MITRAL STENOSIS,CAUSES,PATHOGENESIS,CLINICAL FEATURES,DIAGNOSIS AND MANAGEMENT

1. MITRAL STENOSIS
Dr.G.VENKATA RAMANA
MBBS DNB FAMILY MEDICINE

2. MITRAL STENOSIS
• Stenosis of mitral valve

3. Causes of Mitral Stenosis
• Rheumatic fever
• Congenital (parachute valve, cor triatriatum)
• Severe mitral annular calcification with leaflet involvement
• Systemic lupus erythematosus
• Rheumatoid arthritis
• Myxoma
• IE with large vegetations
• Hunter’s syndrome
• Hurler’s syndrome
• Drugs - Methysergide
• Carcinoid syndrome
• Amyloidosis

4. Pathogenesis
• In rheumatic mitral stenosis, the mitral valve orifice is slowly
diminished by progressive fibrosis, calcification of the valve leaflets,
and fusion of the cusps and subvalvular apparatus
• The mitral valve orifice is normally about 5cm2 in diastole but can
be reduced to < 1cm2 in severe mitral stenosis
• The patient is usually asymptomatic until the orifice is < 2cm2
• As stenosis progresses, left ventricular filling becomes more
dependent on left atrial contraction
• Classically, the mitral valves exhibit leaflet thickening, commissural
fusion and shortening, and thickening and fusion of the chordae
tendineae
• Fibrous bridging across the valvular commissures and calcification
create “fishmouth” or “buttonhole” stenoses
• Microscopic examination shows neovascularization and diffuse
fibrosis that obliterates the normal leaflet architecture

5. CLINICAL MANIFESTATIONS
• Dyspnea
• Results from elevation in left atrial pressure and
pulmonary venous hypertension, which leads to reduced
compliance of the lungs, a decrease in vital capacity, and
increased work of breathing
• Inability to increase the cardiac output with increased
metabolic demands
• Fatigue
• Less common symptom that may occur as the degree of
MS worsens, cardiac output declines, and right heart
failure develops
• Thus, fatigue may be associated with low forward flow
and a low transmitral gradient

6. • Hemoptysis
• The increased pulmonary pressures and vascular
congestion can lead to hemoptysis, which may have a
variety of clinical manifestations:
• Sudden hemorrhage (pulmonary apoplexy) due to the
rupture of thin-walled and dilated bronchial veins when
there is a sudden increase in left atrial pressure
• This complication is rarely life-threatening, despite what
appears to be a large amount of bleeding
• Blood-tinged sputum induced by severe coughing
associated with paroxysmal nocturnal dyspnea or
bronchitis
• Pink frothy sputum resulting from pulmonary edema
associated with left heart failure

7. • Chest pain
• Patients with MS rarely present with chest pain
• May be due to underlying coronary artery disease or a
coronary artery embolism
• Most commonly the result of pulmonary hypertension
(PH) and right ventricular hypertrophy, which may be
associated with right ventricular endocardial ischemia
• Another cause of intermittent chest pain is an atrial
tachyarrhythmia with left atrial and pulmonary vascular
distension

8. Precipitants of symptoms
• Any situation that increases the cardiac output, which
raises transmitral flow or causes tachycardia (which
decreases diastolic filling time), can increase the
transmitral pressure gradient and precipitate symptoms
such as dyspnea or hemoptysis
• Activities or conditions that can provoke symptoms
include exertion, emotional stress, fever, infection (eg,
pneumonia), AF, and pregnancy
• As an example, the increase in heart rate and cardiac
output during pregnancy can substantially increase the
resting transmitral gradient in pregnant patients with MS,
which can lead to symptoms in a previously
asymptomatic (and perhaps undiagnosed) patient or an
exacerbation of symptoms in an already symptomatic
patient

9. General examination
• When MS is severe, causing PH and diminished cardiac
output, cutaneous vasodilation results in pinkish-purple
patches on the cheeks (mitral facies)
• Lung examination may demonstrate crackles (rales)
consistent with pulmonary edema
• Advanced disease may be associated with the signs of
right-sided heart failure such as elevated jugular venous
pressure, lower extremity edema, and ascites

