Chapter 20 — Mitral Regurgitation

📚 Guideline basis

Zoghbi WA, et al. Recommendations for Noninvasive Evaluation of Native Valvular Regurgitation (JASE 2017;30:303–71); 2025 ESC/EACTS Guidelines for the Management of Valvular Heart Disease (Eur Heart J 2025;46:4635–), which recognise atrial secondary MR as a distinct entity with a new Class IIa recommendation for surgery and Class IIb for transcatheter therapy; ASE 2025 diastolic update (MR-specific filling pressure indicators).

Pathophysiology & Mechanisms

Classification

Primary (organic/degenerative) — the leaflets or chordae are the problem. Secondary (functional) — the leaflets are structurally normal and the valve fails because of the geometry of the chamber it sits in.

The Carpentier classification describes leaflet motion and maps to mechanism:

Type	Leaflet motion	Mechanism	Typical cause
I	Normal	Annular dilatation or leaflet perforation	Atrial functional MR, endocarditis, cleft
II	Excessive (prolapse/flail)	Elongated or ruptured chordae, papillary muscle rupture	Myxomatous degeneration, chordal rupture, papillary muscle rupture, endocarditis
IIIa	Restricted in systole and diastole	Leaflet thickening and commissural fusion	Rheumatic, radiation, drug-induced
IIIb	Restricted in systole only	Apical tethering by a remodelled ventricle	Ischaemic and dilated cardiomyopathy (ventricular secondary MR)

The 2025 ESC/EACTS separation of atrial from ventricular secondary MR is clinically substantial. Atrial functional MR arises from left atrial and mitral annular dilatation — typically in long-standing atrial fibrillation or HFpEF — with a normal-sized, normally contracting ventricle and no leaflet tethering. Its mechanism, prognosis and treatment differ from ventricular secondary MR, and it responds to rhythm and volume management in a way that tethered MR does not.

Acute versus chronic haemodynamics

The distinction hinges on left atrial compliance.

	Acute severe MR	Chronic severe MR
LA compliance	Normal (small, stiff atrium)	Increased (large, compliant atrium)
LA pressure	Very high with a giant v wave	Modestly elevated
LA size	Normal	Dilated
LV size	Normal	Dilated
Presentation	Flash pulmonary oedema, cardiogenic shock	Exertional dyspnoea, AF, gradual decline
Murmur	Often soft, short, or absent (early pressure equalisation)	Loud pansystolic
Colour jet	Brief, may be unimpressive; often eccentric	Large

In acute severe MR the ventricle appears hyperdynamic because it ejects into a low-impedance left atrium: EF is supranormal while forward stroke volume is catastrophically low. Reporting "vigorous LV function" in this patient is technically true and clinically misleading.

The masked ejection fraction in chronic MR

Regurgitation into the low-pressure atrium unloads the ventricle, so EF overestimates contractility. An EF of 55% in chronic severe MR represents significant myocardial dysfunction, which is why the intervention thresholds for MR use an EF cut-off of 60%, not 50%.

Diagnostic Synthesis

Severity parameters

Parameter	Mild	Moderate	Severe (primary)	Severe (secondary)
Vena contracta width, cm	< 0.3	0.3–0.69	≥ 0.7	≥ 0.7
EROA, cm²	< 0.20	0.20–0.39	≥ 0.40	≥ 0.20
Regurgitant volume, mL	< 30	30–59	≥ 60	≥ 30
Regurgitant fraction, %	< 30	30–49	≥ 50	≥ 50
CW jet	Faint, parabolic	Dense	Dense, triangular, early-peaking	Dense, triangular
Pulmonary venous flow	Normal S > D	Blunted S	Systolic flow reversal	Blunted or reversed
LA and LV size	Normal	Normal or mildly dilated	Dilated (chronic)	Dilated

The lower secondary MR thresholds are not a different disease definition — they reflect the crescentic, non-circular regurgitant orifice of functional MR, which PISA systematically underestimates, combined with the worse prognosis conferred by a smaller regurgitant volume in an already failing ventricle.

The most useful ICU signs

Dense, triangular, early-peaking CW jet. A dense envelope means many red cells crossing the orifice. Early peaking with a rapid late decline reflects the giant v wave — atrial pressure rises so steeply that the LV–LA gradient collapses before end-systole. This "cut-off sign" is the signature of acute severe MR and is often visible when nothing else is.
Systolic flow reversal in the pulmonary veins. Specific for severe MR. Sample the right upper pulmonary vein; check more than one vein, because an eccentric jet directed into one vein produces reversal there and normal flow elsewhere.
Vena contracta ≥ 0.7 cm measured zoomed in the parasternal long axis.
Mechanism. A flail leaflet or a ruptured papillary muscle head on 2D imaging is severe MR by definition, whatever the Doppler shows in a hypotensive patient.

