2. INTRODUCTION
• Mitral stenosis (MS) is characterized by obstruction to left ventricular
inflow at the level of mitral valve due to structural abnormality of the
mitral valve apparatus.
• Rheumatic fever is the leading cause of mitral stenosis (MS).
• Pure or predominant MS occurs in approximately 40% of all patients
with rheumatic heart disease and a history of rheumatic fever.
• With reductions in the incidence of acute rheumatic fever, the
incidence of MS has declined considerably over the past several
decades
• Two third of the cases are females.
4. NATURAL HISTORY
• Mitral stenosis is a progressive,lifelong disease.
• Usually slow and stable in early years
• Progressive acceleration in later years
• 20-40 years latency from rheumatic fever to symptom
onset.
9. • Rheumatic Heart disease (most common)
• Congenital
• Severe mitral annular calcification
• Rheumatoid arthritis
• Systemic lupus erythematosus
• Amyloidosis
• Drugs - methylsergide
• Carcinoid syndrome
Other causes of LV inflow obstruction
• Left atrial myxoma
• Cotriatrium
• Ball valve thrombus in left atrium Harrison 19E Pg.1539
10. • Why mitral valve is most commonly
involved in rheumatic heart disease?
11. • Mitral valve surface area is more than aortic area
• The pressure gradient across mitral valve is greater than
that across aortic valve.
Hence more prone for injury.
12. • What are the pathological processes that
occur in rheumatic mitral valve?
13. • In rheumatic MS, chronic inflammation leads to diffuse
thickening of the valve leaflets with formation of fibrous
tissue and/or calcific deposits. The mitral commissures
fuse, the chordae tendineae fuse and shorten, the
valvular cusps become rigid, and these changes, in
turn,lead to narrowing at the apex of the funnel-shaped
(“fish-mouth”)valve.
• MS is usually the result of repeated episodes of carditis
alternating with healing.
Hurst's 11E
15. • The initial mitral valvulitis leads to abnormal flow patterns
across the mitral valv that promote thickening,fibrosis
and calcification of leaflets.The thickened leaflets fuse
along their edges i.e commissures, resulting in a
stenosed mitral valve which has a 'fish mouth' or 'button
hole' appearance.
» API 2015
18. • What are the classical physical findings in
a case of mitral stenosis?
19. • Low volume pulse
• Apex Beat - Normal in position. Tapping in character.
• Diastolic thrill may be palpable in mitral area.
• Left Parasternal heave
Auscultation
• Loud S1
• Opening Snap just after S2
• A low pitched rough rumbling mid diastolic murmur with presystolic
accentuation over the apex best heard with the bell of stethescope
in left lateral position during expiration.
• With the development of pulmonary hypertension, Palpable P2,loud
P2, Ejection systolic murmur in pulmonary area and a Pansystolic
murmur may be heard along left sternal border(Functional TR)
23. • It is the pinkish purple patches
on cheeks. As cardiac output is
low in MS, vasoconstriction
produces peripheral cyanosis
in lips,tip of nose and cheeks.
Malar flush is seen in malar
area due to vasodilation. All
these constitute mitral facies
24. • What is the normal mitral valve area and
severity grading of MS according to valve
area?
25. • Normal mitral valve area is 4-6 sq.cm
• Mild MS - 1.5-2.5 sq.cm
• Moderate MS - 1-1.5 sq.cm
• Severe/critical MS - <1 sq.cm
27. • Due to persistent diastolic gradient across the
mitral valve, the valve cusps remain wide open
throughout the diastole and as soon as the
ventricular systole starts, the widely opened
mitral valve cusps close rapidly, giving rise to
loud S1.
• M1T1 summation
• Flow across deformed valve
31. • Associated with mitral or aortic regurgitaion
• Mitral valve calcification
• Active rheumatic carditis(due to prolonged PR interval)
• Digitalis overdose(due to prolonged PR interval)
• Left heart failure
• Atrial fibrillation(varying S1)
• Rotation of the heart due to gross right ventricular
hypertrophy.
• Obesity,emphysema,pericardial effusion,thick chest wall.
33. • Prominent a waves - In presence of PHT
• Prominent v wave - In presence of TR (functional)
• Prominent y descent - In presence of TR (functional)
• Absent a waves - Atrial fibrillation
34. • How can the severity of MS assessed
clinically?
35. Featues of severe MS:
• Narrow S2-OS gap
• Longer duraton of mid diastolic murmur.
Harrison 19E Pg.1540
39. • The interval between closing of aortic valve and opening
of mitral valve is known as 'isovolumetric relaxation
period'. Diastolic murmur is heard as soon as the blood
flows from left atrium to left ventricle after the opening of
mitral valve. There is no blood flow in the isovolumetric
relaxation period and this is why the murmur of MS is
mid-diastolic,not early diastolic.
