Download Mitral Stenosis Etiology

Mitral Stenosis Lori B. Heller, MD Clinical Instructor University of Washington Medical Center Physicians Anesthesia Service Swedish Medical Center Seattle, WA Etiology In the vast majority of cases, mitral stenosis is caused by rheumatic involvement of the mitral valve 1,2 although less than 70% of patients report a history of rheumatic fever3,4 . In a surgical pathology series of 452 patients with MS seen at the Mayo Clinic in 1987, 99 percent had post‐
inflammatory disease that was presumed to be rheumatic in origin. 3 Rheumatic Heart Disease
is the most common cause
of MS
While the overall incidence of rheumatic fever and subsequent rheumatic mitral valve disease has become much less common in the United States, it still remains the most common cause of mitral stenosis. Another study of 1051 consecutive patients presenting for surgical correction of MS determined the etiology was rheumatic in 77 percent and may have been higher if not for the 15 percent of cases in which the etiology was not classified. 2 Infective endocarditis and mitral annular calcification accounted for 3.3 and 2.7 percent of cases, respectively. Other etiologies such as congenital malformation, systemic lupus erythematosus, carcinoid heart disease, Less Common Causes of MS:
endomyocardial fibrosis, and rheumatoid arthritis were implicated in less than 1 percent of cases. Infective Endocarditis
Mitral Annular Calcifications
Congenital
SLE
Carcinoid
While the US prevalence of RHD has sharply declined over the past 40 years, developing countries continue to have a significant prevalence. It is estimated that 15.6 million people suffer from rheumatic heart disease worldwide, with approximately 282,000 new cases and 233,000 related deaths each year.5 Pathophysiology and Course of Disease Patients with MS typically present more than 20 years after an episode of rheumatic fever. It is unclear if it is the initial infection combined with continued turbulent flow over the valve or if there is a smoldering rheumatic process that continues. Progressive thickening, scarring, and calcification of the mitral leaflets and chordae are the hallmark of RHD. Fusion of the commissures and chordae also cause a decrease the orifice size. This obstruction results in the development of a pressure gradient across the valve in diastole and causes an elevation in left atrial and pulmonary venous pressures. Elevated left atrial pressures then lead to left atrial enlargement, predisposing the patient to atrial fibrillation and arterial thromboembolism. Elevated pulmonary venous pressure results in pulmonary congestion and pulmonary edema. In advanced mitral stenosis, patients develop pulmonary hypertension and right‐sided heart failure.6 Secondary Findings
LAE
Afib
Pulmonary Edema
PHTN
Right Heart Failure
MVA Normal 4‐‐6 cm2 Mild Stenosis 1.6‐2.0 cm
m2 Moderate SStenosis 1.1‐1
1.5 cm2 Severe Sten
nosis < 1.0 cm
m2 2D exam Initial evalu
uation of the mitral valve sshould begin with 2D inspeection of the leaflets. Rheumatic mitrral stenosis is characterized by thickeneed, calcified leaflets witth obstruction
n of inflow intto the left ventricle. In rheeumatic heartt disease, the
e thickening b
begins at the leaflet tips and extends down the commissures toward the
e remaining pportions of th
he leaflets. Sin
nce leaflet mo
otion is restricted
d mostly at th
he leaflet tipss, the leaflets have a characteristic dom
ming appearance
e in diastole ((hockey stick deformity). TThe posterior leaflet is ofteen immobile. TThe entire miitral valvular aapparatus is iinvolved in th
his pathologicc Anterrior leaflet. Hock
key
process as t
the chordae b
become thick
kened, shorte
ened, and ofte
en fused‐
stick deformity
therefore ccontributing to the restrictted leaflet mo
ovement. Long Axis View
w of the Left Ventrricle: The anteriorr leaflet appears thickkened and displayys diastolic domin
ng or a Com
mmissural fussion is an impportant feature to distingu
uish rheumatiic hockey‐stick deformity which is characteristic o
of RHD from degenerative MS. It alsoo serves to id
dentify severee MS as comp
plete fussion of both commissures uusually indicaates more advvanced diseasse. Thiis can be seen
n in the ME viiews however is perhaps b
best appreciaated in tthe TG basal SSAX view. Postteromedial Comm
missure Anterrolateral Commisssure
TG Basal SAX alloows inspection of booth com
mmissures MS 2D characteristics
c
s:
Diastolic
c Doming of anterior
a
leaflett
Restricted motion of posterior
p
leafllet
Thickening begins at leaflet tips
ordae
Shortened, fused cho
Commis
ssural fusion
Pressure Gradients Elevvation of the mean pressu
ure gradient iis the hallmark of mitral sstenosis.7,9,10 TTo determinee, obtain the maxim
mal velocity u
using continuo
ous wave Dopppler from th
he mid‐esophageal imagess. Tracce the entire mitral valve sspectral profiile and the coomputer softw
ware will inteegrate the velo
ocities and caalculate the m
mean gradientt. Mean Gradient: Mild < 5 mm Hgg Moderate 5‐12 m
mm Hg Sevvere > 12 mm Hg CW profile of the MV inflow. Tracin
ng over the entire spectral profile w
will yield a mean mitral pressure gradient from thee machine softwarre Calcculation of M
MVA The
ere are severaal methods avvailable to determine MVA
A, each with aadvantages an
nd disadvantaages. It is best to use sseveral techniques for confirmation of ddisease and sseverity. nimetry Plan
Mitral valve areaa can be meassured by plan
nimetry in thee transgastricc basal short aaxis view. Thee ima
age of the mittral valve is frozen in diastole and the opening is trraced. Since tthe mitral vallve is not flat (it formss a funnel shape) the imagiing plane shoould be moved back and fo
orth in order tto e. This will bee the limiting aspect of thee ventricular determine the narrowest part of the valve
inflo
ow. Planimetryy of the mitral vvalve is
performe
ed in the basal short
axis vie
ew. The narrow
west
portion off the valve shou
uld be
traced.
