Mitral Valve Prolapse

Meet the patient

A 28-year-old woman is sent to you by her GP, who heard "an extra sound" at a routine examination. She is thin, mildly anxious, and has occasional palpitations and sharp, fleeting left-sided chest pain that has frightened her more than once in the middle of the night. At the apex you hear a clear mid-systolic click followed by a short late systolic murmur; when she squats, the click moves later, and when she stands, it moves earlier.[1]

Three questions decide her care, and they are the questions that decide every MVP case: is the click-murmur really MVP, and not HOCM? (the manoeuvre response settles it), how much mitral regurgitation is hiding behind the eccentric jet? and — the one that makes MVP an exam topic at all — is this the benign common phenotype, or the rare arrhythmic one that can kill?[1][3]

A structural finding, not a clinical syndrome — and why that matters

MVP is an echocardiographic diagnosis, not an auscultatory one. The definition is operational: abnormal systolic displacement of one or both mitral leaflets at least 2 mm beyond the mitral annular plane in the parasternal long-axis view, with leaflet thickness at least 5 mm defining the "classic" form. The click-murmur is one presentation of MVP — it is not the definition, and a prolapsing leaflet is not automatically pathological.[1][2]

The valve abnormality is driven by myxomatous degeneration: the leaflet spongiosa is infiltrated by proteoglycans, collagen is fragmented, and the chordae elongate (and may rupture). When prolapse produces incomplete coaptation, mitral regurgitation follows — and MR is the mechanical, symptomatic, prognostic and operative determinant of MVP. The mitral annulus may dilate and may separate from the ventricular myocardium — mitral annular disjunction (MAD) — the substrate for the rare arrhythmic syndrome.[4][3]

Two exam mistakes recur. The first is diagnosing MVP from a click alone — confirm it on echo. The second is calling a thin, anxious young person "MVP" without checking that the leaflet displacement is real and pathological, because physiological prolapse at very low body mass is rarely clinically relevant.[1]

Etymology for viva gold: myxomatous comes from the Greek myxa, mucus — the degenerated leaflet looks glistening and jelly-like to the surgeon. Barlow syndrome honours John Barlow of Johannesburg, who in 1979 nailed down the "specific billowing mitral leaflet syndrome"; the older name "click-murmur syndrome" captures the bedside description that preceded the echo era.[5]

The face-off — two morphologies that decide the operation

Before you treat, sort the morphology: focal fibroelastic deficiency, or diffuse Barlow disease? The two look alike at the stethoscope and nothing alike in the operating room.[1]

[1] [5]

The discriminator line: focal P2 with abrupt chordal rupture is fibroelastic deficiency and repairs easily; bileaflet Barlow disease is diffuse, demanding, and best sent to a high-volume mitral centre.[1][2]

How common, who, and the exceptions that matter

Population prevalence is 2 to 3 percent by the modern 2 mm echo criterion; the older 5 to 15 percent figure used looser thresholds and over-diagnosed thin-leaflet billowing. The classic form has a 2:1 female predominance under age 40; in men the prevalence rises with age as fibroelastic deficiency becomes the leading mechanism of primary MR. The Framingham offspring cohort established the modern figure and showed the highest valve-event rates in those with moderate-severe MR or leaflet thickening over 5 mm.[1]

MVP is usually benign — say it out loud, then name the exceptions. Overall event rates are low: mitral surgery roughly 0.5 to 1 percent per year across the whole MVP population, endocarditis roughly 0.05 percent per year (rising above baseline when MR is present), and sudden cardiac death roughly 0.2 to 0.4 percent per year overall — higher in the arrhythmic MVP with MAD subset. The clinical task is not to treat the 97 percent who will never have an event; it is to find the few who will.[1][3]

Risk factors are female sex and younger age for the classic form, older age for fibroelastic deficiency and chordal rupture, the connective-tissue disorders (Marfan, Ehlers-Danlos, Loeys-Dietz, osteogenesis imperfecta), familial non-syndromic MVP (rare monogenic loci FLNA, DCHS1, DZIP1), low body mass, and prior rheumatic fever or endocarditis for secondary MVP. The MASS phenotype (Mitral valve, Aorta, Skeleton, Skin) is the connective-tissue variant — historically grouped with Marfan, now an autosomal-dominant myxomatous degeneration of valve, aorta and skeleton.[1][2]