10. Cardiovascular examination
• Pulse examination
• The arterial pulses are preserved in most patients with
MS, reflecting preserved stroke volume
• In patients with severe MS with AF, the arterial pulses
are reduced in volume due to the decreased stroke
volume
• Findings on jugular venous examination include a
prominent "a" wave (atrial contraction or systole)
reflecting elevated right atrial pressure in the setting of
PH and right ventricular hypertrophy
• The "a" wave is absent in patients with AF and only a
prominent "v" wave (atrial filling during ventricular systole
when the tricuspid valve is closed) is seen
• If present, tricuspid regurgitation can lead to a prominent
"c-v" wave (reflecting regurgitation of blood into the right
atrium) and the neck veins are very pulsatile

11. Cardiac examination
• Identification of characteristic heart sounds, opening
snap, and diastolic murmur may be diagnostic for MS
with appropriate patient positioning in a quiet room
• An apical impulse that is generally normal, although it
may be reduced in magnitude
• However, if PH is present, there may be a right
ventricular heave (parasternal lift) and a palpable S2
• The first heart sound (S1) may also be palpable

12. Heart sounds
• S1 – With stenotic but noncalcified mitral leaflets, the leaflets are
widely separated at the onset of ventricular contraction due to
elevated left atrial pressure, and the first heart sound (S1) is loud,
reflecting the increased excursion of the stiff leaflets
• As the leaflets become more rigid and calcified with severe
obstruction, their motion is limited, and S1 becomes soft
• S2 – The second heart sound is initially normal, but, with the
development of PH, P2 becomes increased in intensity and may be
widely transmitted
• As pressure increases further, splitting of S2 is reduced, and,
ultimately, S2 becomes a single sound
• S3 – A third heart sound of left ventricular origin is not heard in pure
MS because of the obstruction to flow across the mitral valve
• However, it may be present if there is coexisting aortic or mitral
regurgitation or it may be generated from the right ventricle.
• S4 – A fourth heart sound may be heard, generally originating from
the right ventricle when it is hypertrophied and dilated and the
patient is still in sinus rhythm

13. • Opening snap
• In the presence of MS , leaflets with preserved mobility, an opening
snap (OS) of the mitral valve is heard
• The OS is due to the abrupt halt in leaflet motion in early diastole,
after rapid initial rapid opening, due to fusion at the leaflet tips
• It is best heard at the apex and lower left sternal border
• The OS following S2 may be mistaken for a split S2 unless the
examiner recognizes that the two components of S2 are followed by
the OS during the inspiration and that the OS is best appreciated at
the apex, not the base
• As the MS progresses and left atrial pressure increases, the OS
occurs earlier after S2 or A2
• Thus, more severe MS is generally associated with a shorter A2-OS
interval
• However, this relationship is complicated by the effects of other
conditions including tachycardia, hypertension, mitral regurgitation,
and aortic valve disease, as discussed separately
• The OS is loudest when there is preserved excursion of the mitral
leaflets
• The OS is absent when the mitral valve leaflet motion is severely
limited with calcification

14. • Diastolic murmur
• A low pitched, rough, rumbling, mid-diastolic murmur with pre-
systolic accentuation, best heard over the apex, with the bell
of the stethoscope in the left lateral position, in expiration
• Although the intensity of the diastolic murmur does not
correlate with the severity of the stenosis, the duration of the
murmur is helpful since it reflects the transvalvular gradient
and the duration of blood flow across the valve
• When MS is mild, the gradient is confined to late diastole
(during atrial contraction), and, hence, the murmur is heard
late in diastole, just before S1.
• As the stenosis becomes more severe, there is a gradient at
the very onset of the diastolic flow period, immediately
following the OS
• This early diastolic murmur is decrescendo, becoming softer
as the transvalvular gradient decreases
• If the patient is still in sinus rhythm, the increase in atrial
pressure during atrial contraction results in an increase in the
loudness of the murmur, termed "presystolic accentuation"

15. • With more severe MS, there is a continuous gradient throughout all
of the diastolic flow period, from mitral valve opening to mitral valve
closure
• However, the diastolic murmur may be inaudible or absent when MS
is very severe, due to the very slow flow across the mitral valve
• There are several maneuvers that have been used to evaluate heart
sounds in MS
• The diastolic murmur and OS are diminished with inspiration, but
augmented with expiration (in contrast to tricuspid stenosis). With
inspiration, the A2-OS interval widens and a distinct P2 may be
heard
• Increasing venous return (eg, by lying the patient down and lifting
the legs) augments the gradient; as a result, the diastolic murmur
lengthens while the A2-OS intervals shorten
• Similar changes are seen in response to exercise
• In contrast, reducing venous return with amyl nitrate, the Valsalva
maneuver, or standing after squatting shortens the murmur and
lengthens the A2-OS interval