Plan
nimetry Limittations: Exte
ensive calcificcations can m
make determin
nation of the exact locatio
on of the mitrral valve edgee difficult. Patientss with previous commissurotomies are also technicaally challengin
ng. Caution not to ove
er‐gain as this can lead to e
error.10 Pressure Half Tim
me: PHTT uses the rate of pressure
e drop across the mitral vaalve as a meassure of mitrall severity. As the severity of the m
mitral stenosiss increases, th
he time it takkes the pressu
ure between tthe left atrium
m and
d left ventricle
e to equalize during diasto
ole increases. Pressure halff time is the ttime it takes ffor the peak transmitral pressure
e gradient to decrease by hhalf. When th
he mitral valvve area is 1.0 cm2 it taakes 220 ms ffor the pressu
ure gradient aacross the mittral valve to d
drop to half itts original value. The
erefore, 220 d
divided by the
e pressure half time will givve the mitral valve area in
n cm2. MV
VA = 220/PHT Nott all increased
d PHT’s indicaate mitral sten
nosis. Patientts with abnorrmal myocard
dial relaxation
n havve a prolonged
d PHT, but the peak E velo
ocity is not inccreased and iis usually low
wer than 1 m/ssec. In p
patients with atrial fibrillation, several ccycles should be averaged.. Occasionallyy, there are tw
wo separate slopes of mitral velo
ocity – a more
e peaked initi al slope and aa second slop
pe with a longger HT should be measured fro
om the latter.. At faster heaart rates, the E wave and tthe A duration. The PH
wavve begin to fu
use and it mayy be difficult tto distinguishh the slope off the velocity profile. This m
may be o
overcome by decreasing th
he sweep spe
eed of the speectral profile.. Spectral Dopp
pler pattern of m
mitral inflow vvelocity. This caan be obtained ffrom any of the midesophageal LV views. Mostt TEE machines determine PHT have software packages that d
when the E slope is trraced. To m
measure Presssure Half Tim
me: PH
HT underestim
mates MS seve
erity
In AI and impairred LV relaxatiion
Optimize CW mitral inflow velocity 1. O
2. C
Change sweep
p speed to 10
00 mm/s 3. TTrace the slop
pe of the E waave 4. TThe machine ssoftware packkage will provvide you withh PHT and MV
VA manually: Calcculation of the PHT can alsso be done m
1. O
Optimize CW mitral inflow velocity 2. C
Change sweep
p speed to 10
00 mm/s 3. M
Measure the p
peak E wave vvelocity, or VMAX M
4. VMAX ÷ 1.4 = V t1/2 5. D
Draw vertical lines from E sslope to baseline at VMAX aand V t1/2 6. M
Measure time
e interval (T1/22) from VMAX tto V t1/2 7. M
MVA = 220÷ TT1/2 Deceleration Time Alternatively, Deceleration time can be used to calculate MVA. Pressure half time is 0.29% of deceleration time. Therefore MVA = 760/DT PHT = 0.29 x DT PHT/Deceleration Time Limitations: Aortic Insufficiency and abnormal myocardial relaxation will underestimate the severity of MS by PHT. PHT has not been validated in the post CPB patients and has been found inaccurate in post‐commissurotomy patients due to its dependence on net chamber compliance. 8 Continuity Equation on and the conservation off energy statees: The continuity equatio
LVOT (are
ea) x LVOT (TV
VI) = MV (areaa) x MV (TVI)
LVOT areaa = left ventricular outflow
w tract area LVOT (TVII) – left ventriicular outflow
w tract time‐vvelocity integrral MV (TVI) =
= mitral valve
e time‐velocitty integral Mitral Vallve area can ttherefore be d
determined w
with the threee of the other variables in the equation
n. 2
LVOT areaa is determine
ed by calculattion of Πr (th
he formula foor area of a circle), where rr is the ½ the diameter of the LVOT m
measured in tthe aortic LAX
