persistent severe symptoms on optimal GDMT.^[2]

^{[1] [2] [3]}

COAPT versus MITRA-FR

^{[10] [11] [2]}

ESC/EACTS 2025 says the divergence might be explained by effect size, trial design, patient selection and follow-up, echo grading, GDMT use and technical factors.^[1] Grayburn's reading is that MITRA-FR enrolled MR proportionate to LV dilatation, whose clinical outcomes during long-term follow-up did not differ from medically treated controls.^[12]

• COAPT through 5 years: HF hospitalisation 33.1% vs 57.2% per year (HR 0.53); all-cause death 57.3% vs 67.2% (HR 0.72).^[18]
• RESHAPE-HF2 (HF with moderate-to-severe functional MR): HF hospitalisation or CV death 37.0 vs 58.9 events per 100 patient-years at 24 months (rate ratio 0.64). ESC/EACTS 2025 notes CV mortality alone was not significantly reduced.^[26][1]
• Meta-analysis of the three RCTs (cited by ESC/EACTS 2025): HF rehospitalisation at 24 months HR 0.63, with no significant difference in all-cause or CV death.^[1]
• MATTERHORN: TEER was noninferior to surgery within 1 year (16.7% vs 22.5%), with fewer major adverse events within 30 days (14.9% vs 54.8%); 84% had ventricular SMR.^[27][1]
• Beyond COAPT criteria: in the EXPANDed studies, non-COAPT-like patients had MR, HF hospitalisation and quality-of-life improvements at 1 year comparable with COAPT-like patients. Cluster analysis of secondary MR phenotypes in COAPT and MITRA-FR found outcomes after M-TEER better predicted by multidimensional phenotypes (cardiac damage, surgical risk and comorbidity burden) than by any single domain.^[30][32]
• SGLT2 inhibition: in EFFORT (HF with NYHA class II or III, EF 35% to below 50%, and functional MR with EROA above 0.1 cm²), ertugliflozin reduced EROA and regurgitant volume (by 11.2 mL) compared with placebo.^[24]

Surgery in ventricular secondary MR

In ventricular SMR without relevant CAD, ESC/EACTS 2025 keeps indications for isolated MV surgery restrictive, owing to procedural risk and no proven mortality benefit.^[1] Undersized annuloplasty had high recurrence in an RCT, and replacement is usually required when tenting area exceeds 1.35 cm²/m² BSA.^[1] ACC/AHA 2020 prefers replacement over repair. In its cited RCT of repair versus replacement in severe ischaemic MR, survival and LV remodelling did not differ at 2 years, but moderate or severe MR recurred more often after repair, with more HF and repeat hospitalisation.^[2] Treatment of moderate ischaemic secondary MR at CABG remains controversial: meta-analyses including four RCTs of CABG with versus without MV surgery showed lower recurrent MR but no benefit in mortality or clinical outcomes.^[1] ESC/EACTS 2025 says MV surgery may be considered in moderate SMR undergoing CABG (IIb B). In severe ventricular SMR without concomitant CAD, it may also be considered in symptomatic patients without advanced HF who are not suitable for TEER (IIb C).^[1]

Management: atrial secondary MR

• Recognise and treat the underlying causes; manage associated HFpEF and AF according to their guidelines. ESC/EACTS 2025 encourages SGLT2 inhibitors in HFpEF.^[1]
• Rhythm control may reduce atrial SMR and reverse LA dilatation, though data are limited.^[1] ACC/AHA 2020 notes that successful AF ablation may reduce or eliminate MR.^[2]
• ESC/EACTS 2025: MV surgery, surgical AF ablation if indicated, and LAAO should be considered in symptomatic patients with severe atrial SMR under optimal medical therapy (IIa B).^[1] Observational studies suggest surgical annuloplasty is effective and durable because it counteracts the main mechanism; combining it with a Maze procedure and LAAO may add benefit.^[1] ACC/AHA 2020: isolated annular dilation has the highest repair rate in the STS database (85%).^[2]
• ESC/EACTS 2025: TEER may be considered in symptomatic severe atrial SMR when the patient is not eligible for surgery after optimised medical therapy including rhythm control, when appropriate (IIb B). Beware a raised gradient from planar coaptation, a large jet and a limited MV area.^[1]

