MITRAL STENOSIS Flashcards
Most common cause of MS in the world?
Rheumatic heart disease is the most cause of MS in the world
Second most common cause of MS?
Calcific disease
Rare causes of MS?
Inflammatory disease
Carcinoid
Infiltrative disease
Radiation induced
Drug induced
Among patients with rheumatic mitral valve disease what is the proportion of MS and MR?
25% isolated MS
40% mixed MD and MR
Echo features of rheumatic mitral stenosis?
In PLAX view we see hockey stick appearence where as in PSAX view we have the fish mouth appearence
- Thickening at the tip of the leaflets
- Commisural fusion
- Hockey stick pattern in PLAX during opening and closing.
- Leaflet thickening and calcification
- Chordal shortening and fusion
What does this view indicate?
This is the “hockey stick” appearence of rheumatic MS that we see in PLAX view
What does this image indicate?
This is the “fish mouth appearence” we see in PSAX view in rheumatic MS
Pathophysiology of rheumatic heart disease?
Autoimmune disease due to M protein that is common with group A strepp and heart cells. B cells get activated and make antibodies which then attack the heart and cause rheumatic heart disease
This autoimmune process causes fibrosis and endothelial injury mostly at the mitral commissures resulting in commissural fusion.
Natural progression of rheumatic mitral stenosis?
- 10-15 years after RF patients will have MS and then LA dilation, increase LAP and pulmonary edema which then causes dyspnea
- Later on as LA dilates even more patients develop atrial fibrillation
- Later patients can develop Class III/IV heart failure symptoms
Features of degenerative calcific mitral stenosis?
These patients have a chronic degenerative process of calcification due to aging. Calcification causes MAC and can extend to the leaflefts giving reduced mobility.
These patients usually have calcification elsewhere and can have comorbidities.They often can have calcific aortic stenosis.
Pathophysiology: Mitral annular calcification extending into leaflets leading to obstruction of LV inflow
Natural history of calcific MS?
Without intervention if a patient has severe calcific MS then survival is 72% at one year and 52% at 3 years.
Note: Based on Mayo stidy of 200 patients with severe calcific MS from 2003 to 2017
Anatomy of the mitral valve?
Mitral valve has two leaflets.
Anterior leaflet which has scallops : A1 anterior segment, A2, middle segment and A3 posterior segment
Posterior leaflet which has scallops: P1 posterior, P2 middle and P3 anterior
Commisures define the areas where the anterior and posterior mitral leaflets come together at their insertion into the annulus
Mitral valve surgical view?
PSAX view of the mitral valve?
PLAX view of the mitral valve?
Apical 4C view of the mitral valve?
Apical 2 C view of the mitral valve?
3 Chamber view of the mitral valve?
Surgeon view of the mitral valve?
Real specimen of mitral valve?
Surgeon’s view of the mitral valve?
Cardiac auscultation in mitral stenosis?
Loud S1 (closure of MV) initially due to increased LAP. This indicates a pliable valve
Later in more severe disease we have soft S1 as it has less and less excursion
Opening snap followed by diastolic rumbling murmur
Physical exam findings in mitral stenosis?
Left atrial dilation > atrial fibrillation
Pulmonary hypertension > Loud P2, RV heaving
RV hypertrophy and dilation > TR murmur, JVP, edema and asites
EKG findings of mitral stenosis?
LA enlargement
Atrial fibrillation
Signs of RV strain such as RVH and Right axis deviation
Chest X-ray findings of mitral stenosis?
LA appendage enlargement (loss of concave pattern at the arrow)
Right atrium enlarged
Pulmonary hypertension with noticable pulmonary vessels
Pulmonary cephalization/edema
Splaying of the carina
Elevation of left main bronchus
Cardiomegaly
Normal CXR anatomy?
Double density sign on CXR in MS?
In a normal CXR there is only one right heart border which is the right side of the right atrium.
In MS, left atrium becomes so enlarged that the right side of the LA pushes against the lung and can be seen even further to the right than the right side of the right atrium giving the double density sign.
Third mogul sign on CXR in MS?
The left cardiac border just below the main pulmonary artery is the left atrial appendage. Enlargement of this will give rise to a convexirty (loss of flattening or even a bump) in the left heart border at the level of the main pulmonary artery.
Splaying of the carina in CXR on MS?
The LA is located directly inferior to the carina and enlarged LA can cause the main bronchi to move away from each other giving a carina angle greater than 90 degrees.
LAE will cause elevation of the left main bronchus
Morphology in rheumatic MS?
We have thickened tips of the MV leaflets with reduced excursion
Commisural fusion
Thickened sub-valvular apparatus
Hockey stick appearence
Dilated RA
Dilated LA
Morphology in rheumatic MS, doppler evaluation?
Here we can see flow acceleration across the MV during diastole. We should also assess for any MR on doppler
Rheumatic MS morphology?
Here we see commisures are severely thickened with reduced excursion. (Note: Sometimes we might be able to see the fish mouth appearence)
Assessing MS severity
MV mean gradient?
If we do a doppler across the mitral inflow and trace a VTI around the signal we will get a mitral valve mean gradient.
The mean gradient is affected by:
(1) . Heart rate (If slower HR then more time from the blood to go from the LA to LV and the mean gradient will be lower, if tachycardic then the gradient will be higher as diastole would be shorter)
(2) . Mitral regurgitation (there is more preload going back therefore, higher gradient)
(3) . Cardiac output (high output states will increase the gradient)
(5) . Anemia (high flow states will again increase the gradient in anemia)
(6) . Atrial fibrillation (beat to beat variability)
Therefore, anything that causes high flow rates (anemia, MR, tachycardia, thyrotoxicosis) will cause an increase in the gradient whereas low flow states such as bradycardia, cardiomyopathy and low stroke volume will decrease the gradient.
