1. D . B A S E M E L S A I D E N A N Y
L E C T U R E R O F C A R D I O L O G Y
A I N S H A M S U N I V E R S I T Y
Mitral stenosis

2. Etiology
1-Rheumatic heart diseasegreat majority (inflammatory process due
to cross-reactivity between streptococcal antigen and the valve tissue)
2-Infective endocarditis and mitral annular calcification accounted for
3.3 and 2.7 % of cases, respectively.
3-Other etiologies such as congenital malformation (rolled, thickened
leaflet margins, hypoplasia of fusion of the papillary muscles, and
short and thickened chordae tendineae), systemic lupus
erythematosus, carcinoid heart disease, endomyocardial fibrosis, and
rheumatoid arthritis were implicated in less than 1% of cases
4-Picture simulating mitral stenosis can result from obstruction of the
mitral valveleft atrial myxoma or cor triatriatum, an uncommon
congenital abnormality in which there is a membrane within the left
atrium producing two left atrial chambers
5-Prosthetic valve dysfunction in this setting may result from acute or
chronic thrombosis, pannus ingrowth on the atrial side of the valve, or
leaflet calcification

3. PATHOPHYSIOLOGY
--90% of individuals with rheumatic heart disease
--Tiny nodules along the coapting portions of the valve leaflets
leaflets thicken with eventual deposition of fibrin on the cusps and
loss of normal valve morphology Fusion of the leaflet commissures,
Thickening, fusion and shortening of the chordae tendineae
symmetric, central oval-shaped orifice and a classic pattern of
"doming" of the leaflets in diastole due to fusion of the leaflet tips at
the commissures
--Commisural fusion and chordal shortening are due to recurrent
rheumatic fever with repetitive valve scarring, but leaflet thickening
and calcification appear to be primarily due to the stress of chronic
turbulent flow through a deformed valve {recurrent stenosis after
mitral valvuloplasty, without intervening episodes of rheumatic fever,
is due to leaflet thickening and calcification without recurrent
commisural fusion}

4. AHA 2014

6. Cardiac hemodynamics
--Pressure gradient between LA and LV in diastole reflected
backward increase in pulmonary venous, capillary, and arterial
pressures and resistance.
-Mild to moderate MS only apparent with exercise or increase heart
rate
-Severe MS at rest
--Increase LA pressure AF clinical decompensation via two
mechanisms: the loss of atrial contraction; and the rapid ventricular
response (reduction in the duration of diastole)
--Pulmonary hypertension passive increase in pressure due to
backward transmission of the elevated left atrial pressure; and reactive
pulmonary vascular disease {Pulmonary arterial and arteriolar
vasoconstriction; Hypertrophy of the pulmonary artery muscular
layer}right-sided heart failure
** potentially completely reversible**

7. SYMPTOMS
--Many patients with severe MS deny symptoms
because slow progression of disease is "matched" by a
gradual reduction in activity history of maximal
physical activity
--More rapid progression in areas of high prevalence
may be due to the ineffective use of antibiotics and/or
increased virulence of the Streptococcus organism

8. 1-Dyspnea:
-Most common and often only symptomreduced
compliance of the lungs and a decrease in vital
capacity due to vascular congestion and interstitial
edema
-increase with: exertion, emotional stress, fever,
pulmonary infection, sexual intercourse, AF, and
pregnancy at rest orthopnea

9. 2-Hemoptysis:
-Due to increased pulmonary pressures and vascular
congestion
-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 the 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

10. 3-Thromboembolism:
-Over 80 percent of patients with MS who have an embolism are
in AF
-Transient AF and infective endocarditis
-Early percutaneous balloon mitral commissurotomy prevents
systemic embolism in patients with and without AF
-Predictors in absence of AF:
Left atrial thrombus
The degree of reduction in mitral valve area
Significant aortic regurgitation
-LA(most) most common=cerebral circulation,spleen,
kidneys, and the coronary circulation
-RA PE

11. 4-Chest pain:
Most commonly the result of pulmonary hypertension and
right ventricular hypertrophy
May be due to underlying coronary artery disease or a
coronary artery embolism
5-Infective endocarditis:
-Uncommon once the valve becomes calcified and very
rigid
-Antibiotic prophylaxis against endocarditis is NOT
recommended in patients with native valve mitral stenosis
in the absence of prosthetic replacement