^{[1] [2]}

Specific scenarios

Papillary muscle rupture. Complete rupture causes very severe, poorly tolerated MR, and prompt surgery is lifesaving.^[2] Severe acute MR after myocardial infarction has an incidence below 1% but frequently causes haemodynamic instability, pulmonary oedema and cardiogenic shock; medical management has the worst prognosis.^[25] Mechanical complications occurred in 0.27% of STEMI cases, with 42.4% in-hospital mortality.^[4]

Endocarditis. In a population cohort with mitral valve prolapse, the 15-year risk of IE was 1.1%. No cases occurred without previously diagnosed MR, and incidence was higher with moderate or worse MR or a flail leaflet.^[36] Heart failure is the main indication for urgent or emergency surgery in IE.^[5] Emergency surgery is indicated for new-onset NYHA class IV HF symptoms, pulmonary oedema and/or cardiogenic shock, irrespective of infection status, when considered non-futile. Urgent surgery is indicated for milder HF (NYHA II–III) with severe regurgitation or echocardiographic signs of haemodynamic compromise (raised LV end-diastolic or LA pressure, or moderate or severe pulmonary hypertension), or large vegetations.^[5]

Barlow's disease and annular disjunction. CMR-detected fibrosis is linked with ventricular arrhythmias and sudden death.^[1] Ring annuloplasty stabilises the posterior annulus and may lower arrhythmic risk.^[1]

Rheumatic and radiation disease. Rheumatic valves are less suitable for repair than complex degenerative valves.^[2] In radiation-induced MV disease, thickened leaflets with restricted movement often limit M-TEER and risk iatrogenic stenosis.^[1]

Multiple valve disease. ESC/EACTS 2025 recommends MV surgery in patients with severe MR undergoing surgery for another valve (I C).^[1] In a transcatheter strategy, a staged approach starting with the downstream lesion (aortic, then mitral and tricuspid) is generally preferred.^[1]

Complications and pitfalls

• Trusting a normal EF. ACC/AHA 2020: in severe primary MR, an LVEF below 60% or LVESD of 40 mm or more already means LV systolic dysfunction.^[2]
• Grading SMR in the wrong state. Do it after GDMT optimisation, euvolaemic and normotensive.^[1]
• Calling atrial SMR primary. Pseudo-prolapse in advanced stages has occasionally caused misclassification.^[1]
• AF. Patients with valve disease and AF have a high incidence of thromboembolic or bleeding complications.^[1] ACC/AHA 2020: in chronic primary MR, new-onset AF is an indication for repeat TTE to look for change in MR severity and LV status.^[2] In asymptomatic severe primary MR without LV dysfunction, ESC/EACTS 2025 says MV surgery should be considered with AF secondary to MR (IIa B), and AF counts towards the three-criteria Class I repair row (low-risk patients, durable result likely).^[1] It recommends DOACs in preference to VKAs for stroke prevention in AF with MR when OAC is indicated (I A). It does not recommend DOACs with AF and rheumatic MS with an MVA of 2.0 cm² or less (III B).^[1] In AF patients having valve surgery, surgical LA appendage closure is recommended as an adjunct to OAC (I B). Concomitant surgical ablation is recommended in MV surgery with AF suitable for rhythm control, according to an experienced team of electrophysiologists and arrhythmia surgeons (I A).^[1] In LAAOS III, surgical LAAO in AF patients with CHA₂DS₂-VASc 2 or more undergoing cardiac surgery was associated with a 33% reduction in stroke or systemic embolism at a mean follow-up of 3.8 years.^[1]
• After TEER for primary MR. Residual MR and raised gradients are commoner than after surgical repair. Surgery after failed TEER, although rare, is associated with higher peri-operative mortality and low repair rates.^[1]
• After annuloplasty for primary MR. Recurrent MR frequently leads to repeat surgery, usually replacement; transcatheter options are reserved for selected high-risk patients.^[1]

^{[1] [2]}

Prognosis and follow-up

Severe organic MR treated medically carries about 6% yearly mortality in patients aged 50 or older.^[7] Chronic severe primary MR reaches a trigger for surgery at an average rate of about 8% per year.^[2] LA diameter was the strongest independent echo predictor of event-free survival in asymptomatic severe primary MR.^[19] Repair for prolapse at experienced centres gives 87.5% freedom from moderate or severe MR at 20 years.^[1]

