MITRAL REGURGITATION

ETIOLOGIES

ACUTE CHRONIC
Annulus disorder Inflammatory
• Endocarditis (abscess) • Rheumatic heart disease
• Trauma (surgery) • Lupus
• Paravalvular leak by suture interruption (surgery) • Scleroderma
Leaflet disorder Degenerative
• Endocarditis (perforation) • Myxomatous degeneration (Barlow, MVP)
• Trauma (BMV) • Marfan
• Tumor (atrial myxoma) • Ehlers-Danlos
• Myxomatous degeneration • Pseudoxanthoma elasticum
• LED – Libman-Sacks lesion • Calcification of mitral annulus
Rupture of chordae tendineae Infective
• Spontaneous • Endocarditis
• Myxomatous degeneration (prolapse, Marfan, Ehlers-
Danlos)
• Endocarditis
• Acute rheumatic fever
• Trauma
Papillary muscle disorder Structural
• ACS • Rupture chordae tendineae (spontaneous or
• Acute LV dysfunction secondary to ACS, trauma, MV prolapse,
• Infiltrative disease (sarcoidosis, amyloidosis) endocarditis)
• Trauma • Rupture or dysfunction of papillary muscle
• Dilation of mitral valve annulus and LV
cavity
• Hypertrophic cardiomyopathy
• Paravalvular prosthetic leak
Primary mitral valve prosthetic disorder Congenital
• Cusp perforation (endocarditis) • Mitral valve clefts or fenestrations
• Cusp degeneration • Parachute mitral valve with endocardial
• Mechanical failure cushions defects, endocardial fibroelastosis,
• Immobilized disc or ball • Transposition of great arteries
• Anomalous origin of left coronary artery

Carpentier’s classification

• Type I: normal leaflet motion – jet is central

• Type II: increased leaflet motion (leaflet prolapse) – jet is directing towards opposite side
• Type IIIa: restricted leaflet motion during diastole and systole – jet is central or same side
• Type IIIb: restricted leaflet motion predominantly during systole (ischemic) – jet is same side

Primary MR: degenerative (Barlow, IE, connective disease)

Secondary MR: functional (LV dysfunction…)

Coronary artery disease

30% patients with CAD have some degree of MR
- Tethering of posterior leaflet because of regional LV dysfunction
- Worse MR because associated to LV remodeling and systolic dysfunction

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 - Also ischemic damage to papillary muscles, dilation of mitral valve ring and/or loss of systolic annular
contraction contributing to MR
- Severe MR associated to poor prognosis
- 20% MR after ACS – more adverse outcomes

PATHOPHYSIOLOGY

o 50% regurgitant volume is ejected in LA before aortic valve opening

o Orifice size and pressure gradient are labile – gradient depends on SVR and mitral annulus
o Severe MR – LV volume overload (é preload and afterload)
o LV and LA compliance increases = low LV filling pressure - é LVEDV = chronic compensated stage of
severe MR
o émitral annulus + regurgitant orifice = ê contractility LV
o Eccentric hypertrophy (é mass)
o LA can dilate and cause afib
o Eventually LV function deteriorates, EF falls, ESV and EDV é, LV compliance ê, LV filling pressure é
à pulmonary congestion with mild effort and ê CO
o ê SV in late in chronic severe MR
o êEF reflect impaired myocardial function (contractility) and patients do poorly after surgical
correction of MR èEF < 35% = high risk patients without post-op benefits
o LVESV or diameter: predictor of function and survival after surgery (> 40mm)
Acute MR
§ Sudden onset severe reflux into normal sized LA
§ Signs and symptoms depend on size and compliance of pre-existing LA

CLICINAL SYMPTOMS

- Fatigue (low CO), left heart failure symptoms, palpitations (AF), and pulmonary congestion
- Right heart failure present in acute MR