12. 6-Right-sided heart failure:
-Increased jugular venous pressure
-Edema of both legs, 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
7-Hoarseness:
LAcompression of the recurrent laryngeal nerve leading
to hoarseness (Ortner's syndrome or cardiovocal
syndrome)
8-Fatigue due to the reduction in cardiac output

13. PHYSICAL EXAMINATION
-The arterial pulses are reduced in volume due to the decreased stroke
volume, AF.
-When MS is severe vasoconstriction, resulting in pinkish-purple patches
on the cheeks (mitral facies).
-Pulmonary hypertension and right ventricular hypertrophy prominent "a"
wave (atrial contraction). 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.
-Palpation and percussion of the chest wall reveals an apical impulse that is
generally normal.
However, if pulmonary hypertension is present, there may be a right
ventricular heave (substernal lift) and a palpable S2.
-Advanced disease may be associated with the signs of right-sided heart
failure

14. Cardiac auscultation
1-Heart sounds:
As a result of the elevated left atrial pressure, the stenotic (but noncalcified)
mitral leaflets are still widely separated at the onset of ventricular contraction.
Thus, the first heart sound (S1) is loud, reflecting the increased excursion of
the leaflets. As the leaflets become more rigid and calcified, their motion is
limited and S1 becomes soft.
The second heart sound is initially normal but, with the development of
pulmonary hypertension, 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.
A third heart sound of left ventricular origin is never 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 may be
generated from the right ventricle.
A fourth heart sound may be heard, most often originating from the right
ventricle when it is hypertrophied and dilated and the patient is still in sinus
rhythm

16. 2-Opening snap:
An opening snap (OS) of the mitral valve is heard at the
apex when the leaflets are still mobile.
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.
As the MS progresses and left atrial pressure is higher, the
OS occurs earlier after S2 or A2. Thus, the shorter the A2-
OS interval, the more severe the mitral stenosis.

17. 3-Diastolic murmur :
-Low-pitched diastolic rumble that is most prominent at the apex, patient lying on the left side in
held expiration and by using the bell of the stethoscope, after exercise (very light
pressure also may help. (Strong pressure will instead completely eliminate the low frequencies of
MS).
-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.
-This early diastolic murmur is decrescendo, becoming softer as the left atrial pressure falls and the
transvalvular gradient decreases. If the patient is still in sinus rhythm, the increase in atrial
pressure after atrial contraction, results in an increase in the loudness of the murmur, termed
"presystolic accentuation"
-The diastolic murmur may be inaudible or absent when MS is very severe, due to the very slow
flow across the mitral valve.
-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 shortens. Similar
changes are seen in response to exercise. In contrast, reducing venous return with amyl nitrate, the
Valsalva maneuver, or squatting shortens the murmur and lengthens the A2-OS interval.

18. 4-Additional sounds, murmurs:
-A pulmonary ejection sound, which 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 which increases with inspiration.
-A faint and brief 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. 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 sec), 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 waves changes are not seen in patients with atrial
fibrillation. The fibrillatory waves are coarse, generally >0.1 mV
in amplitude, reflecting left atrial hypertrophy.
--Pulmonary hypertension and right ventricular hypertrophy
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. Chest x-ray
-Left atrial enlargement may produce a "double density," the left
heart border becomes straightened, the left bronchus is
elevated, and, on the lateral projection, the left atrium is
displaced posteriorly, impinging on the esophagus.
-Calcification of the annulus may be observed
-Enlargement of the main pulmonary artery due to pulmonary
hypertension, while the aorta and left ventricle are often small.
-Pulmonary vascular congestion with 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

22. Pulmonary arteriogram in pulmonary
hypertension secondary to mitral stenosis

24. Echocardiography
1-Transthoracic:
--(2-D) echocardiography:
-Mitral leaflets are thickened, have reduced motion during diastole, and show doming,
which is indicative of commissural fusion
-The mitral valve area can be accurately measured by planimetry in short axis views.
-Estimates of leaflet motion, the degree of calcification and fibrosis of the leaflets, and
assessment of the subvalvular apparatus can help establish the role for surgical or
balloon valvotomy. Also, commisural calcification
-Left atrial size, and left and right ventricular size and systolic function can be
assessed.
--Doppler:
-Mean transvalvular gradient and the pressure half-time valve area can be accurately
calculated from the diastolic velocity curve. (severe=MVA<1, mean PG>10mmHg)
-Pulsed, continuous wave, and color Doppler are used to evaluate coexisting mitral
regurgitation.
-Pulmonary pressures are calculated from the velocity of the tricuspid regurgitation jet
and right atrial pressure, which is estimated from the size and respiratory variation in
the inferior vena cava