The pathology reads in five layers

MVP is a biomechanical failure of the leaflets and subvalvular apparatus, with downstream atrial, ventricular and — in a minority — arrhythmogenic remodelling. Each layer earns its place because it changes something you do.[1]

1. Leaflet and chordal pathology — myxomatous degeneration. The spongiosa expands with proteoglycans, collagen fragments, the fibrosa thins; leaflets become redundant and thickened (over 5 mm) and prone to prolapse. Chordae elongate (allowing prolapse) and may rupture acutely (fibroelastic deficiency). The annulus dilates, accentuating non-coaptation. Strain on the leaflet accelerates degeneration — a positive-feedback loop.[1][5]

2. Mitral annular disjunction (MAD). The systolic separation of the mitral annulus from the ventricular myocardium, visible on echo as a wide gap between the posterior annulus and the LV wall. First systematically characterised by Carmo et al. in myxomatous MVP, MAD drives abnormal annular motion and mechanical traction on the inferolateral basal myocardium — implicated in the arrhythmic phenotype.[4][3]

3. The inferolateral basal myocardium and ventricular arrhythmia. Cardiac MRI with late gadolinium enhancement in arrhythmic MVP shows focal fibrosis of the inferolateral LV base and papillary muscles, with T-wave inversion in the inferior leads and frequent, complex PVCs (right-ventricular-outflow, fascicular or papillary-muscle origin) on Holter. The combination of mechanical traction from MAD, myxomatous valve disease, and basal fibrosis is the substrate for polymorphic VT and VF.[3][1]

4. MR — the haemodynamic axis. Mild MR is late systolic and eccentric; posterior leaflet prolapse directs the jet anteriorly, hugging the LA wall — easy to underestimate on colour Doppler. Severe MR drives chronic volume overload: LA enlargement, AF onset, pulmonary venous hypertension, and LV eccentric hypertrophy with a falling EF below 60 percent — the surgical trigger.[1]

5. The autonomic axis. A subset has a dysautonomia-like phenotype — exaggerated sympathetic response, orthostatic intolerance, panic-like symptoms — that may account for palpitations and atypical chest pain independent of MR. Beta-blockade is mechanistically rational here.[1][2]

The bedside signature — the click that moves

The single most examined physical sign in MVP is a mid-systolic click whose timing shifts with preload. That shift is the bedside signature, and it tells MVP from HOCM in five seconds.[1]

• Mid-systolic click — high-pitched, best heard at the apex in the left lateral decubitus position, produced by the prolapsing leaflet snapping against the LA wall.
• Late systolic murmur — starts after the click, crescendos to S2; the jet is eccentric (anterior) if the posterior leaflet prolapses, sometimes harsh or musical.
• The dynamic rule, the whole point: anything that shrinks the LV (Valsalva strain, standing) lets the leaflet prolapse earlier — the click moves toward S1 and the murmur lengthens. Anything that fills the LV (squatting, handgrip) delays prolapse — the click moves toward S2 and the murmur shortens.[1][2]

MR signs appear when MR is severe — apical thrill, pan-systolic axillary radiation, a displaced apex from LV dilatation, an S3, and signs of pulmonary hypertension (loud P2, raised JVP). When the click and murmur are absent but the patient is sent for palpitations, the diagnosis rests on echo.[1]

The arrhythmic phenotype — the exception that kills

A small subset of MVP causes sudden cardiac death in the young, and the 2022 EHRA consensus codified it. Recognise the triad before you reassure anyone.[3]

The phenotype is bileaflet prolapse plus mitral annular disjunction plus fibrosis of the inferolateral LV base, often in a young woman (30 to 50 years) with preserved LV function and only mild-to-moderate MR. The bedside markers are T-wave inversion in the inferior leads (II, III, aVF) on ECG, a PVC burden over 10 percent and non-sustained VT on Holter, and late gadolinium enhancement of the inferolateral LV base on cardiac MRI. The annual sudden-death event rate in those with sustained arrhythmia on Holter is roughly 0.4 to 1.9 percent — small in absolute terms, catastrophic in a young patient.[3][4]

Investigations — echo first, then stratify by risk

Transthoracic echo is the diagnostic cornerstone, and it does four jobs at once: confirm the diagnosis, grade MR severity, measure LV and LA size and pulmonary pressures, and look for MAD. The workup then steps up only for the symptomatic or high-risk patient.[1]

