The mitral valve apparatus has five interdependent components:

Additionally, the LV myocardium itself is considered a "sixth component" — LV geometry and contraction directly influence annular size and papillary muscle positioning.

During systole, LV pressure rises above LA pressure. The mitral leaflets are pushed upward toward the closed position by the pressure gradient, while the papillary muscles contract simultaneously to pull the chordae taut and prevent the leaflets from prolapsing (everting) into the LA. The net result is tight coaptation (apposition) of the anterior and posterior leaflets along a "coaptation zone" — this seal prevents regurgitation.

During diastole, the mitral valve opens to allow LA blood to fill the LV. The normal mitral valve area is 4–6 cm².

The posteromedial papillary muscle receives its blood supply from a single artery (usually the posterior descending artery from the RCA), whereas the anterolateral papillary muscle has dual supply (from both the LAD and LCx). This makes the posteromedial muscle highly susceptible to ischaemia/infarction — especially in inferior MI — and is the reason why ischaemic MR disproportionately involves this muscle ^[2].

The valve leaflets or chordae themselves are structurally abnormal. The valve is the problem.

The valve leaflets are structurally normal, but the valve doesn't close properly because the supporting apparatus has been distorted by LV or LA disease. The ventricle (or atrium) is the problem.

This is described as a "casing problem" of the mitral valve ^[1].

In MR, during systole, the LV ejects blood through two exits:

1. Forward through the aortic valve into the aorta (effective stroke volume)
2. Backward through the incompetent mitral valve into the LA (regurgitant volume)

The regurgitant fraction = regurgitant volume / total stroke volume.

This means:

• Forward cardiac output is reduced (→ fatigue, weakness)
• LA receives an abnormal volume load (→ raised LA pressure → pulmonary congestion)
• LV receives increased volume in diastole (regurgitant blood returns from LA → volume overload)

Chronic MR develops gradually — the heart has time to compensate.

Phase 1 — Compensation (may last ≥ 10 years):

• Gradual LA dilation with ↑pressure only during systole → the large, compliant LA acts as a "buffer," absorbing regurgitant volume without much rise in mean LA pressure
• Usually little or no symptoms early on for ≥ 10 years (cf. MS, which is symptomatic much earlier)
• The LV also dilates (eccentric hypertrophy) to accommodate the increased total stroke volume
• ↑LA compliance results in exaggerated regurgitant fraction — paradoxically, as the LA becomes more compliant, it "invites" more regurgitant flow (because the impedance to backward flow decreases)
• Early symptoms dominated by low forward cardiac output: fatigue, weakness ^[2]
• Pulmonary hypertension only occurs late when the LV fails due to volume overload ^[2]

Phase 2 — Decompensation:

• Once severe, MR is NOT benign ^[2]
• Patients develop symptoms at 10%/year, AF in 1/3 ^[2]
• 90% of asymptomatic patients with normal LVEF will need surgery at 10 years ^[2]
• The LV gradually fails from chronic volume overload → LV systolic dysfunction (↓LVEF)
• Rising LA pressure → pulmonary venous hypertension → pulmonary arterial hypertension → RV failure

Key concept — LVEF is deceptively normal in MR: In MR, the LV ejects into two low-pressure chambers (aorta AND LA). The LA is a very low-impedance circuit. This means the LV can maintain a "normal" LVEF even when intrinsic myocardial contractility has already declined significantly. By the time LVEF drops below 60% in MR, the ventricle is already significantly impaired. This is why the surgical threshold for LVEF in MR is ≥ 60% (not 50% as in other conditions) — once it drops below 60%, irreversible LV damage may have occurred ^[2].

Acute MR is a completely different beast — and a medical/surgical emergency.

Causes: chordal rupture, papillary muscle rupture (post-MI), leaflet perforation (IE), acute rheumatic fever, prosthetic valve dehiscence.

