"Starr-Edwards-Mitral-Valve" by Dr. Mirko Junge

My DDU point form notes on mitral regurgitation…

The rest of my DDU notes are here.



annulus, leaflets, chordae, papillary muscles (LA, LV walls)


D shaped

saddle shaped

anterior and posterior points superior (towards LA)
shape changes during cycle

anteromedially shares wall with aortic annulus

=aortomitral curtain, next to left and noncoronary cusp
more rigid than elsewhere

posterior annulus longer than anterior

dilates > anterior



2/3 of area, thicker, D shaped
no true anatomic separations • 3 segments


crescent, 2/3 of attachment to annulus
3 scallops


3 types

primary to margins

rupture → flail / prolapse

secondary to body
tertiary to base

from papillary mm


more prone to infarction (RCA territory)


which is actually on the posterolateral wall!

Carpentier nomenclature

1’s are antero1ateral, 3’s are postero3edial


determines therapy

primary (valvular)

leaflets / chordal – Mx usually surgical


MVP commonest 1° cause, myxomatous change
ruptured chordae
thickening / Ca2+

MAC may have mitral stenosis also




Libmann-Sacks lesions

rheumatic, radiation, and drugs

all cause leaflet thickening / restricted posterior leaflet


cleft / endocardial cushion defect

secondary (functional)

term sometimes used to mean non-ischaemic, usually ischaemic
commonest cause

Δ geometry

commonly myocardial dilation and ↓ systolic function (especially posterior / inferior wall)
→ papillary muscle dysfunction (lateral / posterior and apical displacement) and annular flattening / dilatation
→ tethering, incomplete coaptation

“ischaemic” MR

commonly due to remodelling, but occasionally

papillary m rupture

acute and transient with AMI

functional MR → higher periop mortality for CABG

TTE assessment

A4C best
tenting seen best on anterior valve leaflet

bend in leaflet from 2° cord

normal convex shape → concave
can measure

tethering height: distance from mitral annulus plane to coaptation point in systole, ≥11mm significant

tethering area


ACEI, statins, β blockers,… ie Rx CHF
consider biventricular pacing
± surgical intervention

MR due to LVOT obstruction

underfilling, tachycardic hyperdynamic LV with low afterload → high velocity jets → AMVL sucked into jet by Venturi (SAM)

common post MV repair

potentially with undersized annuloplasty ring or long posterior leaflet → anterior coaptation point → redundant mitral tissue sucked in

echo features

CFD: jet usually directed slightly posteriorly → systolic aliasing in LVOT
spectral Doppler: dagger shape CWD with late systolic peak (since LVOT gradient ↑ progressively during systole)

see in TG mid long axis or deep TG LV


displacement of mitral leaflets during systole > 2mm from annular plane
spectrum from minimal prolapse to flail
thick (>5mm) leaflets, ≥ moderate MR and LVEF <50% → worse prognosis

Carpentier classification

based on leaflet motion

type 1: normal leaflet motion

annular dilatation, perforation

type 2: ↑ motion

billowing / scalloping: body protrudes above annular plane in systole but point of coaptation below annular plane
prolapse: tip above annular plane in systole
flail: mitral leaflet flows freely into LA, loss of normal concave shape

usually ruptured chordae

always significant, often severe MR

type 3: ↓ motion

3a: systole and diastole

eg rheumatic heart disease

3b: systole only

commonly functional



thickened, Ca2+?



motion: normal, excessive, restricted?

coaptation point: below, at, above annular plane? no coaptation?


TOE: diameter in bicommisural (~60°) and anteroposterior (~150°)

normal 28-32 mm; dilates posteriorly

consider loading conditions / rhythm

GA will ↓ apparent severity by 1 full grade

colour Doppler

gain, Nyquist optimised

jet direction

functional slightly posterior
very eccentric (>45°) → structural

type 1 (N motion): usually central

type 2 (↑ motion): usually away from diseased leaflet

type 3a (↓ motion): usually toward diseased leaflet

type 3b (↓ motion, but because posteromedial PM attaches to both → affects both leaflets): slightly posterior

jet surface area


>40% of LA better than absolute area vs angiographic standard, but measure both in same systolic frame

