Cardiovascular · PANCE / PANRE

Mitral Regurgitation

Backflow of blood from LV to LA in systole; acute presents catastrophically, chronic insidiously.

Also known as: MR, mitral regurgitation, mitral insufficiency, MVP, mitral valve prolapse

Overview

Retrograde flow from the LV into the LA during systole due to incompetence of the mitral valve apparatus (leaflets, chordae, papillary muscles, annulus, or LV geometry). Subdivided into primary (organic — valve itself is diseased) and secondary (functional — valve is structurally normal but LV/LA pathology causes regurgitation).

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Risk factors

  • Primary MR:
  • • Mitral valve prolapse (most common cause in developed countries) — myxomatous degeneration
  • • Rheumatic heart disease (most common globally)
  • • Infective endocarditis (acute leaflet destruction)
  • • Papillary muscle rupture or dysfunction (post-MI, classically inferior MI affecting posteromedial papillary muscle — single blood supply from PDA)
  • • Connective tissue disease (Marfan, Ehlers-Danlos)
  • Secondary (functional) MR:
  • • Ischemic cardiomyopathy
  • • Non-ischemic dilated cardiomyopathy
  • • Severe LV dysfunction — annular dilation, papillary muscle displacement

Pathophysiology

Regurgitant volume increases LA pressure and reduces forward stroke volume. Acute MR: no time for LA compliance to develop → flash pulmonary edema and cardiogenic shock. Chronic MR: gradual LA dilation buffers pressure; LV dilates from volume overload (eccentric hypertrophy) and initially compensates, but eventually LV systolic dysfunction develops irreversibly.

Clinical presentation

Symptoms

  • Acute MR (papillary muscle rupture, endocarditis with cordal rupture):
  • • Sudden severe dyspnea, flash pulmonary edema, cardiogenic shock
  • • Hypotension, tachycardia
  • Chronic MR (insidious onset):
  • • Dyspnea on exertion, fatigue, decreased exercise tolerance
  • • Palpitations (often from new AFib as LA dilates)
  • • Late: signs of LV failure
  • MVP often asymptomatic; symptomatic patients may report atypical chest pain or palpitations

Signs / physical exam

  • Holosystolic murmur at the apex, radiating to the axilla (classic)
  • S3 gallop (volume overload) — common in severe MR
  • Laterally displaced, hyperdynamic PMI (LV dilation)
  • Soft S1 (severely incompetent valve)
  • Mitral valve prolapse: mid-systolic click followed by late systolic murmur; click moves earlier and murmur lengthens with decreased preload (standing, Valsalva)
  • Acute severe MR: rales/pulmonary edema, hypotension, may have a SHORTER murmur than chronic (pressure equalizes quickly across non-compliant LA)

Differential diagnosis

  • Tricuspid regurgitation — Holosystolic at LEFT lower sternal border; INCREASES with inspiration (Carvallo sign); prominent cv waves in JVP; pulsatile liver if severe
  • Ventricular septal defect (post-MI or congenital) — Holosystolic at LSB with palpable thrill; consider post-MI VSD if days after infarct presenting with new murmur and shock
  • Hypertrophic obstructive cardiomyopathy (HOCM) — Dynamic outflow murmur, LOUDER with Valsalva/standing (decreased preload), softer with squatting/handgrip — opposite maneuvers from MR
  • Aortic stenosis — Crescendo-decrescendo at RUSB, radiates to CAROTIDS (not axilla); pulsus parvus et tardus; carotid murmur from radiation
  • Mitral valve prolapse without significant MR — Mid-systolic click followed by late systolic murmur; click moves EARLIER and murmur LENGTHENS with decreased preload (standing, Valsalva)
  • Hyperdynamic flow states (anemia, hyperthyroidism, pregnancy, fever) — Functional systolic flow murmurs; address underlying cause; murmur resolves when state corrected

Diagnostic workup

Labs

  • BNP, BMP, troponin (if acute presentation), blood cultures (if endocarditis suspected)