PHYSICAL EXAM

JVP, carotid, precordial motion directly related to severity of leak not cause

CAROTID
- Mild – normal
- Moderate-severe – brisk, often êpulse volume (if presence of heart failure)
o b/c N or decrease forward SV ejected more rapidly than normal during early systole
- Severe – quick rising, poorly sustained, low amplitude
JVP
- Large V waves
- AF – loss a, V more prominent
PRECORDIAL
LV impulse
- Hyperdynamic
- Displaced
- Dilated
- +/- Palpable S3 – early diastole, pt hold breath end-exp (decubitus)
Parasternal impulse
- Pulm HTN – sustained RV lift, holosystolic
o More common in combined MR/MS

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 o Also loud P2, RV S4, TR/PR
- Systolic expansion of enlarged LA = late systolic thrust
S1
- êS1 amplitude (masked by murmur)
- Loud if holosystolic prolapse of MV
S2
- Severe – wide split and early A2 (shortening of LV ejection)
- P2 louder if pHTN P2>A2
S3
- Common – means large regurgitation volume
- Also present if LV dysfct with dilation
S4
- LV S4 never seen in rheumatic MR b/c LA dilated and can’t generate force
- S4 common in acute or papillary muscle dysfunction due to cardiomyopathy
- RV S4 if PHTN (louder with insp, max intensity at LLSB)

MURMUR

SYSTOLIC
- Starts with S1 and extends to S2 – beyond A2 (pressure gradient between LV-LA after Ao valve
closure)
o 50% of entire regurg vol reflux to LA before AV open
- Holosystolic
o Late systolic: mild MR – PVM or papillary muscle dysfunction
o Early systolic: Acute MR – diamond shaped decreasing in late systole (é pressure non
compliant LA)
o Holosystolic: Severe MR – long murmur + diastolic rumble
- High pitch
- Loudest at apex
- Radiate
o Axilla or left scapula (murmur directed posteriorly – anterior leaflet involvement)
o Towards sternum and base (murmur directed anterior – prolapse of posterior leaflet)
- Ruptured chordae – murmur usually harsh, loud (>gr 3)
- Not amplified post PVC
- Regurgitant murmur – fremitus
- ê upward position, Valsalva
- é handgrip, squatting
- Little correlation between intensity of systolic murmur and severity of MR
- Silent MR: LV dilatation, ACS, paraprosthetic valvular regurgitation, emphysema, obesity, chest
deformity, prosthetic valve

DIASTOLIC
- short mid-diastolic flow murmur, brief, low- to med-pitched apically best heard with bell when pt
decubitus, light pressure - é flow during filling in diastole

DIFFERENTIAL DIAGNOSIS

TR
- hard to separate if RV enlarged
- TR usually increase with inspiration (Carvallo), MR softer

VSD
- maximum location at LLSB

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HOCM
- also has long SEM
- may not have typical radiation
- attn to change with posture, maneuver, drugs

ddx MR and AS – carotid, length of murmur, murmur post PVC (murmur increases with AS)

ECHOCARDIOGRAPHY

Primary MR
- Assess LV size and function, RV function, left atrial size, PA pressure, mechanism and severity of
primary MR
- CMR is indicated in chronic primary MR to assess LV and RV volumes, function or MR severity

Secondary MR
- Assess the etiology of chronic secondary MR and extend and location of wall motion abnormalities and
LV function, severity of MR and pulmonary hypertension.

★ Suggested reference: Zoghbi W. et al. Recommendations for the evaluation of the severity of native valvular
regurgitation with two-dimensional and Doppler echocardiography. 2003 J Am Society
Echocardiography;16:777-802.