• 12-lead ECG — usually normal; inferior T-wave inversion (II, III, aVF) and biphasic lateral T-waves mark arrhythmic MVP with basal fibrosis. ST elevation as in pericarditis should not be attributed to MVP.
• TTE — parasternal long-axis for leaflet displacement at least 2 mm above the annulus (usually P2), leaflet thickness, annular diameter, and MAD; apical views for coaptation, billowing and MR severity by vena contracta, EROA and regurgitant volume (PISA). An eccentric, anterior, wall-hugging jet is characteristic of posterior leaflet prolapse and is easy to underestimate.
• LV size and EF (end-systolic diameter, end-diastolic diameter, Simpson biplane), left atrial volume index (over 40 mL per metre squared marks chronic MR), and pulmonary artery systolic pressure from tricuspid regurgitation velocity (over 50 mmHg is a surgical trigger).[1][2]
• 24 to 48 hour Holter (or 14-day patch) for any symptom or risk stratification — PVC burden, NSVT, PSVT, paroxysmal AF. PVC burden over 10 percent and NSVT mark arrhythmic MVP.
• Cardiac MRI with late gadolinium enhancement for arrhythmic MVP, syncope or a family history of SCD — to detect inferolateral basal and papillary-muscle fibrosis.
• Signal-averaged ECG (late potentials), TOE and 3D TTE/TOE for preoperative repair planning (leaflet segmentation A1 to A3, P1 to P3), and contrast CT chest if a thymoma-equivalent question arises — though MVP has no thymic equivalent; imaging targets the aorta only when connective-tissue disease is present.[1][3]

Two drug-dose lists to carry into the viva, verbatim with their cites:[1]

• Symptomatic palpitations or atypical chest pain — metoprolol 25 to 100 mg twice daily (start low, titrate); bisoprolol 2.5 to 10 mg daily (once-daily alternative); verapamil 80 to 240 mg daily when a beta-blocker is not tolerated.
• Ventricular arrhythmia in arrhythmic MVP — amiodarone 200 mg three times daily loading then 200 mg daily; catheter ablation for drug-refractory papillary-muscle or fascicular PVCs; ICD for secondary prevention.[1][3]

Two emergencies that do need resuscitation

Most MVP patients never need acute care — but two presentations do, and both are surgical.[1]

1. Acute severe MR from chordal rupture (the fibroelastic-deficiency presentation). Sudden posterior or anterior leaflet flail produces sudden severe MR, flash pulmonary oedema and cardiogenic shock in the unprepared ventricle. The bedside triad is sudden dyspnoea, a new loud pan-systolic murmur (often with thrill), and acute decompensated heart failure in a previously well patient.[1]

• Resuscitate: ABCDE and oxygen, large-bore IV access, IV furosemide 40 to 80 mg bolus repeated, vasodilator (sodium nitroprusside 0.5 to 10 microgram per kg per minute titrated to systolic BP 100 to 110) to cut afterload, inotropes if hypotensive (dobutamine 2 to 20 microgram per kg per minute), an intra-aortic balloon pump for afterload reduction and forward flow (note: IABP is helpful in acute MR — the opposite of AR), and non-invasive or invasive ventilation.
• Urgent TTE plus or minus TOE to confirm anatomy, then emergency mitral repair (preferred) within 24 hours; percutaneous edge-to-edge repair (MitraClip) is a bridge or palliative option when surgical risk is prohibitive.[1][2][4]

2. Out-of-hospital cardiac arrest or polymorphic VT in arrhythmic MVP with MAD. Standard ACLS — high-quality CPR, defibrillation for VF, amiodarone 300 mg IV bolus (then 150 mg) for refractory VT or VF, lidocaine 1 to 1.5 mg per kg IV second line. After ROSC, manage in a cardiac ICU with targeted temperature management, antiarrhythmic therapy (amiodarone 200 mg three times daily loading then 200 mg daily, or sotalol), and ICD evaluation for secondary prevention — indicated after cardiac arrest or sustained VT regardless of LV EF.[3]

The stepped, risk-stratified plan

MVP management is staged by MR severity, LV and LA consequences, rhythm, and the arrhythmic phenotype — not by the click.[1][2][3]