• Rapid ↑LA pressure (no time to dilate) — the LA is small and non-compliant
• Acute severe pulmonary hypertension with acute pulmonary oedema and intense distress ^[2]
• The sudden volume overload is transmitted directly backward to the pulmonary veins → flash pulmonary oedema
• Forward cardiac output drops precipitously → cardiogenic shock
• The murmur in acute MR may be shorter and softer than in chronic MR (because the LV-LA pressure gradient equilibrates rapidly in late systole — the murmur may have a decrescendo quality ^[2])
• This is a surgical emergency — medical therapy is a temporizing bridge

The lecture slides specifically illustrate this mechanism:

In ischaemic heart disease, the "casing problem" of the mitral valve involves: ^[1]

1. Papillary muscle displacement — LV remodelling (post-MI dilation/scar) displaces the papillary muscles posterolaterally
2. Restricted leaflet closure — the displaced papillary muscles pull the chordae taut, tethering the leaflets and preventing them from coapting at the annular plane
3. Annular dilation — LV dilation stretches the mitral annulus, further widening the gap between leaflets

The result is a valve that is structurally normal but functionally incompetent — the leaflets simply cannot reach each other.

This classification describes leaflet motion relative to the annular plane and is the standard framework used by cardiac surgeons:

Exception — MVP murmur: In MVP, manoeuvres that ↓LV volume (Valsalva, standing) cause the click to come earlier and the murmur to become longer and louder — because a smaller LV means the prolapse occurs earlier in systole.

• Definition: Displacement of one or both mitral leaflets ≥ 2 mm above the mitral annular plane during systole
• Occurs in 2–3% of the population ^[4]
• More common in young women (for non-syndromic MVP)

• Degenerative: myxomatous degeneration — enlargement of leaflet with replacement of normal dense collagen and elastin matrix of valvular fibrosa by loose myxomatous connective tissue ^[4]
• Congenital: primary AD inheritance with variable penetrance or associated with connective tissue disorders (Marfan syndrome), secundum ASD, Turner syndrome, PDA, WPWS, polycystic kidney disease, DCMP/HCMP ^[4]

• Asymptomatic (most patients)
• Arrhythmia: palpitation, atypical chest pain ('systolic click-murmur syndrome')
  • Mechanism: mitral valve prolapse → excessive stress on papillary muscle → ischaemia and chest pain ^[4]
• Symptoms of MR: presents acutely (due to chordal rupture) or chronically (due to progressive MR) ^[4]

• Mid-systolic click followed by late systolic crescendo murmur loudest at the LLSB / apex
• The click is generated by sudden tensing of the redundant leaflet and chordae as they reach maximum prolapse
• Murmur: late systolic, crescendo — not pansystolic (unless MR is severe)

• Embolic stroke (rare — platelet-fibrin deposits on redundant leaflet)
• Endocarditis (abnormal valve surface predisposes to bacterial seeding)
• Arrhythmia (prolonged QT)
• Progression to severe MR (chordal rupture, progressive myxomatous degeneration)

Why does TR get louder with inspiration? Inspiration increases venous return to the right heart (↓intrathoracic pressure → ↑pressure gradient from systemic veins to RA). This ↑RV preload → ↑RV volume → ↑regurgitant flow across the tricuspid valve → louder murmur. This is Carvallo's sign — the single most useful bedside manoeuvre to distinguish TR from MR ^[3].

Why does MR NOT increase with inspiration? The left heart is "downstream" of the pulmonary circulation. While inspiration transiently pools blood in the pulmonary vasculature (↓LV preload slightly), the effect on MR murmur intensity is minimal or slightly decreasing — the opposite of TR.

The Gallavardin phenomenon — a common trap: AS can present as an ejection systolic murmur (ESM) best heard at the apex, mimicking MR. This is the Gallavardin phenomenon, more common in the elderly ^[3]. Why does this happen? In calcific AS, the murmur has two components — a low-frequency component transmitted to the apex (sounding like MR) and a high-frequency component transmitted to the carotids. The carotid radiation and slow-rising pulse help distinguish it.