Poor prognosis when ERO ≥ 20 mm2

TEE
- Not recommended for routine evaluation and follow-up
- Performed when TTE images are inadequate
- Useful in IE – better visualization of underlying infected structures
- More precise quantification of regurgitation severity and better evaluation of likelihood of success of
MV repair

Follow-up
- Severe primary MR (C1): annual or biannual
- Moderate MR: 1-2 years
- Mild MR: 1-2 years

★ Suggested reference: Nishimura R. A. et al. 2014 ACC/AHA guidelines for the management of patients with
valvular heart disease. J Am Coll Cardiol 2014;63:e57-185 – Tables 15-16

CATHETERIZATION

- Ventriculography and hemodynamic measurements when noninvasive testing are inconclusive

o Severity of MR
o LV function
o Need for surgery
- Discrepancy between noninvasive testing and clinical symptoms

★ Suggested reference: Nishimura R. A. et al. 2014 ACC/AHA guidelines for the management of patients with
valvular heart disease. J Am Coll Cardiol 2014;63:e57-185.

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EXERCISE TESTING

Can be used to establish the presence of symptoms in patients with chronic primary MR and exercise tolerance.

TREATMENT

★ Suggested reference: Nishimura R. A. et al. 2014 ACC/AHA guidelines for the management of patients with
valvular heart disease. J Am Coll Cardiol 2014;63:e57-185 – Table 17, 18, figure 4

MEDICAL
Acute MR
- Vasodilators
- IABP
- Prompt mitral surgery

INTERVENTIONS
Primary MR
MV repair >> MV surgery if possible (especially when posterior leaflet involved)
- LVEF greater than 30% and symptoms
- LVEF between 30-60% and asymptomatic, with LVESD of 40 mm or more

Surgical repair
- Pliable valves
- Degenerative MR due to MVP
- Annular dilatation
- Papillary muscle dysfunction due to ischemia or rupture
- Chordal rupture
- Perforation of mitral leaflet cause by IE

Older valves with calcium, deformed, rigid, severe subvalvular chordal thickening and loss of leaflet substances
= MVR necessary
ê EF 10% if valve apparatus not preserved!

Minimal invasive procedures vs. conventional sternotomy showed similar performance results when performed
by experienced surgeons.
Annuloplasty and repair of posterior leaflet shows better outcomes than MVR – mortality < 1%, 95% freedom
of reoperation, 80% with MR < ¾ at 15-20 years post-op.
Annuloplasty and repair is more complex with 2 leaflets but shows better outcomes than MVR – 80% freedom
of reoperation, 60% with MR < ¾ at 15-20 years post-op. Durability of the procedure is uncertain.

MitraClip
- Clip is safe (Everest I) but less effective than surgical repair (Everest II)
- Residual MR by creating 2 regurgitant orifice – similar to Alfieri procedure
- Reduce symptoms by reducing MR, reverse LV remodeling
- For patients with chronic severe MR with symptoms NYHA 3-4 despite medical therapy for HF and
are not candidate for surgery
o Degenerative MR with malcoaptation A2-P2, functional MR
o Coaptation depth < 11 mm
o Coaptation length > 2 mm
- Class IIb indication in guidelines

★ Suggested reference: Mauri L. et al. 4-Year results of a randomized controlled trial of percutaneous repair versus
surgery for mitral regurgitation. J Am Coll Cardiol 2013;62:317-328.

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Secondary chronic MR
- Reasonable if severe secondary MR undergoing surgery for CABG
- If patient has persistent symptoms despite optimal medical therapy
- Recent data not conclusive….

★ Suggested reference: Asgar A. et al. Secondary mitral regurgitation in heart failure. J Am Coll Cardiol 2015;65:1231-
48.

Content of this summary from these references:

• Otto C & Bonow R. Valvular Heart Disease. (2012) In Bonow R. et al. Braunwald’s Heart Disease, 9th
edition, pp. 1468-1539. Philadelphia, PA: Elsevier.
• Nishimura R. A. et al. 2014 ACC/AHA guidelines for the management of patients with valvular heart
disease. J Am Coll Cardiol 2014;63:e57-185.
• Zoghbi W. et al. Recommendations for the evaluation of the severity of native valvular regurgitation
with two-dimensional and Doppler echocardiography. 2003 J Am Society Echocardiography;16:777-
802.

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