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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Question 1CardiovascularEasy
A 45-year-old female with mitral valve prolapse and severe mitral regurgitation (effective regurgitant orifice (ERO) 0.45 cm2) is asymptomatic. EF is 62%. Left ventricular end-systolic diameter is 38mm. Transesophageal echo shows complex bileaflet prolapse with extensive annular calcification, and the valve team judges a durable repair unlikely. Which of the following is the most appropriate management?
AStress echocardiography now
BMitraClip procedure
CMitral valve replacement
DSurveillance with annual echo
EMitral valve surgical repair
Reveal answer & full explanation
Correct answer: D — Surveillance with annual echo
AStress echocardiography now
BMitraClip procedure
CMitral valve replacement
DSurveillance with annual echo✓
EMitral valve surgical repair
Why surveillance with annual echo is correct
This patient has asymptomatic severe primary mitral regurgitation (MR) (effective regurgitant orifice (ERO) 0.45 cm2; severe is 0.40 cm2 or more) with preserved ejection fraction (EF) of 62% and left ventricular end-systolic diameter (LVESD) of 38mm.
The 2020 ACC/AHA valvular heart disease guideline recommends surgery for severe primary MR when (1) symptoms are present, regardless of EF (Class 1), or (2) the patient is asymptomatic with EF 60% or less or LVESD 40mm or more (Class 1); in an asymptomatic patient with a normal left ventricle, early repair is reasonable (Class 2a) only when a durable repair is more than 95% likely with expected mortality under 1% at a Primary or Comprehensive Valve Center.
This patient's EF is 62% (above 60%) and LVESD is 38mm (below 40mm), so neither Class 1 threshold is met, and her complex, calcified valve makes a durable repair unlikely, so early repair is not reasonable; surveillance is appropriate.
Mitral valve surgical repair — the Class 1 thresholds (EF 60% or less or LVESD 40mm or more) are not met, and early repair in an asymptomatic patient is reasonable only when a durable repair is highly likely, which is not the case with this valve.
MitraClip procedure — a transcatheter option generally reserved for high-surgical-risk patients; not indicated when the patient does not meet surgical criteria in the first place.
Stress echocardiography now — not the recommended next step when current resting parameters fall below surgical thresholds; continued surveillance is the guideline-directed approach.
Mitral valve replacement — tempting because the valve team judges a durable repair unlikely, but a poor repair outlook is not an indication to operate; with no symptoms, EF above 60%, and LVESD below 40mm, no Class 1 threshold is met, and early surgery in an asymptomatic patient is reasonable only when a durable repair is highly likely.
Question 2CardiovascularMedium
A 60-year-old man is evaluated for a blowing holosystolic murmur heard best at the apex, radiating to the axilla. He denies exertional dyspnea or reduced exercise tolerance and remains asymptomatic on his current medications. Echo shows severe mitral regurgitation with an ejection fraction (EF) of 63% and a left ventricular end-systolic diameter of 34 mm. When should surgery be recommended?
AWhen EF falls below 60% or LV end-systolic diameter exceeds 40 mm
BWhen EF falls below 55% or LV end-systolic diameter exceeds 50 mm
CWhen the regurgitant volume first exceeds 30 mL per beat
DWhen the mean transvalvular gradient exceeds 40 mmHg
Why EF falls below 60% or LV end-systolic diameter exceeds 40 mm is correct
2020 ACC/AHA surgical thresholds for severe primary mitral regurgitation (MR): surgery is recommended (Class 1) when the patient is (1) symptomatic, regardless of ejection fraction (EF), or (2) asymptomatic with EF 60% or less or left ventricular end-systolic diameter (LVESD) 40 mm or more
At EF 63% with an LVESD of 34 mm, this patient has not yet crossed either threshold — close monitoring every 6-12 months is appropriate
Once EF drops below 60% or LVESD exceeds 40 mm, the window for repair before irreversible left ventricular (LV) dysfunction is closing
Why the others are wrong
When the regurgitant volume first exceeds 30 mL per beat — a regurgitant volume of 30 mL per beat is only moderate regurgitation, and regurgitant volume grades severity rather than triggering surgery
When the mean transvalvular gradient exceeds 40 mmHg — mean gradient criteria apply to valvular stenosis, not regurgitation
When pulmonary artery systolic pressure exceeds 70 mmHg — elevated pulmonary artery pressure is not a primary surgical trigger for mitral regurgitation in current ACC/AHA guidelines
When EF falls below 55% or LV end-systolic diameter exceeds 50 mm — these are the aortic regurgitation triggers (EF 55% or less, LVESD above 50 mm); in MR the low-impedance ejection into the left atrium makes EF overstate true LV function, so surgery is triggered earlier, and waiting for the AR cutoffs risks irreversible LV dysfunction
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• 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)
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
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
Feature
Acute MR
Chronic Compensated MR
Chronic Decompensated MR
Onset
Sudden (hours)
Years
Years
LA size
Normal (no time to dilate)
Dilated
Markedly dilated
LA pressure
Markedly elevated
Mildly elevated
Elevated
LV size
Normal
Dilated
Markedly dilated
LV systolic function
Hyperdynamic
Normal / preserved
Reduced
Presentation
Pulmonary edema, shock
Asymptomatic / mild DOE
DOE, fatigue, AFib
Murmur
Often short, may be soft
Holosystolic at apex → axilla
Holosystolic + S3
Management
Emergent surgery + afterload reduction
Surveillance ± surgery
Surgery if EF ≤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, regardless of LVEF
• Asymptomatic severe MR with LVEF ≤60% or LV end-systolic diameter ≥40 mm (Class 1); with a normal LV, early repair is reasonable (Class 2a) if a durable repair is >95% likely with <1% mortality at an experienced valve center
• 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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