X view and thhe respective VTI’s are obttained using spectral D
Doppler. LVOTT VTI can be o
obtained with
h PWD in the deep transgaastric position
n and the VTI of the MV ob
btained in the
e mid‐esophaageal position
n using CWD. LVOTAREA
x VTI = MVAREAA x VTI
A
Dooppler through LVO
OT Diameter of the LVOT MVAREA =
x
CW through MV
V Con
ntinuity equation demonsstrated Associated Findiings The
e increased left atrial presssure associate
ed with mitraal stenosis leaads to left atrial enlargemeent, pid regurgitaation. Left atrial pulm
monary hype
ertension, right ventriculaar enlargemen
nt and tricusp
size
e should be m
measured in th
he short axis vview of the aoortic valve, ass this view haas best been corrrelated with ttransthoracic images. Left atrial dilationn with low flo
ow and high p
pressure can lead to thrombus form
mation and th
he left atrium
m and appenddage should b
be inspected tthoroughly beefore and
d after surgeryy. Regional w
wall motion aabnormalitiess of the posteerior‐basal myyocardium in patients withoutt CAD occur w
with severe rh
heumatic mitrral stenosis and may indicated a mechaanical teth
hering of the myocardium caused by a sscarred mitraal valve. All off these secondary findingss can help
p confirm the
e diagnosis off mitral stenossis and aid in the determin
nation of seveerity. LA
LAE
RA
Leftt atrial enlarggement Bowing inteeratrial septu
um LA >
> 39 mm indicative of LAEE Inte
eratrial septu
um bowing to
o the right ind
dicative of inccreased LAP
Leftt atrial size sh
hould be meaasured in the short axis vi ew of the AV
V 12 Mean gradient ((mmHG) PHT
T (msec) MV
VA (cm2) Mitraal Stenosis Seeverity Mod
derate MILD 6 100
0‐150
1.5
5‐2.0 6‐122 150‐‐200 1.0‐11.5 Severre >12 >220
0 <1.0
0 References 1. Olson LJ, Subramanian R, Ackermann DM, et al. Surgical pathology of the mitral valve: a study of 712 cases spanning 21 years. Mayo Clin Proc 1987; 62:22. 2. Horstkotte D, Niehues R, Strauer BE. Pathomorphological aspects, aetiology and natural history of acquired mitral valve stenosis. Eur Heart J 1991; 12 Suppl B:55. 3. WOOD P. An appreciation of mitral stenosis. I. Clinical features. Br Med J 1954; 1:1051. 4. ROWE JC, BLAND EF, SPRAGUE HB, WHITE PD. The course of mitral stenosis without surgery: ten‐ and twenty‐year perspectives. Ann Intern Med 1960; 52:741. 5. Carapetis JR, Steer AC, Mulholland EK, et al: The global burden of group A streptococcal diseases. Lancet Infect Dis. 2005, 5: 685‐694. 6. Bruce C., Nishimura R. Valvular Heart Disease CLINICAL ASSESSMENT AND MANAGEMENT OF MITRAL STENOSIS. Cardiology Clinics. Volume 16 (3) August 1998 7. Zaroff J., Picard M Transesophageal Echocardiographic Evaluation of the Mitral and Tricuspid Valves. Cardiology Clinics. Volume 18 • Number 4 • November 2000 8. Thomas JD, Wilkins GT, Choong CY, et al. Inaccuracy of mitral pressure half‐time immediately after percutaneous mitral valvotomy. Dependence on transmitral gradient and left atrial and ventricular compliance. Circulation, Vol 78, 980‐993 9. Savino J Transesophageal Echocardiographic evaluation of Native Valvular Disease and Repair. Critical Care Clinics Vol 12(2). April 1996. 10. Porembka D. Transesophageal Echocardiography. Critical Care Clinics. Vol 12 (4) Oct 1996 11. Block M. Comparison of left atrial dimensions by transesophageal and transthoracic echocardiography. Journal of the American Society of Echocardiography. Volume 15 • Number 2 • February 2002 12. Block M, Hourigan L, Bellows W H. et al Comparison of left atrial dimensions by transesophageal and transthoracic echocardiography. J Am Soc Echocardiogr 2002. (15) 143–149.