Imaging

  • ECG: LA enlargement (broad notched P in lead II — 'P mitrale'), LVH, AFib in chronic MR
  • CXR: cardiomegaly (LA enlargement causes elevation of left main bronchus and 'double density' at right heart border), pulmonary edema in acute or decompensated
  • TTE — first-line: identifies mechanism, measures severity (regurgitant volume, regurgitant fraction, EROA), LA and LV size/function
  • TEE — superior for mechanism assessment, surgical planning, evaluating for endocarditis vegetations, and intra-op monitoring
  • Cardiac MRI — useful when TTE/TEE inadequate or to quantify regurgitant volume

Diagnostic algorithm

FeatureAcute MRChronic Compensated MRChronic Decompensated MR
OnsetSudden (hours)YearsYears
LA sizeNormal (no time to dilate)DilatedMarkedly dilated
LA pressureMarkedly elevatedMildly elevatedElevated
LV sizeNormalDilatedMarkedly dilated
LV systolic functionHyperdynamicNormal / preservedReduced
PresentationPulmonary edema, shockAsymptomatic / mild DOEDOE, fatigue, AFib
MurmurOften short, may be softHolosystolic at apex → axillaHolosystolic + S3
ManagementEmergent surgery + afterload reductionSurveillance ± surgerySurgery if EF 30-60% or LVESD ≥40
Acute vs chronic MR — physiology and clinical presentation differ markedly. Acute MR is a surgical emergency; chronic MR is monitored until specific thresholds trigger intervention.

Treatment

First-line

  • Acute severe MR — surgical emergency:
  • • Stabilize: afterload reduction with IV nitroprusside or nitroglycerin, intra-aortic balloon pump if shock
  • • Diuresis for pulmonary edema
  • • Emergent surgical repair or replacement
  • Chronic primary MR — surgery indicated when:
  • • Symptomatic severe MR
  • • Asymptomatic severe MR with LVEF 30-60% or LV end-systolic diameter ≥40 mm
  • • Asymptomatic severe MR + new AFib or pulmonary HTN (selected cases)
  • Mitral repair >> replacement for primary MR — better LV function preservation, no anticoagulation, lower mortality. Refer to high-volume center.

Second-line / adjunct

  • Chronic secondary (functional) MR:
  • • Optimize HF GDMT first (ACEi/ARB/ARNI, BB, MRA, SGLT2i, diuretics, CRT if indicated)
  • • Persistent severe MR despite optimal medical therapy → transcatheter edge-to-edge repair (MitraClip) in selected patients (COAPT trial)
  • • Surgical mitral repair/replacement in selected secondary MR patients

Complications

  • Heart failure (acute pulmonary edema in acute MR; chronic LV failure in chronic MR)
  • Atrial fibrillation (LA dilation)
  • Pulmonary hypertension, right HF
  • Infective endocarditis (regurgitant jet creates susceptible 'kissing' lesion on LA wall)
  • LV thrombus (rare), systemic embolization
  • Sudden cardiac death (more common in severe MVP with redundant leaflets)

PANCE pearls

  • Murmur intensity does NOT correlate with severity — acute severe MR often has a SHORTER, softer murmur due to rapid pressure equalization with a non-compliant LA.
  • Maneuvers: MVP click/murmur moves EARLIER and LENGTHENS with decreased preload (standing, Valsalva strain phase); LATER and SHORTER with increased preload (squatting, leg raise).
  • Inferior MI + new holosystolic murmur + cardiogenic shock = posteromedial papillary muscle rupture. Echo confirms. Emergent surgery; bridge with IABP and afterload reduction.
  • Severe acute MR with sudden hypotension after MI may have ONLY mild murmur or none — high index of suspicion.
  • MVP affects ~2% of population; most asymptomatic and benign. Risk stratifiers for adverse outcome: severe MR, LV dysfunction, AFib, bileaflet involvement, prolonged QT.

References

  • ACC/AHA 2020 VHD — 2020 ACC/AHA Guideline for the Management of Patients with Valvular Heart Disease (Otto et al., Circulation 2021)
  • COAPT — Transcatheter Mitral-Valve Repair in Patients with Heart Failure (Stone et al., NEJM 2018)
  • MITRA-FR — Percutaneous Repair or Medical Treatment for Secondary Mitral Regurgitation (Obadia et al., NEJM 2018)
  • EVEREST II — Percutaneous Repair or Surgery for Mitral Regurgitation (Feldman et al., NEJM 2011)

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