Acute severe MR in the ICU

Cause	Features	Timing
Papillary muscle rupture	Posteromedial in ~75–80% (single blood supply from the posterior descending artery, versus dual supply to the anteromedial); a mobile mass attached to chordae prolapsing into the LA; massive eccentric MR	2–7 days post-MI; often after a small inferior infarct
Chordal rupture	Flail segment with unrestricted leaflet tip motion into the LA	Myxomatous disease, endocarditis, trauma, spontaneous
Endocarditis	Vegetation, leaflet perforation, aneurysm	Any time
Acute ischaemic tethering	Type IIIb, no structural leaflet lesion, dynamic — worsens with ischaemia and hypertension	During ischaemia; may resolve with revascularisation
Dynamic MR from systolic anterior motion	Posteriorly directed jet, late-systolic, with an LVOT gradient; worsens with inotropes	Iatrogenic — see Chapter 28

Distinguishing the SAM-related jet matters because its treatment (stop inotropes, volume load, beta-blockade) is the opposite of the treatment for the others.

Papillary muscle rupture demands immediate surgical referral; medical stabilisation is a bridge measured in hours, not days.

ICU-Specific Limitations

Confounder	Effect	Response
Hypotension	Reduced LV–LA gradient shrinks the jet; severe MR looks moderate	Record the MAP; weight the mechanism and CW density
Vasopressors / hypertension	Increased afterload increases regurgitant volume	Severity may be over-called; reassess at a controlled blood pressure
Sedation and mechanical ventilation	Reduced preload and afterload reduce regurgitant volume	Findings under general anaesthesia routinely under-grade functional MR
Atrial fibrillation	Beat-to-beat variation in PISA and vena contracta	Average multiple beats
Eccentric wall-impinging jet (Coandă)	Colour jet appears small	Vena contracta; 3D vena contracta area; pulmonary venous flow
Dynamic secondary MR	Severity varies hour to hour with loading and ischaemia	State the conditions; consider repeat assessment
Prosthetic or repaired mitral valve	Acoustic shadowing from TTE	TEE required (Chapter 23)

The ASE 2025 diastolic guideline additionally notes that in significant MR, average E/e′ is useful only when EF is depressed, that LA reservoir strain does not track LA v-wave or mean pressure in significant MR, and that IVRT/T(E-e′) < 5.6 (or < 3 for PCWP > 15 mmHg) is the more reliable filling-pressure index in this population.

Therapeutic Logic

Situation	Action
Acute severe MR with pulmonary oedema	Afterload reduction (nitroprusside, nitrates) to redirect flow forward; diuresis; non-invasive or invasive ventilation
Acute severe MR with cardiogenic shock	Afterload reduction plus intra-aortic balloon pump (reduces afterload and augments coronary perfusion — genuinely helpful here, unlike in AR); urgent surgery
Papillary muscle rupture	Emergency surgical referral; stabilise, do not observe
Ischaemic dynamic MR	Treat ischaemia; revascularisation; afterload control
SAM-related MR	Stop inotropes, volume load, vasoconstrictor, beta-blockade
Chronic severe primary MR decompensated by illness	Treat the precipitant; rate and rhythm control; diuresis; defer valve decisions to the Heart Team

The 2025 ESC/EACTS guidelines retain surgery as the preferred treatment for primary MR, with transcatheter edge-to-edge repair reserved for anatomically suitable patients at high surgical risk, and add the new atrial secondary MR recommendations noted above.

🛑 Critical pitfall: Reading a hyperdynamic ventricle with a small colour jet in a hypotensive, flash-pulmonary-oedema patient as "mild MR". This is the classic presentation of acute severe MR. Look at the leaflets, look at the CW envelope density, and look at the pulmonary veins.

🛑 Critical pitfall: Grading functional MR under general anaesthesia or deep sedation. Reduced preload and afterload can convert severe MR into "mild" on the operating table.

🛑 Critical pitfall: Assuming that TTE excludes prosthetic or post-repair mitral regurgitation. Acoustic shadowing from the mitral position makes TTE unreliable for this question; TEE is required.

💡 Clinical pearl: A dense, triangular, early-peaking CW jet with a "cut-off" late-systolic decline indicates a giant v wave and severe acute MR, even when everything else looks unimpressive.
💡 Clinical pearl: Interrogate more than one pulmonary vein. An eccentric jet produces flow reversal only in the vein it is aimed at.
💡 Clinical pearl: In new severe MR after inferior infarction, look specifically for a mobile echodensity attached to chordae swinging into the left atrium — a ruptured papillary muscle head — and call surgery before completing the rest of the study.

References

Zoghbi WA, Adams D, Bonow RO, et al. Recommendations for noninvasive evaluation of native valvular regurgitation. J Am Soc Echocardiogr 2017;30:303–71.
ESC/EACTS. 2025 Guidelines for the management of valvular heart disease. Eur Heart J 2025;46:4635–.
Nagueh SF, Sanborn DY, Oh JK, et al. ASE 2025 diastolic function update. J Am Soc Echocardiogr 2025;38:537–69.
Lancellotti P, et al. Acute valvular heart disease. J Am Coll Cardiol 2021. PMID 34850332.
Champion S, et al. Dynamic left ventricular outflow tract obstruction. Can J Cardiol 2020. PMID 33173359.