40. • What is the cause for presystolic
accentuation?
41. • The last part of ventricular diastole actually coincides
with atrial systole. atrial systole increases the blood flow
across the stenotic valve and thus there is presystolic
accentuation.
43. • Opening snap is produced due to bellowing down of the
closed mitral valve cusps at the onset of ventricular
diastole.
It has the following characteristics:
• Sharp and high pitched
• Best heard with diaphragm of stethescope
• Best heard after expiration with the patient in standing
position
• Loudest in between the apex and left sternal border
• Present in early diastole (at the end of isovolumetric
relaxation period)
45. • MS is organic
• Valve cusps are pliable
• Significant MS
• High atrioventricular pressure gradient
• Severe AR,MR,atrial fibrillation,left heart failure absent
• MS is readily amenable for surgery
• Diminishing S2-OS gap indicates increasing severity.
To differentiate OS from splitting of S2
• Ask the patient to stand.As standing reduces the venous return, S2-
OS gap increases and A2-P2 gap decreases (dynamic auscultation).
47. • Mild MS
• Severe MS
• Calcific MS
• Congenital MS
• MS with associated significant MR/AR/AS
48. • What is the cause of Atrial fibrillation in
MS?
49. • Left atrial enlargement results in disorganisation of atrial
muscle bundles coupled with inhomogenous refratory
periods
50. • What are the changes noticed when Atrial
fibrillation develops in MS?
51. • Irregularly irregular pulse with a pulse deficit >10
• Varying intensity of S1
• Presystolic accentuation of diastolic murmur disappears
as atria contracts in an uncordinated and ineffective
manner. But presystolic accentuation may be present in
short cycles in AF.(Crile's hypothesis)
• Opening snap may not heard
• No a waves in JVP
52. • What is the mechanism behind acute
pulmonary edema in presence of AF in
MS?
53. • Decrease in the diastolic flow period caused by
increased heart rate
• Loss of atrial contribution to cardiac output.
54. • What are the changes that occur after left
atrial failure in MS?
55. • S1 becomes muffled
• Opening snap is not heard
• Presystolic accentuation of the murmur disappears
57. • Atrial fibrillation
• Pulmonary hypertension
• Haemoptysis
• Congestive cardiac failure
• Pressure symptoms - compression of recurrent laryngeal(Ortners
Syndrome)and esophagus.Pressure on left main bronchus may
result in bronchiectasis.
• Infective endocarditis(rare)
• thromboembolic manifestations
• Recurrent brochopulmonary infections
58. • What are the possible explanations for
haemoptysis?
59. • Due to rupture of thin walled bronchial or pulmonary
veins resulting from sudden rise in LA pressure.
• Chronic bronchitis
• Acute pulmonary edema (Pink frothy sputum)
• Pulmonary infarction
• Overdose of anticoagulant therapy
• Pulmonary haemosiderosis
61. (1) passive backward transmission of the elevated LA
pressure;
(2) pulmonary arteriolar constriction (the so called“second
stenosis”), which presumably is triggered by LA and
pulmonary venous hypertension (reactive pulmonary
hypertension);
(3) interstitial edema in the walls of the small pulmonary
vessels; and
(4) at end stage, organic obliterative changes in the
pulmonary vascular bed(active PHT)
63. • When the pulmonary venous pressure increases fluid
passes into alveolar walls and promotes thickening and
fibrosis of the wall resulting in hypoxemia. This
hypoxemia is sensed by chemoreceptors that lead to
reflex pulmonary vasoconstriction.This triad of passive
pressure transmission,reflex vasoconstriction and
obliterative changes in the vascular bed causes
Pulmonary Hypertension.
» API 2015
64. • What are the possible explanations for
syncope in MS?
65. • Cerebral embolism from atrial fibrillation
• Due to low cardiac output ( PHT,AF with RVR)
70. • Carey-Coombs murmur - Soft MDM in active rheumatic
carditis
• Austin Flint murmur : Functional MDM in a patient with
severe AR
• Left atrial myxoma - MDM varying with posture
• Ball valve thrombus in left atrium obstructing mitral
orifice.
• Cotriatrium
• Other functional MDM : Due to increased flow through
normal mitral valve as occurs in severe MR,
ASD,VSD,PDA etc.
73. • Symptoms and signs depend upon the dominant lesion
MS>MR MR>MS
• Pulse Low volume Large volume
• BP Low sys BP Normal
• Apex outward shift down and out
Tapping Hyperdynamic
• Thrill Diastolic thrill systolic thrill
• S1 Short,sharp,snapping Soft/muffled
• OS Usual Absent
• S3 Absent Present
• Murmur Classical MDM PSM with radiation
PSM not radiating MDM without
presys accentuation
• CXR,ECG LAH+RVH LVH+LAH
74. • In presence of significant MR Mitral valve
replacement is the treatment of choice.