25. Hatle formula

26. 2-Three-dimensional:
This technique can provide an en-face cross sectional view of the mitral orifice, to which
planimetry can be applied to determine the valve area.
3-Stress echocardiography:
-Is helpful when symptoms seem to be more severe than expected based on resting hemodynamics
(such as resting valve area); these patients often have exertional pulmonary hypertension.
-Mechanical relief of MS is recommended in patients with elevated pulmonary pressures (>60
mmHg systolic) with exertion.
4-TEE:
-To assess the presence of absence of left atrial thrombus and to further evaluate the severity of
mitral regurgitation in patients being considered for percutaneous mitral balloon valvotomy
-To assess mitral valve morphology and hemodynamics if transthoracic echocardiography provides
suboptimal data
AHA 2014:
I-TEE should be performed in patients considered for percutaneous mitral balloon
commissurotomy to assess the presence or absence of left atrial thrombus and to
further evaluate the severity of mitral regurgitation (MR) . (Level of Evidence: B)

27. AHA 2014

29. Cardiac catheterization and angiography
--To assess the severity of MS if noninvasive tests are
not conclusive or there is a discrepancy between the
results of noninvasive tests and clinical findings
related to the severity of MS.
--When there is a discrepancy between mitral valve
area and the Doppler-derived mean gradient;
catheterization should include left ventriculography to
evaluate the severity of mitral regurgitation
--To assess the cause of severe pulmonary arterial
hypertension if it is out of proportion to the severity of
MS determined by noninvasive testing.

30. AHA2014:
Class IIa
1. Exercise testing is reasonable in selected
patients with asymptomatic severe VHD to 1)
confirm
the absence of symptoms, or 2) assess the
hemodynamic response to exercise, or 3)
determine
Prognosis . (Level of Evidence: B)

32. EVALUATION AND FOLLOW-UP
--Too early unnecessary risk for a complication of the
procedure with little or no short-term benefit, since the MS
may remain asymptomatic and stable for many years.
--Delaying intervention  irreversible pulmonary
hypertension and/or right heart failure
--ACC/AHA repeat echocardiography to assess
pulmonary artery pressure in asymptomatic stable patients
every year in those with severe MS, every one to two years
with moderate MS, every three to five years with mild MS,
and any time there is a change in clinical status

33. PHYSICAL ACTIVITY AND EXERCISE
--Exercise should be symptom-limited. This will prevent extreme elevations in
the transmitral gradient that may lead to pulmonary edema
--Patients in sinus rhythm with mild MS with peak pulmonary artery systolic
pressures less than 50 mmHg can participate in all competitive sports.
--Patients with moderate MS who are in sinus rhythm or atrial fibrillation
(AF) and have peak pulmonary artery systolic pressures less than 50 mmHg
can participate in low and moderate static and dynamic competitive sports.
--Patients with severe MS who are in sinus rhythm or atrial fibrillation and
patients with peak pulmonary artery systolic pressures greater than 50 mmHg
should not participate in any competitive sports.
--Patients with MS of any severity who are in or have a history of AF and are
treated with anticoagulation should not participate in any competitive sports
associated with a risk of bodily contact or possible trauma

34. Diuretics
--Usually with a loop diuretic+ dietary salt restriction
are appropriate when there are manifestations of
pulmonary vascular congestion
--Right-sided heart failure

35. Digoxin
--Symptomatic left and/or right ventricular systolic
dysfunction.
--Controlling a rapid ventricular rate during AF,
although it should not be considered a first-line drug
for this indication