16. • Other sounds
• A pulmonary ejection sound is heard in early systole; the
sound diminishes with inspiration when the pulmonary
arteries dilate
• With the development of tricuspid regurgitation, there is
a holosystolic murmur best heard along the right sternal
border that increases with inspiration
• A faint and brief early diastolic murmur of pulmonic
regurgitation (Graham Steell murmur) may be heard at
the base
• Murmurs of mitral or aortic regurgitation may also be
present if these valve lesions coexist with MS

19. Investigations in mitral stenosis
• Electrocardiogram
• The QRS amplitude and morphology are normal unless there
is mitral regurgitation or coexistent aortic valve disease
• Left atrial hypertrophy and enlargement results in a P wave
that becomes broader (duration in lead II >0.12 s), is of
increased amplitude, and is notched (due to the delay in left
atrial activation). This is termed P-mitrale
• The left atrial changes also produce a prominent negative
terminal portion of the P wave in lead V1
• The P-wave changes are not seen in patients with AF
• The fibrillatory waves are coarse, generally >0.1 mV in
amplitude, reflecting left atrial hypertrophy
• Additional changes occur with the development of pulmonary
hypertension (PH) and right ventricular hypertrophy
• The frontal axis shifts to the right (S>R in lead I and aVL) and
a tall R wave develops in V1 and V2 (R>S or R/S ratio >1).

20. • P Mitrale
• The presence of broad, notched (bifid) P waves
in lead II is a sign of left atrial enlargement,
classically due to mitral stenosis

21. P waves with terminal portion > 1mm deep in V1

22. Chest X-ray
• The chest radiograph in mild MS may be normal,
although there is often evidence of some
enlargement of the left atrium and appendage
• Left atrial enlargement may produce the following
findings
• A "double density" (double right heart border
caused by the right side of the left atrium
extending behind the right cardiac shadow
• Straightened left heart border
• Elevated left bronchus
• On the lateral projection, posterior displacement of
the left atrium, impinging on the esophagus

23. • Other findings :
• Calcification of the mitral annulus may be observed on
an overpenetrated film in older adult patients with
calcified rheumatic mitral disease
• Enlargement of the main pulmonary artery may be
caused by PH, while the aorta and left ventricle are
often small
• Pulmonary vascular congestion causes redistribution
or "cephalization" of pulmonary blood flow to the upper
lobes, dilated pulmonary vessels, Kerley B lines at the
bases, and interlobar effusions (Kerley C lines)
• In more severe cases, Kerley A lines (straight dense
lines running toward the hilum) may be seen

30. Investigations in mitral stenosis
nosis
• Echo
• Thickened immobile cusps
• Reduced valve area
• Enlarged left atrium
• Reduced rate of diastolic filling of left ventricle
• Doppler
• Pressure gradient across mitral valve
• Pulmonary artery pressure
• Left ventricular function
• Cardiac catheterisation
• Coronary artery disease
• Pulmonary artery pressure
• Mitral stenosis and regurgitation

31. STAGING

32. • Conditions Simulating MS
1. Left atrial myxoma
2. Cortriatriatum
3. Ball valve thrombus of left atrium
4. Diastolic flow murmurs across normal mitral valve as in
VSD, PDA, severe MR, etc.
5. Carey-Coomb’s murmur of mitral valvulitis.
6. TS (also masks the features of MS)
7. Austin-Flint’s murmur

33. COMPLICATIONS
• Atrial fibrillation
• Thromboembolism
• Pulmonary hypertension
• Right heart failure
• Infective endocarditis
• Hoarseness

34. Atrial fibrillation
• Due to the elevation of left atrial pressure and left atrial
enlargement
• Two independent risk factors for AF were left atrial
diameter and increasing age
• AF can lead to clinical decompensation via two
mechanisms
• 1.The loss of atrial contraction, which plays an important
role in the generation of adequate left atrial pressure to
maintain blood flow across the stenotic valve
• 2.Rapid ventricular response, which diminishes the time
available for filling of the left ventricle
• AF is suggested by an irregularly irregular pulse on
physical examination and confirmed by
electrocardiogram (ECG)

35. Thromboembolism
• Thromboembolic risk in patients with rheumatic MS is
primarily related to the presence of AF and blood stasis
in the left atrium
• First presentation of MS in some patients
• Most common site for clinically evident embolism is the
cerebral circulation, any organ may be involved,
especially spleen, kidneys, and the coronary circulation,
resulting in a myocardial infarction
• Most emboli in patients with MS arise from the left
atrium, emboli can also arise from the right atrium when
there is pulmonary hypertension (PH) and right
ventricular and atrial dilation
• Emboli from this site lead to pulmonary embolism and
infarction
• The risk of thromboembolism is higher in older patients
(with a longer duration of disease), more severe MS, and
heart failure, and is further increased with associated
atherosclerotic risk factors including hypertension and
diabetes