Step 1 — Asymptomatic, no MR or only mild MR. Reassure, advise lifestyle and good dental hygiene, give no antibiotics for routine procedures (the modern position is no endocarditis prophylaxis except for the highest-risk subset), and repeat echo in 3 to 5 years unless symptoms change.[1][2]

Step 2 — Symptomatic palpitations, atypical chest pain, mild-moderate MR. Beta-blocker first line — metoprolol 25 to 100 mg twice daily, or bisoprolol 2.5 to 10 mg daily, or verapamil 80 to 240 mg daily as an alternative. Treat coexisting anxiety or panic; reassure about the overall benign prognosis.[1]

Step 3 — Arrhythmic MVP with complex PVCs or NSVT. Optimise beta-blockade; add amiodarone for sustained or highly symptomatic VT; consider catheter ablation of papillary-muscle or fascicular PVCs; ICD for secondary prevention after cardiac arrest or sustained VT. The EHRA consensus advocates individualised risk stratification for primary-prevention ICD (family history of SCD, syncope, NSVT, LGE on MRI).[3]

Step 4 — Severe primary MR reaching a surgical trigger. This is the decision that matters. The 2020 ACC/AHA and 2014 AHA/ACC guidelines give Class I triggers: symptoms (NYHA II to IV), asymptomatic severe MR with LV EF below 60 percent, or asymptomatic severe MR with LVESD over 40 mm. Class IIa triggers add PASP over 50 mmHg, new-onset AF, and progressive LA enlargement.[1][2]

[1] [2]

Type of operation. Mitral valve repair is preferred over replacement — lower operative mortality, better long-term survival, freedom from reoperation, better LV preservation, and avoidance of anticoagulation in patients without AF. Repair rates exceed 90 percent at dedicated centres. Techniques include triangular or quadrangular resection of the prolapsing segment, neochordoplasty with artificial PTFE chordae, and ring or band annuloplasty. Replacement (bioprosthesis, or mechanical for chronic AF needing long-term anticoagulation) is reserved for repair failure, extensive calcification, or the elderly.[1][2]

Anticoagulation for AF is standard, CHA2DS2-VASc-driven, with a NOAC preferred over warfarin when there is no mechanical valve or moderate mitral stenosis. Endocarditis prophylaxis is restricted to the highest-risk subset — prosthetic valves, prior endocarditis, uncorrected cyanotic congenital heart disease, repaired congenital disease with prosthesis in the first 6 months, or repaired congenital lesions with a residual defect. MVP without MR is NOT in this list; MVP with severe MR undergoing high-risk dental work may warrant amoxicillin 2 g orally 30 to 60 minutes before the procedure (alternatives ampicillin, clindamycin 600 mg, azithromycin 500 mg by allergy status).[1][2]

Surveillance: TTE annually for moderate MR or asymptomatic severe MR, 3 to 5 yearly for mild MR, and immediately for any new symptom.[1]

The scenarios that change the answer

• Fibroelastic deficiency with acute chordal rupture — sudden severe MR; urgent repair with neochordoplasty plus annuloplasty within days; operative mortality well under 5 percent at high-volume centres.
• Diffuse Barlow disease with chronic severe MR — bileaflet, multi-segmental; repair by experienced surgeons, durable but technically demanding, higher recurrence than fibroelastic deficiency.
• MASS phenotype — flail leaflet plus aortic-root dilation plus skeletal and skin features; monitor the aortic root, screen the family.
• Arrhythmic MVP with MAD and cardiac arrest or sustained VT — ICD for secondary prevention, beta-blockade, amiodarone, catheter ablation for drug-refractory arrhythmia; mitral repair may reduce arrhythmia burden in selected patients.
• MVP with new-onset AF — anticoagulate per CHA2DS2-VASc; rate or rhythm control; surgery for severe MR plus MAZE or pulmonary-vein isolation at repair.
• MVP with endocarditis — Duke criteria apply; three blood cultures, TTE then TOE, intravenous antibiotics per local protocol; early surgery for heart failure, uncontrolled infection, embolic phenomena or vegetations over 10 mm.[3][4]

