Mitral stenosis

My DDU point form notes on mitral stenosis…

The rest of my DDU notes are here.

ASSESSMENT

anatomy, mobility, calcification
mean transmitral gradient
valve area by

planimetry 2D/3D

pressure half time

pulmonary artery pressures
MR

TTE good
TOE better

except subvalvular

3D useful

degree and asymmetry of commissural fusion

planimetry

CAUSES

rheumatic disease

commonest cause by far

tips affected most

(cf MAC)
bowing / doming due to commissural fusion → tips restricted > base and mid
tip thickening ± base and mid

commonly also affects subvalvular apparatus

chordal shortening, fusion, fibrosis, Ca²⁺

assessment

leaflet

thickening

Ca²⁺

mobility

subvalvular involvement

mitral annular calcification (MAC)

commonly found in elderly
is a CV risk factor
LV side of posterior annulus → entire posterior annulus ± AMVL (especially if calcific AS)
can cause mild-moderate MR
occasionally, extends onto base of leaflet → functional MS

D/DX

other causes of pulmonary congestion

LV systolic / diastolic dysfunction
AV disease
MR
rarities

myxoma

cor triatrium

QUANTITATION

mean transmitral gradient

uses CWD VTI → simplified Bernoulli averaged over curve

if PWD used will underestimate if not placed at narrowest area of flow

depends on transmitral volume flow rate as well as area

∴ if SV down (e.g. due to LV diastolic problems) → relatively low mean gradient

also, with tachycardia and significant MR, gradient can ↑ without MS → in this case deceleration slope of early diastolic filling will not be ↓ (cf MS)

VALVE AREA

planimetry

orifice elliptical, more planar than AS ∴ planimetry useful

validated cf catheter determined valve area, area at surgery

approach

PSAX + zoom
funnel shaped inflow ∴ start mid-pap in PSAX, tilt slowly slightly medially and superiorly until entire orifice just visible
use the highest possible transducer frequency
optimise gain, dynamic range and focus so the
mitral orifice is clearly delineated
use mid-diastolic frame
inner margins of the leaflets at the blood-tissue interface
average 3-5 beats

ideally consecutive, avoid post ectopic beats

3D more reproducible (align image in plane of minimal orifice)

pressure half time valve area

assumptions

assumes rate of pressure decline relates to CSA orifice

neglects LAP, LV compliance issues

PHT

time to halve from max early diastolic pressure gradient

defined invasively initially

for an individual, independent of exercise induced Δ flow rate
Doppler equivalent: time from V_max to V_max / √2
empirically: MVA = 220 / PHT

correlates with invasive valve areas

technical considerations

parallel

CFD helpful to align

PWD or CWD

Bonita seems to use CWD

PWD “better definition of maximum velocity and early diastolic slope” per Otto

fails if

arrhythmias

average multiple beats, exclude v short early diastolic periods (can’t measure slope accurately due to next beat / A wave)

non-linear or curvilinear diastolic slopes

if can’t get a linear slope, use mid-diastolic slope

acute changes in LA compliance, LV diastolic dysfunction

∴ not true for 72 hrs post balloon commisurotomy

significant aortic regurgitation (severe)

fills LV → ↓ PHT

can cause functional MS (Austin-Flint) → ↑ PHT

atrial shunt

continuity equation

MVA = transmitral SV / VTI_{MS jet}
VTI_{MS jet} from CWD
SV from

CSA_LVOT x VTI_LVOT (if no MR or AR)

CSA_PA x VTI_PA

only accurate if

no significant MR, AR if using LVOT to get SV

parallel VTI_{MS jet}
useful with Δ chamber compliance

other

PISA not used – doesn’t work due to need to integrate volume flow rate over diastolic filling period

CONSEQUENCES

left atrial enlargement / thrombosis

pressure → enlargement
enlargement + low volume flow rate due to MS → stasis → thrombus
thrombi in LAA > on wall, IAS (laminated)
more common in AF
TTE <50% sensitive

can’t see LAA well

best views

PSAX @ aortic valve + lateral angulation

A2C + superior tilt

beamwidth artefact / poor penetration contribute

TOE 99% specific and sensitive

high frequency (5-7MHz)

closer

pulmonary hypertension

MS → ↑ LAP → pulmonary venous HT → arterial HT

initial passive ↑ pulmonary arterial pressures (PVR unΔ)

reversible

later Δ vascular bed → ↑ PVR

exercise testing if symptoms > expected for degree of MS

measure immediately post exercise

mitral regurgitation

common
significant → CI to commisurotomy
PHT valve area and planimetry still accurate, continuity not accuate

rheumatic heart disease of other structures

aortic valve

AR and MS jets together can complicate assessment of AR
assess just proximal to AV (in LVOT) to avoid problems

tricuspid valve

TS hard to see on 2D
Doppler useful
assess TR carefully – may need annuloplasty at time of MV surgery

LV response

usually LV is small

dilated → look for MR, AR, IHD etc

diastolic function impaired due to small orifice

SPECIFIC PATIENT POPULATIONS

pre commisurotomy

scoring systems predict haemodynamic results and complications

leaflet mobility, thickness, Ca²⁺

commissural Ca²⁺

subvalvular involvement

CI if moderate or worse MR
LA thrombus

may be dislodged by procedure

post commisurotomy

MR
ASD size @ transeptal puncture site
PHT valve area method inaccurate
PASP

from BSE except where noted

Cover image: Streptococcus pyogenes (Lancefield Group A) on Columbia Horse Blood Agar – Detail