The reverse trap — ischaemic MR mimicking AS: In ischaemic papillary muscle dysfunction, the regurgitant jet may be directed to the anterior LA → best heard at LSB/aortic areas (mimicking ESM of AS) ^[2]. Here, the posterior leaflet is tethered by the displaced papillary muscle, directing the jet anteriorly. The key differentiator is the pulse character (normal or small volume in MR vs. slow-rising in AS) and echocardiography.

Why does HOCM cause MR? Asymmetric septal hypertrophy (ASH) → anterior displacement of papillary muscles → systolic anterior motion (SAM) of the mitral valve anterior leaflet toward the septum → MR. The severity of MR is directly proportional to the LV outflow obstruction ^[5]. So in HOCM, MR and LVOT obstruction are linked — anything that worsens obstruction worsens MR.

Critical distinction with dynamic manoeuvres: HOCM is the only common murmur that gets louder with Valsalva (strain phase). All other systolic murmurs generally get softer. This is because ↓preload in HOCM → ↓LV cavity size → the hypertrophied septum and anterior mitral leaflet are brought closer together → ↑obstruction → louder murmur.

Why is VSD a PSM? During systole, the LV pressure greatly exceeds RV pressure. Blood is shunted from LV → RV through the defect throughout systole, creating a continuous pressure gradient and therefore a pansystolic murmur. The mechanism is analogous to MR (constant systolic pressure gradient driving flow), but the flow goes from LV → RV rather than LV → LA, so the murmur is located at the LLSB (over the septum) rather than the apex.

Paradox of VSD murmur intensity: A small, restrictive VSD produces a louder murmur than a large, non-restrictive VSD. This is because in a small VSD, the pressure gradient is high → high-velocity turbulent flow → loud murmur. In a large VSD, pressures equalize between ventricles → low-velocity flow → soft murmur (or even absent in Eisenmenger syndrome when the shunt reverses).

Effective regurgitant orifice area (EROA) is the most recommended tool in MR severity assessment ^[1].

Why is EROA the best parameter?

EROA measures the cross-sectional area of the regurgitant orifice at its narrowest point (the "vena contracta"). It is flow-independent — meaning it reflects the actual anatomical size of the leak rather than being influenced by loading conditions (preload, afterload, heart rate). It is calculated using the PISA method (Proximal Isovelocity Surface Area):

• The regurgitant blood accelerates as it approaches the narrow regurgitant orifice, forming concentric hemispheric shells of equal velocity (like water approaching a drain)
• On colour Doppler, the aliasing boundary (where colour changes from blue to red) represents a hemisphere of known velocity
• The flow through this hemisphere equals the flow through the regurgitant orifice: EROA = 2πr² × aliasing velocity / peak MR velocity

Why different thresholds for primary vs. secondary MR?

The 2021 ESC guidelines use lower thresholds for severe secondary MR (EROA ≥ 20 mm², RVol ≥ 30 mL) compared to primary MR (EROA ≥ 40 mm², RVol ≥ 60 mL). This is because in secondary MR:

• The LV is already dilated and dysfunctional — even a "moderate" amount of regurgitation has a disproportionately negative impact on an already failing ventricle
• The regurgitant orifice in secondary MR is often crescent-shaped (along the coaptation line) rather than circular, so the PISA method may underestimate the true EROA

Why does severe MR cause pulmonary vein systolic flow reversal? Normally, blood flows from the pulmonary veins into the LA during both systole and diastole (systolic dominant pattern). In severe MR, the regurgitant jet increases LA pressure so much during systole that it exceeds pulmonary venous pressure — blood is actually pushed backwards into the pulmonary veins. This is a highly specific sign of severe MR.

The ECG does not diagnose MR but provides important clues about chronicity, haemodynamic severity, and aetiology.