36. Beta blockers
--Decrease heart rate and cardiac output at rest, causing a decrease in the
transmitral gradient, pulmonary capillary wedge pressure, and mean
pulmonary pressure.
--Blunt the heart rate and cardiac output responses to exercise
--Exercise capacity may not be increased by beta blockers but it is not reduced
--In NYHA IV {exclude HF}
AHA 2014:
Class IIa
1. Heart rate control can be beneficial in patients with MS and AF
and fast ventricular response.
(Level of Evidence: C)
Class IIb
1. Heart rate control may be considered for patients with MS in
normal sinus rhythm and symptoms
associated with exercise . (Level of Evidence: B)

37. Secondary prevention of rheumatic fever
-Preventing repeated attacks of rheumatic fever may
play a role in delaying the progression of MS
{progressionresponse to turbulent blood flow
through the rheumatically deformed valve}

38. Prevention of endocarditis
The 2007 American Heart Association guidelines on
the prevention of bacterial endocarditis recommended
that only patients with the highest risk of the
development of endocarditis receive antimicrobial
prophylaxis—not MS--

39. Prevention of thromboembolism
--The 2014 ACC/AHA valvular disease guidelines and 2008 Eighth
ACCP consensus conference recommended long-term oral
anticoagulation (target INR 2.5, range 2.0 to 3.0) in patients with MS
who have a prior embolic event, left atrial thrombus, or paroxysmal,
persistent, or permanent AF, since all forms of AF carry a similar risk
for thromboembolism
--The ACCP consensus conference suggested the addition of low-dose
aspirin (50 to 100 mg/day) in patients who have an embolic event or
have left atrial thrombus despite oral anticoagulation at a therapeutic
INR. An alternative strategy is to adjust the oral anticoagulant dose to
achieve a higher target INR (target INR 3.0, range 2.5 to 3.5)
--The ACC/AHA guidelines suggested that oral anticoagulation may be
considered in patients with severe MS, an enlarged left atrium>55mm,
and spontaneous echo contrast, although the evidence was less well
established {??bleeding}

40. Statin therapy
The rates of decrease in mitral valve area and increase
in mean transmitral gradient were lower in the statin
group compared with the untreated group  Further
study in randomized controlled trials is required

41. AF
--Hemodynamically unstable immediate electrical
cardioversion is indicated.
--Hemodynamically stable patients controlling the ventricular
rate (with a beta blocker without intrinsic sympathomimetic
activity, calcium channel blocker [verapamil or diltiazem], or,
less preferably, digoxin) and anticoagulation {2-3}
--Cardioversion is not indicated before intervention unless
unstable
--Rate control strategy is generally preferred, with a rhythm
control strategy, long-term anticoagulation is still required in
most patients
----Substitution of vitamin K antagonists by new agents is not
recommended, because specific trials in patients with VHD are
not available

42. RFA
--The 2006 ACC/AHA/ESC guidelines on AF
concluded that catheter ablation is a reasonable
alternative to pharmacologic therapy for the
prevention recurrent AF in symptomatic patients with
little or no left atrial enlargement. The presence of left
atrial enlargement would exclude many patients with
MS
----Surgical ablation should be considered in patients
with symptomatic AF and may be considered in
patients with asymptomatic AF, if feasible with
minimal risk

43. Pregnancy
--COP= 30-50% increase
--During active labor, additional increases in cardiac output and
stroke volume occur with each uterine contraction (additional
50 percent)
--Following delivery, there is an abrupt increase in preload,
resulting from the autotransfusion of uterine blood into the
systemic circulation and to aortal caval decompression in the
absence of a gravid uterus up to six weeks postpartum
--To minimize medical treatment failures during pregnancy,
women with MS should be evaluated before pregnancy:
Symptomatic mitral stenosis (NYHA class II to IV) or severe
pulmonary hypertension (pulmonary artery pressure >75
percent of systemic pressure) intervention pre

44. --Management:
-Diuretic therapy for pulmonary congestion(safe) avoid hypovolemia
(placental hypoperfusion).
-If symptoms progress despite diuretic therapy, a beta blocker should be tried,
beginning with very low doses. A cardioselective drug may be preferred.
-fail  PMBV at experienced centers or surgical closed commissurotomy
-Severe mitral stenosis at labor invasive hemodynamic monitoring with a
right heart catheter is appropriate  goal pulmonary capillary wedge
pressure of approximately 14 mmHg. Invasive hemodynamic monitoring
should be continued in the immediate postpartum period because of large
intravascular volume shifts
{Cesarean section should be performed only for obstetric indications, better in
patient on warfarin  for foetus}
--Routine endocarditis prophylaxis is not necessary for either cesarean or
vaginal delivery