36. Pulmonary hypertension
• Patients with MS commonly develop PH (Mean pulmonary artery
pressure [mPAP] >20 mmHg)
• In patients with MS, pulmonary artery pressure elevation is
associated with more severe MS (smaller mitral valve area and
higher mitral valve gradient) and lower atrioventricular compliance
• PH caused by MS is a type of PH due to left heart disease (PH-LHD;
group 2 PH), which is most commonly postcapillary PH but, in a
minority of patients, is combined pre-and postcapillary PH
• Postcapillary PH
• Among patients with MS with PH, most have postcapillary PH due
to chronically elevated pulmonary venous pressure
• The postcapillary PH phenotype is characterized by an mPAP >20
mmHg, pulmonary artery wedge pressure of >15 mmHg, a diastolic
pressure gradient (diastolic pulmonary artery pressure – pulmonary
artery wedge pressure) of <7 mmHg, and a pulmonary vascular
resistance ≤3 Wood units
• Another metric is the transpulmonary gradient (TPG = mPAP –
pulmonary capillary wedge pressure) which is normal (≤12 to 15
mmHg) in patients with postcapillary PH

37. • Combined pre- and postcapillary PH
• A minority of patients with MS and PH develop combined pre- and
postcapillary PH
• Precapillary PH is caused by vasoconstriction and pathologic
remodeling of the pulmonary vasculature and may be, in part,
mediated by the potent vasoconstrictor endothelin-1 (ET-1)
• The combined pre- and postcapillary phenotype is characterized by
an mPAP >20 mmHg, pulmonary artery wedge pressure of >15
mmHg, a diastolic pressure gradient (diastolic pulmonary artery
pressure – pulmonary artery wedge pressure) of ≥7 mmHg, and a
pulmonary vascular resistance ≥3 Wood units
• The TPG is elevated (>15 mmHg) is elevated in patients with
combined pre-and postcapillary PH

38. Right heart failure
• Chronic PH increases right ventricular afterload which
can lead to right ventricular enlargement, right ventricular
dysfunction, secondary tricuspid regurgitation, and signs
of right-sided heart failure
• Signs of right-sided heart failure include
• Increased jugular venous pressure
• Lower extremity edema, which may progress to involve
the upper thighs, sacral area, and abdominal wall;
ascites and pleural effusions can also occur
• Hepatomegaly in which the liver may be pulsatile if
tricuspid regurgitation is present

39. • Infective endocarditis
• Since the rheumatic mitral valve is deformed
with disturbed blood flow patterns, there is a risk
of infective endocarditis
• Hoarseness
• If the left atrium becomes very large, there may
be compression of the recurrent laryngeal nerve,
leading to hoarseness (Ortner syndrome or
cardiovocal syndrome) or coughing

40. General management
• Management of rheumatic MS includes
• Patient education regarding the need for ongoing care
• Periodic monitoring, rheumatic fever prophylaxis
• Management of heart failure
• Management of atrial fibrillation (AF)
• Prevention of thromboembolism
• Endocarditis prophylaxis
• Counseling on physical activity
• Management of risk associated with pregnancy
• Management of risk of noncardiac surgery
• Cardiovascular risk reduction

41. • Monitoring
• For all patients with MS, follow-up should include yearly
history and physical examination to assess for symptoms
and signs of disease progression and development of
indications for intervention
• Follow-up transthoracic echocardiography should be
performed with frequency based upon the severity of
disease.
• 2020 American College of Cardiology/American Heart
Association (ACC/AHA) valve guideline recommendation
for echocardiography every three to five years if the
mitral valve area (MVA) is >1.5 cm2, every one to two
years if the MVA is 1.0 to 1.5 cm2, and every year if the
MVA is <1.0 cm2
• More frequent monitoring may be required in these
patients and in those with concurrent mitral regurgitation
or disease affecting other valves
• All patients should undergo reevaluation whenever there
is a change in clinical status