MVP-specific ECG findings ^[4]:

• Normal ± non-specific ST depression in inferior leads ^[4]
• ST-T changes may reflect papillary muscle traction/ischaemia
• Rarely: prolonged QT interval (associated arrhythmia risk)

The CXR provides indirect evidence of MR and its haemodynamic consequences:

Acute MR on CXR: Fulminant pulmonary oedema with a normal-sized heart — this is a critical clue. The LA and LV have not had time to dilate, so the cardiac silhouette is normal despite severe pulmonary congestion. If you see acute pulmonary oedema with a normal heart size, think acute MR (or other acute valvular catastrophe/flash pulmonary oedema from renal artery stenosis/hypertensive emergency).

Cardiac catheterisation is not routinely done for MR diagnosis ^[2]. Its role has been largely supplanted by echocardiography. However, it still has specific indications:

Why does a tall v wave appear on the PCWP trace? The pulmonary capillary wedge pressure (PCWP) approximates LA pressure. Normally, the LA pressure trace shows a gentle a wave (atrial contraction) and a gentle v wave (venous filling during ventricular systole). In MR, the regurgitant jet adds a large volume to the LA during systole → a very prominent v wave — sometimes called a "giant v wave." This is a classic catheterisation finding of severe MR.

The goal of medical therapy in acute MR is to bridge to emergency surgery — NOT to be the definitive treatment. The aim is to:

• ↓Pulmonary oedema (↓preload)
• ↑Forward cardiac output (↓afterload → diverts blood forward through the aorta rather than backward through the incompetent mitral valve)
• Support haemodynamics if in cardiogenic shock

Why does ↓afterload help in MR? In MR, blood takes the path of least resistance. The LA is a low-pressure chamber, so without intervention, a large fraction of each stroke volume flows backward into the LA. By reducing systemic vascular resistance (afterload), you make the aortic outflow pathway "easier" — more blood goes forward through the aorta, less goes backward. This is the opposite of what you'd do in aortic stenosis (where ↓afterload is dangerous because the fixed obstruction means ↓SVR → ↓coronary perfusion).

Acute severe MR requires emergency surgery — either repair or replacement, depending on the pathology:

Medical therapy in chronic MR does NOT alter disease progression or reduce regurgitation ^[1][2]. Its roles are limited to:

Surgery should be done early to avoid development of irreversible ↓LV function ^[2].

Severe primary MR — Surgical indications (2020 ACC/AHA / 2021 ESC guidelines):

Summary of triggers for surgery in asymptomatic severe primary MR:

Symptoms → Operate. LVEF < 60% → Operate. LVESD ≥ 40 mm → Operate. New AF → Operate. PASP > 50 mmHg → Operate. None of the above → Watch and wait (but consider early repair at expert centre).

This is the first-line approach for secondary MR. Treating the underlying LV dysfunction may reduce MR severity by:

• ↓LV volume → ↓annular dilation → improved coaptation
• ↓Afterload → ↑forward flow → ↓regurgitant fraction
• Reverse remodelling → restoration of LV geometry → improved papillary muscle alignment

Severe secondary MR: surgery only when symptomatic (NYHA III–IV) or concomitant CABG/AVR ^[2].

This is much more restrictive than primary MR because:

• The underlying LV disease persists even after valve surgery → outcomes are worse
• Trials (CTSN trials) showed limited survival benefit of MV repair/replacement for ischaemic MR in many patients
• Medical optimisation alone may sufficiently reduce functional MR

• MR is generally well-tolerated in pregnancy (unlike MS). The ↓SVR of pregnancy → ↓afterload → ↓regurgitant fraction → may actually improve symptoms.
• Medical management: diuretics if symptomatic (avoid ACEi/ARB — teratogenic); beta-blockers safe.
• If prosthetic valve: mechanical valve + warfarin is problematic (warfarin is teratogenic in 1st trimester; heparin bridging protocols are complex and carry risk). Bioprosthetic valve avoids this issue but has limited durability.

Routine antibiotic prophylaxis is NOT recommended ^[3].