Ventricular SMR carries the worse long-term outlook of the two secondary forms.^[1] In HF with LV systolic dysfunction, chronic secondary MR of any severity is associated with a worse prognosis than no MR.^[2] Even after TEER, 73.6% of COAPT device patients died or were hospitalised for HF within 5 years.^[1]

^{[1] [2]}

Special populations

Women. One recent study found higher long-term mortality after repair for primary MR in women, and ESC/EACTS 2025 cites evidence for considering lower women-specific LVESD cut-offs. Atrial SMR affects more women than men.^[1]

Pregnancy. Regurgitant lesions are generally well tolerated.^[1] Most women with asymptomatic severe MR tolerate the haemodynamic changes of pregnancy, and there is no evidence that pregnancy accelerates LV dysfunction. Depressed LV systolic function and PASP above 50 mm Hg are high-risk features for HF during pregnancy.^[2] Valve surgery during pregnancy is reasonable only in the rare woman with severe regurgitation and NYHA class IV symptoms refractory to medical therapy.^[2] Intervention thresholds are higher in an asymptomatic woman who might become pregnant, because repair may fail and a prosthetic valve be needed.^[2]

Older and high-risk patients. High-risk and elderly patients with chronic primary MR, though uncommon, may benefit from M-TEER.^[1] GDMT alone is the only option for very frail patients with ventricular SMR or limited life expectancy.^[1]

Non-cardiac surgery. In asymptomatic severe MR with preserved LV function, NCS can usually be performed safely. Before elective NCS in severe ventricular SMR, medical therapy should be optimised. If symptoms persist and NCS is intermediate or high risk, the ESC/EACTS 2025 text, which has no recommendation-table row for this, says TEER should be considered after Heart Team discussion based on clinical and anatomical selection criteria.^[1]

Guidelines and regional differences

^{[1] [2] [3]}

What is new in ESC/EACTS 2025 for MR starts with separating atrial from ventricular secondary MR. In primary MR it brings refined intervention criteria in asymptomatic patients, minimally invasive surgery to shorten stay and large-scale data on TEER in high-risk patients. In ventricular SMR it adds longer-term follow-up data and two new RCTs.^[1] The list below gives every new and revised row in its MR sections (9.1, 9.2 and 13.3), each with its own population. It then gives the revised CAD and AF rows whose 2021 or 2025 wording names SMR, MV or transcatheter valve procedures.^[1]