42. Secondary prevention of rheumatic fever

43. •

44. Prevention of infective endocarditis
• As noted in the 2007 AHA guidelines on the prevention
of bacterial endocarditis, only patients with the highest
risk of the development of endocarditis (eg, patients with
prosthetic heart valves, patients with prior endocarditis)
are advised to receive antimicrobial prophylaxis
• Most patients with native valvular heart disease,
including those with MS, are not included in this group
and therefore do not require antimicrobial prophylaxis

45. Physical activity and exercise
• Most patients with severe MS are symptomatic with exertion, leading them
to adopt a more sedentary lifestyle
• However, all patients should be encouraged to participate in at least a low-
level exercise regimen to maintain cardiovascular fitness
• Patients should be informed that sudden death in MS is extremely rare,
which may alleviate certain fears about exercising
• Each patient's exercise tolerance will vary depending upon the severity of
their disease and the intensity and type of exercise
• The following recommendations were included in the 2014 AHA/ACC
recommendations for competitive athletes with MS
• Annual evaluation should be performed in athletes with MS to determine
whether sports participation can continue
• In athletes with MS, exercise testing to at least the level of activity achieved
in competition and training is useful in confirming asymptomatic status
• For athletes with MS with MVA >2.0 cm2 and mean gradient <10 mmHg at
rest, participation in all competitive sports is reasonable
• Athletes with severe MS (MVA ≤1.5 cm2) should not participate in
competitive sports, with the possible exception of low-intensity (class IA)
sports
• Individuals with MS with AF treated with anticoagulation should not
participate in sports involving risk of bodily contact

46. MEDICAL MANAGEMENT OF HEART FAILURE
• The role of medical therapy for heart failure caused by MS is limited
• The onset of symptoms is an indication for intervention in patients
with severe MS
• Pharmacologic therapy is appropriate to improve symptoms and
hemodynamic conditions prior to intervention, for persistent
symptoms after intervention, and for management of symptoms
precipitated by an intercurrent illness or during pregnancy
• Diuretic therapy (usually with a loop diuretic such as furosemide)
• Dietary salt restriction
• Agents for heart rate control (in patients in sinus rhythm or AF)
include beta blockers, nondihydropyridine calcium channel blockers,
and ivabradine
• These agents can significantly decrease heart rate and cardiac
output at rest, causing a decrease in the transmitral gradient,
pulmonary venous pressure, and mean pulmonary artery pressure in
patients with MS
• Beta blockers can blunt the heart rate and cardiac output responses
to exercise, while attenuating the rise in transmitral gradient that
normally occurs

47. • The role of digoxin in patients with MS is limited since
most patients have preserved ventricular systolic
function
• Digoxin may be helpful in selected patients who have
symptomatic left and/or right ventricular systolic
dysfunction, as in patients with other causes of systolic
heart failure
• Digoxin may also be helpful in controlling a rapid
ventricular rate during AF, although digoxin is not a first-
line drug for this indication for most patients

48. MANAGEMENT OF ATRIAL FIBRILLATION
• In many patients with MS, the onset of AF contributes to
the onset of symptoms
• AF in patients with MS may be poorly tolerated for two
reasons, with the hemodynamic consequences
depending upon the severity of the stenosis:
• If AF is associated with a rapid ventricular rate, the
shortened diastolic filling time causes left atrial and
pulmonary pressures to rise, potentially leading to
pulmonary edema
• The loss of atrial contraction contributes to a decrease in
left ventricular filling and an increase in left atrial
pressure

49. • Initial management
• In patients who are hemodynamically unstable,
immediate electrical cardioversion is indicated
• For hemodynamically stable patients, the initial
management consists of controlling the ventricular rate
(with a beta blocker, calcium channel blocker
[verapamil or diltiazem], or, less preferably, digoxin) and
anticoagulation

50. Anticoagulation
• Patients with rheumatic MS with left atrial thrombus or
prior embolic event require anticoagulation
• In addition, for patients with rheumatic MS with
paroxysmal, persistent, or permanent AF, recommend
long-term oral anticoagulation
• For patients with rheumatic MS requiring anticoagulation
(for AF, left atrial thrombus, or a prior embolic event),
recommend chronic anticoagulation with a vitamin K
antagonist (VKA: eg, warfarin) rather than with a direct
oral anticoagulant (DOAC)
• The target international normalized ratio (INR) is 2.5
(range 2.0 to 3.0)