How MVP patients come to harm — the preventable list

• Reassuring the arrhythmic phenotype as benign and missing bileaflet prolapse with MAD, inferior TWI and complex PVCs — the preventable sudden death.[3]
• Reading the eccentric, wall-hugging MR jet as "mild" on colour Doppler and under-grading severe MR — quantify with PISA, vena contracta and EROA.[1]
• Waiting for the EF to fall below 50 in MR — by then the ventricle has decompensated and may not recover; the trigger is EF below 60.[1]
• Starting high-dose prednisolone-style steroids for "palpitations" — beta-blockade is the rational first line, not anxiolysis alone.[1]
• Confusing the HOCM murmur with the MVP click — the Valsalva and squatting responses are opposite; get them right.[1]
• Giving endocarditis prophylaxis for routine MVP — restricted to the highest-risk subset.[1]
• Sending diffuse Barlow disease to a low-volume centre where repair fails and the patient gets a replacement they did not need.[1]

Prognosis, disposition, and what to tell the patient

The prognosis of MVP is overwhelmingly benign. Most patients have mild MR, a normal life expectancy, and never need surgery. The clinical task is to identify the high-risk subsets and act.[1]

• Mild MR, asymptomatic — normal life expectancy, follow-up every 3 to 5 years.
• Moderate MR, asymptomatic — close follow-up and re-imaging 1 to 2 yearly; risk of progression to surgery roughly 10 to 15 percent at 10 years.
• Severe MR treated conservatively — roughly 10 percent annual mortality in older data; surgery restores life expectancy to normal when performed before LV dysfunction sets in.
• Severe MR after repair — operative mortality under 2 percent at high-volume centres, 10-year survival 85 to 90 percent, freedom from reoperation 90 to 95 percent.
• Arrhythmic MVP with MAD after cardiac arrest — high recurrence; ICD improves survival.[1][3]

Disposition: asymptomatic MVP is outpatient follow-up at the echo intervals above; symptomatic or severe MR belongs in a valve clinic with cardiology, cardiac surgery and imaging; acute severe MR, syncope or pulmonary oedema is admitted for medical stabilisation and surgical decision; cardiac arrest or sustained VT goes to a cardiac ICU or arrhythmia service for ICD evaluation.[1][2][3]

What to tell the patient: most MVP is benign; avoid dehydration, stay active, report any new breathlessness, palpitation or syncope immediately, and keep good dental hygiene. The reassurance matters — a label of "heart disease" handed to an anxious young person can do more harm than the valve.[1]

Special populations

Pregnancy — most MVP is well tolerated. Severe MR with symptoms is managed medically with diuretics and a beta-blocker (metoprolol preferred, long safety record); surgery in pregnancy carries high fetal risk and is reserved for refractory cases, preferably postpartum. Avoid ACE inhibitors and ARBs throughout pregnancy.[1]

Athletes — asymptomatic MVP without MR is not a bar to competitive sport; MVP with severe MR, LV dilatation, previous arrhythmia or systemic connective-tissue disease may require restriction. Systolic anterior motion with MVP raises the differential of HOCM.[1]

Marfan and connective-tissue disease — measure the aortic root regularly (TTE annually if over 40 mm or rising), use beta-blocker plus or minus losartan for aortic protection, and combine MVP surgery with aortic-root replacement when the root approaches 50 mm.[1]

Elderly — fibroelastic deficiency predominates; chordal rupture is a common presentation; repair is still preferred; transcatheter edge-to-edge repair (TEER, MitraClip) is an option for the high-risk elderly.[1]

Children — MVP is rare, usually associated with Marfan or connective-tissue disease; the MASS phenotype may appear in younger siblings of an index case.[1][2]

The evidence and the regions

The 2020 ACC/AHA guideline (Otto et al.) and 2014 AHA/ACC guideline (Nishimura et al.) set the Class I surgical triggers for severe primary MR and the endocarditis-prophylaxis position; the 2022 EHRA consensus (Sabbag et al.) is the modern authority on arrhythmic MVP and MAD. Barlow and Pocock (1979) anchored the diffuse phenotype, and Carmo et al. (2010) first systematically characterised MAD in myxomatous MVP.[1][2][3][4][5]

Regional deltas: the framework (echo diagnosis, dynamic manoeuvres, repair-preferred surgery) is globally consistent. In India and resource-limited settings, rheumatic mitral disease dominates and Barlow-type myxomatous MVP is relatively less common; pyridostigmine is irrelevant here — the backbone of MVP therapy is reassurance, beta-blockade, and mitral repair at the trigger. Access to cardiac MRI for arrhythmic-MVP risk stratification and to high-volume mitral-repair centres varies, which is why the EHRA bedside markers (bileaflet prolapse, MAD, inferior TWI, PVC burden over 10 percent) matter most where MRI is scarce.[1][3]