• New: surgical repair in low-risk asymptomatic severe primary MR without LV dysfunction, when a durable result is likely, if at least three criteria are present: AF, resting SPAP above 50 mmHg, LA dilatation (LAVI 60 mL/m² or more or LA diameter 55 mm or more), and secondary TR of at least moderate grade (I B).^[1]
• New: in severe primary MR, minimally invasive MV surgery at experienced centres, to reduce length of stay and accelerate recovery (IIb B).^[1]
• New: MV surgery, surgical AF ablation if indicated, and LAAO in symptomatic severe atrial SMR under optimal medical therapy (IIa B).^[1]
• New: TEER in symptomatic severe atrial SMR not eligible for surgery after optimised medical therapy including rhythm control, when appropriate (IIb B).^[1]
• New: MV surgery in moderate SMR undergoing CABG (IIb B), and in severe MR undergoing surgery for another valve (I C).^[1]
• Revised, TEER in primary MR: IIb B in 2021, for symptomatic patients meeting echo eligibility criteria, inoperable or at high surgical risk per the Heart Team, and in whom it was not futile. In 2025 it is IIa B, for symptomatic severe primary MR in patients who are anatomically suitable and at high surgical risk per the Heart Team.^[1]
• Revised, TEER in ventricular SMR: IIa B in 2021, for selected symptomatic patients not eligible for surgery who met criteria suggesting an increased chance of responding. In 2025 it is I A in severe ventricular SMR without concomitant CAD, for haemodynamically stable, symptomatic patients with LVEF below 50% and persistent severe SMR despite optimised GDMT and CRT (if indicated), meeting specific criteria.^[1]
• Revised, TEER outside the criteria: IIb C in 2021, in selected high-risk symptomatic patients not eligible for surgery and not fulfilling the criteria suggesting a response, after careful evaluation for a ventricular assist device or transplant. In 2025 it is IIb B, for symptom improvement in selected symptomatic patients with severe ventricular SMR without concomitant CAD not meeting the criteria, after careful evaluation of LVAD or transplantation.^[1]
• Revised, PCI before TEER: IIa C in 2021, for symptomatic patients judged not appropriate for surgery by the Heart Team, with TEER in case of persisting severe SMR. In 2025 it is IIb C, in symptomatic chronic severe ventricular SMR with non-complex CAD, with TEER after re-evaluating MR.^[1]
• Revised, surgery with PH or AF in primary MR: IIa B in 2021, in asymptomatic patients with preserved LV function (LVESD below 40 mm and LVEF above 60%) and AF secondary to MR or PH (SPAP at rest above 50 mmHg). In 2025 it stays IIa B, in asymptomatic severe primary MR without LV dysfunction (LVESDi below 20 mm/m² is added), with PH or AF secondary to MR.^[1]
• Revised, repair with LA dilatation: IIa B in 2021, in low-risk asymptomatic patients with LVEF above 60%, LVESD below 40 mm and significant LA dilatation (LAVI 60 mL/m² or more or LA diameter 55 mm or more), in a Heart Valve Centre when a durable repair is likely. In 2025 it stays IIa B, now specifying severe primary MR without LV dysfunction, including LVESDi below 20 mm/m².^[1]
• Revised, isolated surgery in ventricular SMR without concomitant CAD: IIb C in 2021, valve surgery in symptomatic patients judged appropriate for surgery by the Heart Team. In 2025 it stays IIb C, MV surgery in symptomatic severe ventricular SMR without advanced HF in patients not suitable for TEER.^[1]
• Revised CAD row: coronary angiography in the evaluation of severe SMR (I C in 2021) became invasive coronary angiography in the evaluation of CAD in severe ventricular SMR (I C).^[1]
• Revised CAD row, PCI before transcatheter valve intervention: in 2021 there were two rows. PCI should be considered with a primary indication for TAVI, or for transcatheter MV intervention, and coronary diameter stenosis above 70% in proximal segments (IIa C each). In 2025 these became one row: PCI may be considered in patients with a primary indication to undergo transcatheter valve interventions and coronary artery stenosis of 70% or more in proximal segments of main vessels (IIb B).^[1]
• Revised AF row: concomitant AF ablation should be considered in valve surgery (IIa A in 2021). In 2025, concomitant surgical ablation is recommended in MV surgery with AF suitable for a rhythm control strategy, according to an experienced team of electrophysiologists and arrhythmia surgeons (I A).^[1]

Australia and New Zealand

Exam pearls

• Primary MR is a valve disease; secondary MR is a ventricular or atrial disease. Name the mechanism before naming a treatment.^[1][2]
• In primary MR, ESC/EACTS 2025 lists LVESDi 20 mm/m² or more alongside LVEF 60% or less and LVESD 40 mm or more; ACC/AHA 2020 uses LVEF and LVESD only.^[1][2]
• In asymptomatic severe primary MR without LV dysfunction, ESC/EACTS 2025 recommends repair in low-risk patients when a durable result is likely if at least three criteria are present (I B). The criteria are AF, resting SPAP above 50 mmHg, LAVI 60 mL/m² or more or LA diameter 55 mm or more, and secondary TR of at least moderate grade.^[1]
• TEER selection: ESC/EACTS 2025 Table 7 and ACC/AHA 2020 (which calls the COAPT enrolment criteria the current standard) share NYHA II or more, LVEF 20–50%, LVESD 70 mm or less, SPAP 70 mmHg or less.^[1][2]
• TEER in ventricular SMR moved from Class IIa, level B in 2021 (selected symptomatic patients not eligible for surgery who met criteria suggesting an increased chance of responding) to Class I, level A in ESC/EACTS 2025. That row covers severe ventricular SMR without concomitant CAD in haemodynamically stable, symptomatic patients with LVEF below 50% and persistent severe SMR despite optimised GDMT and CRT if indicated, meeting its criteria.^[1] The 2026 ESC heart failure guideline grades TEER Class I, level B1 for haemodynamically stable, symptomatic HFrEF with persistent severe secondary MR despite optimised therapy and CRT if indicated, who fulfil specific clinical and echo criteria.^[3]
• In acute severe MR the murmur may be short and unimpressive (ACC/AHA 2020); ESC 2023 ACS says immediate echocardiographic assessment is indicated when a mechanical complication is suspected.^[2][4]

References42ShowHide

1. [1]Praz F, Borger MA, et al. 2025 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J, 2025.PMID 40878295
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