76. • Aortic involvement present in one third of cases of MS.
• Combined MS and AS is usually of rheumatic origin.
• Other cause - Congenital SHONE COMPLEX - MS+AS+COA
• Decreased cardiac output more pronounced in combined lesion.
• Signs of AS are masked in presence of severe MS. Ejection systolic
murmur may decrease in intensity, Apical impulse is less than
heaving
• In presence of significant AS,Signs of MS i.e. S1 may not be loud
and opening snap and classical MDM may not be heard.
• If the degree of AS appears to be mild and the mitral valve is
acceptable for balloon valvotomy, this should be attempted first. If
mitral balloon valvotomy is successful, the aortic valve should then
be reevaluated.
78. • When both AR and MS coexist, severe MS usually coexists with
mild AR.However, the coexistent AR is occasionally severe.
• The combination of coexistent severe MS and severe AR may
present confusing pathophysiology and often leads to misdiagnosis.
MS restricts LV filling, blunting the impact of AR on LV volume.Thus,
even severe AR may fail to cause a hyperdynamic circulation, so
that typical signs of AR are absent during physical examination.
• Likewise, echocardiographic LV cavitary dimensions may be only
mildly enlarged.
• In most cases, it is advisable to perform mitral valvotomy first and
then follow the patient for symptomatic improvement. If symptoms
disappear, correction of AR can be delayed.
80. • It is important to establish whether tricuspid regurgitation
is primary or secondary to pulmonary hypertension.
• In general, if pulmonary hypertension is severe and the
tricuspid valve anatomy is not grossly distorted,
improvement in TR can be expected after correction of
MS.
• On the other hand, if there is severe rheumatic deformity
of the tricuspid valve, competence is likely to be restored
only by surgery.(tricuspid annuloplasty)
86. • Mitralisation of heart - Straightening of left heart border d/t small
aortic knuckle, dilated pulmonary artery and prominent left atrial
appendage.
• Double contour of right heart border (shadow within shadow) - LA
enlargement.
• Evidence of pulmonary hypertension - Dilated pulmonary arteries at
hilum with peripheral pruning.
• Elevation of left upper lobe bronchus and splaying of carina - LA
enlargement.
• Kerley Blines - dense,short, horizontal lines in costophrenic region
when pulmonary venous pressure is between 20-30mmHg.
• Kerley A lines - Straight,dense lines running towards hilum when
pulmonary venous pressure is >30mmHg.
• Upturned apex - inverted moustache sign
87.
88. • RAO view - Barium swallow
may demonstrate sickling of
barium filled esophagus due to
compression by enlarged LA.
• Lateral view - Obliteration of
retrosternal air space.
Chamber enlargement can be
looked for.
92. • Simultaneous measurement of cardiac output and the
gradient between the LA and the LV and calculation of
valve area by cardiac catheterisation remains the "gold
standard" method for assessing the severity of MS
Hurst's 11E
93. • What is the role of cardiac catheterisation
in MS?
94. • To measure arterial pressures and valvular pressure
gradient
• Valve area
• cardiac output
• other valvular lesions
• assess the coronaries
• LV function
98. • Restrict strenous physical activity
• Heart failure measures
• Rheumatic fever prophylaxis
• Anticoagulation in AF
• Patients with mild MS and moderate asymptomatic MS
usually managed conservatively. Interventional
procedures done usually in symptomatic MS.
100. • Significant symptoms
• Isolated MS
• No/mild MR
• Mobile non-calcified valve
• LA free of thrombus
• Asymptomatic- Severe PHT - Pulmonary systolic pressure greater
than 50 mm Hg at rest or 60 mm Hg with exercise.
Pregnant women - PBMV is the procedure of choice
Harrison 19E
107. CLOSED VALVOTOMY:
• Rarely done nowadays. Replace by PBMV
• Pliable valve
• No associated MR
OPEN MITRAL VALVOTOMY:
• Mitral valves are distorted or calcified.
• Left atrial thrombi
Preferred procedure in young patients Harrison 9E
109. • Associated severe MR
• Restenosis
• Severe MS
• Valve has been severely distorted(extensive
commissural calcification, severe fibrosis, and
subvalvular fusion)
Braunwald 9E
111. Mechanical prosthesis :
• Caged ball valve (Starr-Edwards prosthesis)
• Tilting disc valve (St.Jude,Bjork-Shiley valves)
A mechanical valve is preferred when MV replacement for MS is
necessary when AF is present because of the need for chronic
anticoagulation and in patients younger than 65 years in sinus
rhythm.
Bioprosthesis:
• Porcine prosthesis
• Pericardial xenograft prosthesis
A bioprosthetic valve is appropriate in patients who cannot take
warfarin and is reasonable in all patients older than 65 years
Braunwald 9E