45. + AF:
--Hemodynamically unstable  electrical cardioversion is
both safe and effective. If an antiarrhythmic drug is needed
to maintain sinus rhythm  quinidine and procainamide
are the drugs of choice.
--Beta blockers are preferred for control of the ventricular
rate. CCB (verapamil or diltiazem) are more likely to cause
maternal hypotension, especially when given intravenously
--Anticoagulation should be continued during pregnancy.
Warfarin is typically avoided in the first trimester because
of its known teratogenic effects, particularly between the
sixth and ninth weeks.

46. NB. Warfarin+ pregnancy
--Teratogenic effects:
-Potentially teratogenic (low MW, cross placenta) Embryopathy ,
spontaneous abortion and stillbirth.
-The teratogenic effect appears to be dose related, with doses less than 5
mg/day providing the highest margin of safety {regardless of INR}
-most common bone and cartilage nasal and limb hypoplasia
--CNS abnormalities (including optic atrophy, microcephaly, mental
retardation, spasticity, and hypotonia)
-Immaturity of fetal enzyme systems and the relatively low concentration of
vitamin K-dependent clotting factors render the fetus more sensitive than the
mother to the anticoagulant effects of warfarin  risk of hemorrhagic fetal
death during vaginal delivery warfarin should be discontinued after 34 to
36 weeks of gestation
-Preterm cesarean delivery may prevent hemorrhagic fetal death, and fresh
frozen plasma should be administered to the neonate, mother
-safe in lactation

47. --UFH (c):
-Relative difficulty of maintaining a stable therapeutic response, the inconvenience of
parenteral administration, and the complications of heparin-induced
thrombocytopenia and bone demineralization in patients treated for more than seven
weeks
-Guided by APTT
--LMW heparin (B):
-Sustained, stable therapeutic response
-Reduce the inconvenience of parenteral administration
-Laboratory monitoring of the anticoagulant effect of LMW heparin is generally not
performed in nonpregnant patients, but some authors recommend measuring anti-
factor Xa levels four hours after injection in pregnant patients
-Less likely to precipitate heparin-associated thrombocytopenia, unclear whether bone
loss may be significantly reduced
-American College of Obstetricians and Gynecologists has stated that LMW heparin
can be considered in women who are candidates for prophylactic or therapeutic
anticoagulation during pregnancy
- Patients should be switched to subcutaneous unfractionated heparin about two weeks
prior to the expected delivery; this will permit regional anesthesia for labor {epidural
haematoma}

48. Mechanical prosthetic heart valves:
--FDA  LMWH is not recommended for
thromboprophylaxis in pregnant women with
prosthetic heart valves.
--However, other expert panels disagree, and the
American College of Chest Physicians recommended
that LMWH remain a therapeutic option in this setting

49. 2008 ACCP Guidelines
One of three approaches for anticoagulation during pregnancy:
--Aggressive adjusted-dose unfractionated heparin throughout the pregnancy;
heparin is administered subcutaneously every 12 hours in doses adjusted to
keep the mid-interval aPTT at least twice control or to attain an anti-Xa level
of 0.35 to 0.70 U/mL. After a stable dose is achieved, the aPTT should be
measured at least weekly.
--Adjusted-dose subcutaneous LMW heparin therapy throughout the
pregnancy in doses adjusted according to weight to achieve the
manufacturer's recommended anti-Xa level four hours after subcutaneous
injection.
--Unfractionated or LMW heparin therapy (as above) until the thirteenth
week, a change to warfarin until the middle of the third trimester, and then
restarting unfractionated or low molecular weight heparin until delivery
Heparin can be restarted 12 hours post-cesarean delivery and 6 hours post-
vaginal birth, if no significant bleeding has occurred replaced with warfarin
(stopping the heparin when the INR is therapeutic)

50. Other indications for AC in pregnancy
Venous thromboembolism
Atrial fibrillation associated with significant
underlying heart disease
Antiphospholipid antibody syndrome
Heart failure, particularly in the presence of a
ventricular thrombus
Eisenmenger syndrome
Paroxysmal nocturnal hemoglobinuria

51. AHA 2014
The patient and family should be sufficiently
educated by the Heart Valve Team about all
alternatives for treatment so that their expectations
can be met as fully as possible using a shared decision-
making approach.