The mantra, and the mnemonic

[1]

The mantra: click earlier with Valsalva, later with squatting; most patients never need surgery, but the arrhythmic phenotype can kill.[1][3]

Ward-round test — three stems, thirty seconds each

Stem 1 — the woman from the top of the topic (answer)

The 28-year-old with a mid-systolic click and late systolic murmur that moves earlier on standing and later on squatting, mild palpitations and atypical chest pain. Echo shows bileaflet MVP, mild MR, normal LV, no MAD. What do you tell her, and what do you do? Model: This is benign classic MVP — the manoeuvre response is diagnostic (earlier with reduced preload, opposite to HOCM). Reassure her about the prognosis, advise good dental hygiene and hydration, prescribe a beta-blocker (metoprolol 25 to 100 mg twice daily, titrated) for the symptomatic palpitations and atypical chest pain, treat any coexisting anxiety, and arrange surveillance echo in 3 to 5 years. Do not give endocarditis prophylaxis for routine procedures — it is restricted to the highest-risk subset. Tell her to report any new breathlessness, syncope or sustained palpitations immediately.[1][2]

Stem 2 — sudden breathlessness and a new murmur (answer)

A 62-year-old man who was well yesterday presents with acute pulmonary oedema and a new loud pan-systolic murmur with a thrill at the apex. He has a history of a "click" found years ago. What happened, and what is the first 15 minutes? Model: This is acute severe MR from chordal rupture on a fibroelastic-deficiency valve. Sit upright, give high-flow oxygen and non-invasive ventilation, IV furosemide 40 to 80 mg bolus repeated, and an IV vasodilator (sodium nitroprusside 0.5 to 10 microgram per kg per minute titrated to systolic BP 100 to 110) to cut afterload — here, unlike in aortic regurgitation, an intra-aortic balloon pump is helpful because it reduces afterload and improves forward flow. Confirm with urgent TTE plus or minus TOE, then arrange emergency mitral repair (preferred) within 24 hours. The mortality climbs with every day of delay. Do not reach for afterload reduction without securing the airway and circulation first.[1]

Stem 3 — the young woman who collapsed (answer)

A 34-year-old woman with known MVP is admitted after an out-of-hospital cardiac arrest, successfully resuscitated. Her ECG shows T-wave inversion in II, III and aVF; Holter shows frequent complex PVCs and runs of non-sustained VT; cardiac MRI shows late gadolinium enhancement at the inferolateral LV base. What is the diagnosis and the next step? Model: This is arrhythmic MVP with mitral annular disjunction — the codified EHRA 2022 syndrome of bileaflet prolapse plus MAD plus inferolateral basal fibrosis, driving polymorphic VT and sudden cardiac arrest. After stabilisation in a cardiac ICU with targeted temperature management and antiarrhythmic therapy (amiodarone 200 mg three times daily loading then 200 mg daily), she needs an ICD for secondary prevention — indicated after cardiac arrest or sustained VT regardless of LV EF. Refer to a tertiary valve-and-arrhythmia service; consider catheter ablation of the culprit PVCs if drug-refractory; and reassess the mitral valve for repair if severe MR coexists. This is the exception that makes MVP an exam topic at all.[3]

References

1. [1]Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines Circulation, 2021.PMID 33332150
2. [2]Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Circulation, 2014.PMID 24589853
3. [3]Sabbag A, Essayagh B, Barrera JA, et al. EHRA expert consensus statement on arrhythmic mitral valve prolapse and mitral annular disjunction complex in collaboration with the ESC Council on valvular heart disease and the European Association of Cardiovascular Imaging endorsed cby the Heart Rhythm Society, by the Asia Pacific Heart Rhythm Society, and by the Latin American Heart Rhythm Society Europace, 2022.PMID 35951656
4. [4]Carmo P, Andrade MJ, Aguiar C, et al. Mitral annular disjunction in myxomatous mitral valve disease: a relevant abnormality recognizable by transthoracic echocardiography Cardiovasc Ultrasound, 2010.PMID 21143934
5. [5]Barlow JB, Pocock WA. Mitral valve prolapse, the specific billowing mitral leaflet syndrome, or an insignificant non-ejection systolic click Am Heart J, 1979.PMID 420065