Mean gradient : < 5 (mild MS)
5-10 (moderate MS)
>10 (severe MS)
NOTE: We cannot use the mean gradient alone to assess the severity of the mitral stenosis. We have to make sure high output states and other states are not present which might give us a false value.
Assessing MS severity
Pressure half time
Pressure half time is the time it takes from the instantaneous initial MV gradient between the LA and LV to decline to half of it’s original value. In a way it is the rate of decay of the MV gradient. The longer it takes for the pressure to decline to half of it’s value, the more severe the stenosis
MVA = 220/PHT
(220 is a constant derived from the cath lab)
Assessing MS severity
Pressure half time
When measuring PHT we use continuous wave doppler across the mitral valve in diastole
If the signal has an early sharp decline and then a flatter bed, we should use the flatter portion of the signal to measure PHT and not the early part. In some cases we just have one slope and we should use that.
Assessing MS severity
Pressure half time calculations?
To calculate MV area we can use 220/PHT
We can also use deceleration time (only validated in rheumatic heart MS and not in calcific MS) : Decel time x 0.29 = PHT which then gives us MVA = 750/deceleration time
Deceleration time in MS?
Deceleration time is the time it takes for the peak E velocity to reach 0. Normally deceleration time is between 150 and 200 ms.
In MS deceleration time will increase due to stenosis of the valve
We measure deceleration time by tracing from top of the E wave to the horizontal axis.
Limitations of pressure half time?
We cannot use PHT if there is underlying compliance issues of the LV such as diastolic dysfunction
We cannot use it if there is severe aortic regurgitation as then there will be higher end diastolic LV pressures and this would not give us the true pressure decay
We should not use it if the slope of the curve is not linear and does not show a constant decay
We cannot use PHT right after PMBV as we don’t know how this affects the gradient
Assessing MS severity
Continuity equation?
Note we can use the continuity equation to determine MVA but there are following limitations:
(1) SV is not constant if there is severe AR or MR present
(2) If there is atrial fibrillation then stroke volume might change from beat to beat (we could average a few cycles to find a value especially if the R-R intervals are fairly constant).
Assessing MS severity?
Planimetry
Planimetry is the reference method for determining severity of MS by measuring the mitral valve area.
We must first zoom the image to make sure we don’t make any errors when measuring
Make sure there is enough gain to have the contours visible but not too much gain so that it might underestimate the area
Make sure that the orifice is at the mitral valve leaflet tips and perpendicular to the blood flow
Measure in mid diastole
Include the commisures if they are open
Assessing MS severity?
Planimetry
In order to be certain that we are getting an image at the leaflet tips perpendicular to the flow, we can use biplane imaging or 3D imaging.
Note: We want to cut where the orifice is the smallest and flow is perpendicular to the plane of cutting (red line in the image)
Stages of rheumatic MS
Severe MS is defined as MVA less than 1.5 or PHT > 150 ms
If any of these are present then patient is either Stage C or Stage D
Stage C if assymptomatic and Stage D if symptomatic
If MVA >1.5 or PHT <150 ms with mild LA enlargement then we can have progressive MS which is Stage B
Management of rheumatic mitral stenosis?
(Pliability of the valve)
First we have to assess if the MV is pliable or not. To determine the suitability of the MV for percutaneous balloon valvuloplasty we use the Wilkin’s score. This looks at mobility, thickening of the leaflets, calcification and subvalvular thickening.
It is important to also look at commisural calfcification as very high amount of calcification can make it difficult to expand the balloon to open the valve orifice.
Management of rheumatic mitral stenosis?
(Pliability of the valve)
Here we see that favorable features include
(1) High mobility of the rest of the leaflet other than the tip
(2) Less amount of leaflet thickening and if present mostly at the tips
(3) Less amount of calcium in the leaflets
Management of rheumatic mitral stenosis?
(Pliability of the valve)
Here we see that high amount of commisural calcium is unfavorable compared to low calcium for intervention
Management of rheumatic mitral stenosis?
(Pliability of the valve)
Here we analyze the subvalvular apparatus and mainly the chordae. If chordae are thickened, shortnened and have calcium then these are unfavorable characeteristics.
When to intervene in rheumatic MS?
If we have severe MS and symptomatic, i.e stage D and patient has a pliable valve with Wilkin’s score and no LA clot or MR >2+ then Class I indication is to do a PMBC. If patient does have a contraindication such as non pliable valve, LA clot or MR, but has NYHA Class III/IV symptoms then surgery
If patient has stage C and is therefore assymptomatic then if no LA clot, MR and pliable valve then if PASP > 50 then we should consider PMBC (IIa) or if new atrial fibrillation then PMBC (IIb)
If patient has Stage B and has exertional symptoms, we should do stress testing with exercise and if hemodynamically significant disease then PMBC (IIb)
Medical management of rheumatic MS?
Secondary prophylaxis of rheumatic fever:
This can be done with penicillin IM every 4 weeks or oral 200 mg bid
Duration is long.
Degenerative/calcific MS?
As opposed to rheumatic MS which begins at the leaflet tips and then goes to the base, degenerative MS begins at the annulus with severe calcification and then moves to the leaflet tips.
These patients usually have other comorbidities and we should also assess for other calcific valvular lesions
Degenerative/calcific MS?
Mean gradients in patients with MAC is independently associated with long term survival after 10 years and independent of the heart rate.