52. Heart Valve Centers of Excellence
1) are composed of experienced healthcare providers with
expertise from multiple disciplines;
2) offer all available options for diagnosis and
management, including complex valve repair, aortic
surgery, and transcatheter therapies;
3) participate in regional or national outcome
registries;
4) demonstrate adherence to national guidelines;
5) participate in continued evaluation and quality
improvement processes to enhance patient outcomes; and
6) publicly report their available mortality and success
rates.

54. TECHNIQUE
-- Transseptal puncture is used to gain access to the mitral
valve from the left atrium.
A single deflated balloon or a double-balloon is advanced
from the venous circulation to the right atrium, across the
interatrial septum to the left atrium, and across the
stenotic mitral valve.
Inflation and rapid deflation of the balloon opens the
stenotic valve via separation of the fused commissures
--TEE can guide the procedure  general anesthesia
--Intracardiac echocardiography can delineate the extent of
valvular deformity and may also be useful in visualizing
several key steps cost, inability to accurately measure
mitral valve area or adequately assess mitral regurgitation

55. --OUTCOMES:
-Short-term:
Excellent from 1.0 cm2 to approximately 2.0 cm2
Decrease in left atrial pressure and the transmitral
pressure gradient, a reduction in pulmonary artery
pressure, and an increase in cardiac output.
An additional benefit is a reduction in left atrial
stiffnessincrease in left atrial pump function in patients
in sinus rhythm and an increase in left atrial reservoir
function in those with atrial fibrillation
-Long-term:
Pulmonary vascular resistance declines and normalizes in
many patients.

56. Predictors of adverse events (death, mitral valve surgery,
and repeat PMBV):
-Echocardiographic score >8, which was associated with
lower success rates and smaller increases in mitral valve
area
-Increasing age (palliative in elderly with CI to surgery)
-Prior surgical commissurotomy
-NYHA functional class IV
-Higher postprocedural pulmonary artery pressure
-Preprocedural mitral regurgitation ≥2+
-Postprocedural mitral regurgitation ≥3+

58. --PMBV versus surgical commissurotomy:
The outcome after PMBV was as good or better than
after surgery in patients who are candidates for
valvotomy.
--Mitral valve replacement combined with TV repair
may produce better outcomes in patients with severe
MS and severe TR than PMBV

61. AHA 2014
IIb
Percutaneous mitral balloon commissurotomy may be
considered for symptomatic patients with mitral valve area
greater than 1.5 cm2 if there is evidence of hemodynamically
significant MS based on pulmonary artery wedge pressure
greater than 25 mm Hg or mean mitral valve gradient greater
than 15 mm Hg during exercise. (Level of Evidence: C)
Mitral valve surgery and excision of the left atrial appendage
may be considered for patients with severe MS (mitral valve
area ≤1.5 cm2, stages C and D) who have had recurrent embolic
events while receiving adequate anticoagulation. (Level of
Evidence: C)

64. Noncardiac surgery
--In symptomatic patients or in patients with systolic
pulmonary artery pressure >50 mmHg, correction of MS—
by means of PMC whenever possible—should be attempted
before non-cardiac surgery if it is high risk. If valve
replacement is needed, the decision to proceed before non-
cardiac surgery should be taken with
caution and individualized.
--Asymptomatic patients with significant MS and a systolic
pulmonary artery pressure <50 mmHg, non-cardiac
surgery can be performed safely
----Control heart rate (particularly in MS), to avoid fluid
overload as well as volume depletion and hypotension
(particularly in AS)

65. Other valvular lesions
--When either stenosis or regurgitation is predominant,
management follows the recommendations concerning the
predominant VHD
--Interaction between the different valve lesions ex. associated
MR may lead to underestimation of the severity of AS
--Indications for intervention are based on global assessment of
the consequences of the different valve lesions, i.e. symptoms
or presence of LV dilatation or dysfunction
--The decision to intervene on multiple valves should take into
account the extra surgical risk
--The choice of surgical technique should take into account the
presence of the other VHD.

66. Thank you