CardiologyTier 1Disease (DEADMAN)

Mitral regurgitation

Description

	Primary (degenerative)	Secondary (functional)
Problem	The valve	The ventricle or atrium
Lesion	Leaflet, chordae, papillary muscle	Annular dilatation + leaflet tethering
Causes	MVP, rheumatic, endocarditis, chordal rupture	IHD, DCM, long-standing AF
Treatment	Fix the valve	Treat the ventricle first

Different diseases with different evidence bases - classify before treating
Acute vs chronic turns on LA compliance
- Chronic: LA dilates, stays compliant -> symptoms late
- Acute: stiff LA -> abrupt inc LA pressure -> flash pulmonary oedema

Primary - by component

Leaflet - myxomatous degeneration/MVP (commonest), rheumatic, endocarditis, CTD, anorectic drugs, radiation
Chordae - spontaneous rupture -> flail leaflet
Papillary muscle - rupture in acute MI
- Posteromedial muscle has a single blood supply -> the one that ruptures
Annulus - calcification

Secondary

Ventricular - LV dilatation -> annular dilatation + apical leaflet tethering
- IHD (esp. inferolateral/LCx territory), DCM
Atrial - LA dilatation in long-standing AF

Mechanism

Regurgitant volume -> LA + LV volume overload
- -> eccentric LV hypertrophy
- -> preload reserve exhausted
- -> LV dysfunction, PHT, RV failure
MR unloads the LV into a low-pressure LA -> EF overstates true contractility
- An EF in the "normal" range in severe MR already signals impairment

Exam

Displaced thrusting apex, systolic thrill, AF pulse
Pansystolic murmur at apex radiating to axilla - left lateral, expiration
Soft S1, widely split S2 (early A2), S3
MVP: mid-systolic click + late systolic murmur
- Standing/Valsalva -> click earlier, murmur longer; squatting -> the opposite
Acute severe MR: soft or absent murmur, tachycardia, pulmonary oedema, shock

Investigations

TTE - severity, mechanism, LV size and EF, LA size, PASP
Severe if any of:
- Vena contracta >0.7 cm
- EROA >0.4 cm2
- Regurgitant volume >60 mL, or regurgitant fraction >50%
TOE for mechanism and repairability before any intervention
ECG: P mitrale, AF, ischaemic change. CXR: LA + LV enlargement, pulmonary oedema
"60/60" rule - LVEDD <60 mm and EF >60% = still compensated
Exercise testing or stress echo for the apparently asymptomatic

Acute severe MR

Surgical emergency
Afterload reduction - nitroprusside; IABP does help here, unlike in AR
Treat the cause - reperfusion for papillary rupture, antibiotics for endocarditis

Chronic primary MR

Operate if any of:
- Symptomatic severe MR with EF >30%
- Asymptomatic + EF <=60% or LVESD >=40 mm
- Asymptomatic + new AF or PASP >50 mmHg
- Undergoing other cardiac surgery
Repair >> replacement - better survival, no anticoagulation, preserves subvalvular apparatus
- Repair rate is operator-dependent - refer to a high-volume centre
TEER (edge-to-edge clip) if surgical risk prohibitive
Medical therapy does not alter the natural history of primary MR - never use it to defer surgery

Chronic secondary MR

Optimise heart failure therapy first - four pillars, CRT if indicated
- MR frequently improves on reverse remodelling alone
TEER if severe MR persists despite optimal HF therapy (COAPT)
- MITRA-FR was negative - benefit requires MR severe out of proportion to LV size
Revascularisation if ischaemic; surgery otherwise has a limited role
Atrial functional MR - rhythm control for the AF

Asymptomatic severe primary MR: ~5-10%/yr develop symptoms, LV dysfunction or AF
LV dysfunction may be irreversible once established - the rationale for the EF <=60% trigger
Secondary MR marks worse prognosis in HF, but is a marker as much as a cause

Monitor

Complications

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