Only for high-risk groups ^[3]:

• Prosthetic valve replacement/repair
• Previous IE
• Congenital heart disease: unrepaired cyanotic CHD, repaired with residual defects, completely repaired within the first 6 months

For dental procedures: amoxicillin 2g PO / ampicillin IV; single dose 30–60 min before procedure; clindamycin 600 mg PO/IV if allergic to penicillin ^[3].

AF occurs in approximately 1/3 of patients with severe chronic MR ^[2].

Pathophysiology from first principles:

• Chronic MR → regurgitant volume enters the LA during every systole → LA volume overload → LA dilation
• LA dilation causes mechanical stretch of atrial myocytes → structural remodelling (fibrosis of the atrial wall) + electrical remodelling (shortened refractoriness, altered conduction velocities)
• This creates the substrate (patchy fibrosis → areas of slow conduction) and triggers (stretched myocytes → ectopic foci, especially from the pulmonary veins) for re-entrant circuits → AF

Why does AF matter so much in MR?

1. Loss of atrial contraction → loss of the "atrial kick" (normally contributes ~15–25% of LV filling). In a heart already compromised by MR, this loss of the atrial contribution precipitates decompensation
2. Rapid ventricular rate → ↓diastolic filling time → ↓forward CO + ↑LA pressure → acute pulmonary congestion
3. Blood stasis in the dilated LA → thromboembolism risk (see below)
4. New-onset AF is an indication for surgery even in asymptomatic patients ^[2][3] — it signals that LA remodelling has progressed to the point of electrical instability

Management: AF: anticoagulation, rate control ^[3]. Warfarin (INR 2–3) or DOAC for stroke prevention. Rate control with beta-blockers, digoxin, or non-DHP CCB.

Embolic stroke is listed as a specific complication of MR and MVP ^[3].

Pathophysiology:

• LA dilation + loss of effective atrial contraction (AF or even in sinus rhythm with a severely dilated, "stunned" LA) → blood stasis in the LA, especially in the left atrial appendage (LAA)
• Stasis → thrombus formation (Virchow's triad: stasis + endothelial injury + hypercoagulability)
• Thrombus embolisation → systemic embolism, most devastatingly to the brain (embolic stroke), but also to kidneys (renal infarction), spleen (splenic infarction), mesenteric vessels (mesenteric ischaemia), and peripheral arteries (acute limb ischaemia)

In MVP specifically: Embolism due to microthrombus formation behind redundant valve tissue ^[4]. The redundant, billowing leaflet creates a "dead space" on its atrial surface where flow is turbulent and stagnant → platelet-fibrin deposition → microthrombi → embolic events.

Clinical significance: Stroke in a young patient with MR or MVP should always prompt echocardiography (TTE/TEE) to look for LA thrombus, severe LA dilation, and valve pathology.

This is the most important complication of chronic MR because it determines prognosis and surgical timing.

Pathophysiology — the vicious cycle:

• Chronic MR → LV volume overload → eccentric LV hypertrophy (sarcomere addition in series → LV dilation)
• Initially compensatory: the Frank-Starling mechanism maintains stroke volume
• Over years, the chronically overloaded myocardium undergoes adverse remodelling: myocyte apoptosis, interstitial fibrosis, neurohumoral activation (RAAS, sympathetic nervous system)
• This leads to intrinsic myocardial contractile dysfunction (↓LVEF)
• Once LV systolic function declines, the heart enters a decompensated phase: ↓forward CO + ↑LV filling pressures → clinical heart failure

Once severe, MR is NOT benign: patients develop symptoms at 10%/year, AF in 1/3 ^[2].

90% of asymptomatic patients with normal LVEF will have surgery at 10 years ^[2] — meaning that even initially "benign-looking" severe MR progresses inevitably.

Pulmonary hypertension only occurs late when the LV fails due to volume overload ^[2].