>10 cm2

big Otto

Nyquist ≥ 50 cm/s

avoid including low velocity nonturbulent blood flows in measurement

average area on multiple views

easy to miss / underestimate eccentric jets

MR jet size affected by containment by LA wall, flow influences by pulmonary veins ∴ don’t overinterpret

wall hugging

coanda effect → jets appear smaller
nearly always structural


peak velocity

LV to LA gradient

density varies with machine setting and alignment of CW beam ∴ supportive only

dense, sharp, complete → more severe

pulmonary blood flow supportive only per Otto

PWD 1-2cm into pulmonary vein
S wave blunting or reversal S2 wave first → haemodynamically significant

big Otto: any cause of ↑ LAP (LV dysfunction, AF) will blunt S wave cf reversal fairly specific

Oxorn: “in presence of MR, (reversal is) specific but not sensitive”

if v eccentric can be just one pulmonary vein → pulse all if possible


vena contracta

per big Otto

area is effective orifice area

remember flow continues to converge for a short distance beyond the anatomic orifice

less influenced by loading / haemodynamic factors / wall impingement than jet area methods

use views orthogonal to MV coaptation line ie long axis PLAX, A3C

per Oxorn

MO long axis, zoomed

Nyquist ~55 cm/s

<3 mm mild, >7 severe


may be oval vena contracta → don’t rely on this one measurement

need to see whole jet in continuity (flow convergence → vena contracta → distal jet) to be reliable

PISA (proximal isovelocity surface area)

presence of a PISA suggests significant MR
if peak MR velocity ~5 m/s AND Nyquist 40 cm/s shift baseline then regurgitant orifice area = r2 / 2

simplification of flow = area x velocity

at orifice: ROA x peak MR velocity

at PISA shell: Nyquist x 2πr2

these flows are the same

so solving for ROA = Nyquist x 2πr2 / peak MR velocity

if incomplete PISA shell, needs angle correction (α / 180)

> 0.4 cm2 (40 mm2) → severe

ROA x MR VTI = regurgitant volume (>60 ml)
RV / LVOT SV = regurgitant fraction (>50%)

many assumptions

regurgitant orifice is round
one orifice
PISA is complete hemisphere, not cone or flattened hemisphere

big Otto

∴ Nyquist needs to be low cf regurgitant velocity,

inaccurate with flail due to constraint,

results vary widely when radius measured at different distances from orifice

measure along beam, not across (underestimation due to colour dropout)

all measurements made at same point in cardiac cycle

big Otto: ROA Δ during systole

→ avoid PISA radius measurement v early or late in systole, flow rate not at equilibrium

ideally at same time as peak MR velocity, ~mid systole or at T wave

volumetric methods

reproducible results need significant training • many sources of error

basic idea

MR volume = mitral inflow – aortic outflow
= CSAmitral inflow x VTImitral inflow – aortic outflow


PWD at mitral annular plane for VTImitral inflow
CSAmitral inflow = πr2

problem: annulus not circular, though more circular in MR than normal due to dilation

aortic outflow = CSAAo x VTIAo

assumes no AR

alternative approach

MR volume = LV stroke volume by planimetry – aortic outflow volume, again assuming no AR


useful for mechanism, planning surgical Mx, ?role of leaflet stress

direct planimetry of vena contracta area

without geometric assumptions
do full volume 3D colour of 7-14 cycles
narrow sector to ↑ frame rate
correlates well with Doppler, MR volume on MRI
spatial resolution main limitation → don’t bother if not at least moderate


Jet area / LA<20%>40%
<4cm2 Oxorn>10 cm2 Oxorn
Vena contracta (cm)<0.3≥0.7
PISA radius (Nyquist 40 cm/s)<0.4>1.0
Regurgitant volume (mL)<3031-59≥60
Regurgitant fraction (%)<3031-49≥50%
Regurgitant orifice area (cm 2 )<0.20.21-0.39≥0.40
or 40mm2
Other features from Oxorn and Otto
LA and LV size nonspecificnormalnormal / dilatedusually dilated
other 2D featuresmay see ruptured chordae, papillary muscle, flail leaflet
colour Dopplerswirling in LA
pulse wave Doppler
mitral inflowA dominantvariableE dominant
since correlates with D on pulmonary veins
jet densityfaint, incompletedensedense
contourparabolicusually parabolicearly peaking, triangular
PV flowS dominantS bluntedsystolic reversal
other: ↑ RVSP


sudden volume load

no time to adapt

APO, ↑ R sided pressures, SOB
hyperdynamic LV but unable to dilate adequately → ↓ CO, ↓ BP


fast, full and forward
∴ vasodilators (if BP allows), IABP
urgent surgery

Cover image: “Starr-Edwards-Mitral-Valve” by Dr. Mirko Junge


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