51. Indications for intervention
• Decisions on whether and how to intervene are based upon the stage of MS
(which is largely determined by the mitral valve area [MVA] and presence of
symptoms , the feasibility and risk of intervention, and whether the patient is
undergoing cardiac surgery for a concurrent condition
• •Severe MS (MVA ≤1.5 cm2)
• Symptomatic severe MS (stage D)
• For most symptomatic patients (New York Heart Association [NYHA] class
II, III, or IV) with severe rheumatic MS (stage D) , recommend PMBC rather
than either mitral valve surgery or no valve intervention , provided the
patient meets criteria for PMBC
• For those who do not meet criteria for PMBC and are not at high surgical
risk, recommend mitral valve surgery (repair, commissurotomy, or valve
replacement)
• For patients with severe symptomatic rheumatic MS who do not meet
criteria for PMBC and have high surgical risk, management decisions are
individualized
• For patients in this category with severe symptoms (NYHA class III or IV)
and less than moderate mitral regurgitation (MR) and no left atrial thrombus,
suggest attempting PMBC despite unfavorable valve morphology
• Medical management or high-risk mitral valve surgery are reasonable
alternatives

52. • Asymptomatic severe MS (stage C) – For asymptomatic patients
with severe MS (stage C) who have elevated pulmonary artery
systolic pressure (PASP; >50 mm Hg) or AF and are appropriate
candidates for PMBC , suggest PMBC
• Patients without elevated PASP or AF and those who do not meet
criteria for PMBC are managed medically
• An exception is patients undergoing cardiac surgery for a concurrent
condition (eg, coronary artery disease)
• In such patients, suggest concomitant mitral valve surgery

53. • Criteria for PMBC
• Appropriate candidates for PMBC should optimally
meet all of the following criteria
• Favorable valve morphology – This refers to
features of the mitral valve complex (valve and
subvalvular apparatus) associated with effective
PMBC with low risk of induction of MR
• Less than moderate (2+) MR.
• No left atrial thrombus
• No prior failed appropriately performed PMBC

54. • PMBC step-by-step: a transseptal puncture (x-plane), b wire in the LA, c balloon in the LA
with the wire removed, d balloon across the MV (2D and 3D TEE (LA aspect)), e minimal
inflation of the distal part of the Inoue balloon (2D TEE and fluoroscopy), f further inflation of
the distal part of the Inoue balloon (2D TEE/fluoroscopy), g the proximal part of the balloon is
also inflated (2D TEE and fluoroscopy), h maximum inflation of the proximal and the distal
part of the Inoue balloon (2D TEE/ fluoroscopy/ 3D TEE (LA aspect)), and i laminar flow
across the MV in diastole after PMBC (2D TEE with color Doppler)

55. Management of severe rheumatic
mitral stenosis (MVA ≤1.5 cm2)

56. • Nonsevere ("progressive") MS (MVA >1.5 cm2, stage B)
• Isolated nonsevere MS
• Most patients in this stage are asymptomatic, do not require
mitral valve intervention, and should continue to be monitored
• However, for patients with exertional symptoms and evidence
of hemodynamically significant MS with exercise (ie,
pulmonary artery wedge pressure >25 mmHg or mean mitral
valve gradient >15 mmHg) who are appropriate candidates for
PMBC (criteria summarized below), suggest PMBC
• Mixed MS and MR
• Patients with nonsevere MS and MR should be monitored for
development of symptoms
• For symptomatic patients with MS with MVA >1.5 cm2 and
moderate and greater MR, suggest surgical mitral valve
replacement

57. Management of nonsevere (MVA >1.5
cm2) rheumatic mitral stenosis

58. Valve Replacement
• When there is associated MR or when the valve is rigid and calcified, valve
replacement is indicated
• Valve replacement is done using:
• Mechanical Prosthesis
• a. Caged ball valve (Starr-Edwards prosthesis)
• b. Tilting-disc valve (St Jude, Bjork-Shiley valves)
• Bioprosthesis
• a. Porcine bioprosthesis
• b. Pericardial xenograft prosthesis
• c. Homografts—Autograft with pulmonary valve in cases of aortic valve IE or
allografts from cadaveric valves
• Among the mechanical prosthesis, tilting-disc valve is preferred to caged
ball valve because:
• a. It occupies less space and hence useful in patients with a small left
ventricle
• b. Incidence of haemolysis is less common
• c. Incidence of strut fractures is less common

59. • Life long anticoagulation is indicated in patients receiving
mechanical prosthesis
• The advantage of bioprosthetic valve is the low
incidence of thromboembolic phenomenon
• Bioprosthetic valves are not usually used in young
patients < 65 years because of its rapid deterioration.
However, they are useful in pregnancy, when there is
contraindication to the use of anticoagulants and also in
older patients over 65 years of age