Pathophysiology — two components:

Clinical signs of pulmonary hypertension ^[3]:

• Elevated JVP with systolic "v" waves (functional TR)
• Parasternal heave (RV pressure overload)
• Parasternal thrills (functional TR)
• Loud P2
• Pansystolic murmur of TR
• Graham-Steell murmur of PR — PR murmur, associated with loud P2, indicating severe MS ^[3] (though it can occur in any cause of severe pulmonary HTN, including advanced MR)

Why it matters: New-onset pulmonary hypertension (sPAP > 50 mmHg) is an indication for surgery ^[3] — it signals that the backward pressure is now remodelling the pulmonary vasculature. Delay risks irreversible pulmonary vascular disease.

Right heart failure is the end-stage complication of chronic MR, representing the final common pathway of untreated disease.

Pathophysiology chain: Chronic MR → LV failure → ↑LA pressure → pulmonary venous HTN → pulmonary arterial HTN → ↑RV afterload → RV pressure overload → RV hypertrophy → eventually RV dilation and failure

Clinical features of RV failure ^[2][3]:

• Ankle oedema (if RVF) ^[2] — hydrostatic back-pressure in systemic veins → transudation into interstitial space, gravitationally dependent
• Elevated JVP — systemic venous congestion directly reflected by ↑RA pressure
• Hepatomegaly ± pulsatile liver — hepatic venous congestion → hepatic enlargement. If TR is present (functional TR from RV dilation), the liver pulsates with each systolic regurgitant wave.
• Ascites — portal venous congestion → transudation into peritoneal cavity
• Functional TR — RV dilation → tricuspid annulus dilation → TR → further systemic venous congestion (a self-perpetuating cycle)

MR increases the risk of IE because the regurgitant jet creates endothelial damage on the atrial surface of the mitral valve and the LA wall.

Pathophysiology:

• The high-velocity regurgitant jet impacts the atrial surface of the valve leaflets and the adjacent LA endocardium
• This jet lesion creates areas of endothelial denudation → deposition of platelets and fibrin → non-bacterial thrombotic endocarditis (NBTE) — a sterile "landing pad"
• During transient bacteraemia (dental procedures, invasive procedures, even daily activities like tooth-brushing), circulating bacteria adhere to this fibrin-platelet nidus → colonisation → vegetation formation → IE

Valve involvement in IE: MV >> AV > TV > PV ^[3] — the mitral valve is the most commonly affected valve overall.

Infective endocarditis despite optimal medical therapy is an indication for surgery ^[3].

IE complicating MR can worsen the regurgitation through:

• Leaflet destruction/perforation
• Chordal rupture (vegetations weaken chordae)
• Abscess formation at the annulus

This creates a dangerous positive feedback loop: MR → IE → worsened MR → acute decompensation.

Ortner's syndrome: LA enlargement → compression of left recurrent laryngeal nerve (RLN) → hoarseness of voice ^[3].

Pathophysiology from first principles:

• The left RLN loops under the aortic arch and passes between the aorta and the pulmonary artery before ascending to the larynx
• Massive LA dilation (as seen in severe chronic MR, MS, or any cause of giant LA) pushes upward against the left main bronchus and the space between the aorta and pulmonary artery
• This compresses the left RLN → left vocal cord paralysis → hoarseness

This is more classically associated with MS (where LA dilation is typically more extreme), but can occur in severe chronic MR with a giant LA. It is rarely the presenting complaint but can be an exam question.

Acute mechanical complications from MI that cause MR are specific and high-mortality ^[1]:

• MR from rupture of papillary head ^[1] — typically occurs 2–7 days post-MI (when the necrotic tissue is weakest and granulation tissue has not yet formed). The posteromedial papillary muscle is most vulnerable (single blood supply from the PDA/RCA).
• This is high risk for mortality ^[1].
• Presentation: sudden haemodynamic collapse with flash pulmonary oedema, often with a surprisingly soft murmur (because rapid LV-LA pressure equilibration reduces the murmur intensity)
• Other acute mechanical complications listed alongside acute MR ^[1]:
  • Shock from large area (~40%) myocardium involved
  • VSD from transmural infarct and rupture of muscular septum
  • Tamponade from free wall rupture, myocarditis, pericarditis, iatrogenic