For once in my career, I falling in love with the beauty of mitral valve.

1. Management of End Stage
Mitral Stenosis
Dicky A.Wartono
2007

3. Anatomy

4. Anatomy

6. Pathology
Studies of the Mitral Valve: II. Certain Anatomic Features of the
Mitral Valve and Associated Structures in Mitral Stenosis
IAN E. RUSTED, CHARLES H. SCHEIFLEY

7. Studies of the Mitral Valve: II. Certain Anatomic Features of the
Mitral Valve and Associated Structures in Mitral Stenosis
IAN E. RUSTED, CHARLES H. SCHEIFLEY

9. Abnormal Valve Function
• Valve Stenosis
– Obstruction to valve flow during that phase of the cardiac cycle when the
valve is normally open.
– Hemodynamic hallmark -“pressure gradient”
• Valve Regurgitation, Insufficiency, Incompetence
– Inadequate valve closure--- back leakage
• A single valve can be both stenotic and regurgitant; but both
lesions cannot be severe!!
• Combinations of valve lesions can coexist
– Single disease process
– Different disease processes
– One valve lesion may cause another
– Certain combinations are particularly burdensome (AS & MR)

10. Mitral Valve Disease: Etiology
 Mitral Stenosis
 Rheumatic - 99.9%
 Congenital
 Prosthetic valve stenosis
 Mitral Annular Calcification
 Left Atrial Myxoma
 Acute Mitral Regurgitation
 Infective endocarditis
 Ischemic Heart disease
 Papillary ms rupture
 Mitral valve prolapse
 Chordal rupture
 Chest trauma
 Chronic Mitral
Regurgitation
 Ischemic Heart disease
Papillary ms dysfunction
Inferior & posterior MI
 Mitral Valve prolapse
 Infective endocarditis
 Rheumatic
 Prosthetic
 Mitral annular calcification
 Cardiomyopathy
LV dilatation

11. Mitral Stenosis
History:
History of acute rheumatic fever,
History of murmur
Effort-induced dyspnea
Most common complaint
Often triggered by exertion, fever, anemia, onset of Afib,
or pregnancy
Orthopnea, which progresses to paroxysmal nocturnal
dyspnea
Effort-induced fatigue
Hemoptysis, due to the ruptures of thin dilated bronchial
veins (late finding)
Chest pain due to right ventricular ischemia,
concomitant coronary atherosclerosis, or a coronary
embolism
Thromboembolism may be the first symptom of MS.
Palpitations
Recumbent cough
Physical: The physical examination findings depend on
the advancement of the disease and the degree of
underlying cardiac decompensation.
Peripheral and facial cyanosis
Jugular venous distention
Respiratory distress, evidence of pulmonary edema (eg,
rales)
Diastolic thrill that is palpable over the apex
A loud S1 followed by an S2 and the opening snap are
best heard at the left sternal border.
This is followed by a low-pitched, rumbling, diastolic
murmur, which is heard best over the apex
while the patient is in the left lateral decubitus position.
Murmur may diminish in intensity as the stenosis
increases.
The duration, but
mitral narrowing.
holosystolic murmur
Digital clubbing
Systemic embolization
Signs of right heart failure
pulmonary hypertension
second sound; and a
Graham Steell murmur).

12. Mitral Stenosis
• History
– Asymtomatic  Symptmatic
– History of past illness
– Heart Failure
• Physical
– Heart mur-mur
– Heart failure

14. Mitral Valve Disease
• Mitral Stenosis
– Thickened, deformed MV
leaflets
– 2D MVA
– Doppler Gradient
– Associated RVH, PHTN,
TR,MR, LV function
– vegetations
• Mitral Regurgitation
– Determine etiology –
leaflets, chordae, MVP, MI
– Doppler severity of MR jet
– LV function

15. Mitral Stenosis -Pathophysiology
• Restriction of blood flow from
LALV during diastole.
• Normal MVA 4-6cm2.
– Mild MS 2-4cm2.
– Severe MS < 1.0cm2.
• MV Pressure gradient –
• MV grad ~ MV flow//MVA.
– Flow = CO/DFP (diastolic filling
period).
• As HR increases, diastole
shortens disproportionately and
MV gradient increases.

16. Mitral Stenosis-Pathophysiology
• MV gradient Increase LA
press
• Pulmonary HTN
– Passive
– Reactive- 2nd
stenosis
• RV Pressure Overload
– RVH
– RV failure
– Tricuspid regurgitation
– Systemic Congestion

17. Mitral Stenosis- Clinical Symptoms
• Symptoms related to severity of
MVA reduction-
• Symptoms unrelated to severity of
MS-
– Atrial fibrillation
– Systemic thromboembolism
• Symptoms due to Pulmonary HTN
and RV failure-
– Fatigue, low output state
– Peripheral edema and hepato-
splenomegaly

18. complications
• Congestive heart failure.
• Heart enlargement.
• Atrial fibrillation.
• Blood clots.
• Lung congestion

20. Determinants of the
Echocardiographic Mitral Valve
Score

24. Mitral Valve Disease
Hemodinamic Management
• Increase LV pre load
• Decreace HR
• Maintain Contractile
• Maintain SVR
• Reduce PVR

25. Surgery
for Mitral Stenosis
Class III
1. not indicated for patients with mild MS.
2. Closed commissurotomy should not be
performed in patients undergoing MV
repair; open commissurotomy is the
preferred approach.
Class I
1. symptomatic (NYHA functional class
III–IV) moderate or severe MS* when 1)
percutaneous mitral balloon valvotomy is
unavailable, 2) percutaneous mitral balloon
valvotomy is contraindicated because of left atrial
thrombus despite anticoagulation or because
concomitant moderate to severe MR is present, or
3) the valve morphology is not favorable for
percutaneous mitral balloon valvotomy in a
patient with acceptable operative risk.
2. Symptomatic patients with moderate to severe
MS* who also have moderate to severe MR should
receive MV replacement, unless valve repair is
possible at the time of surgery.
Class IIb
asymptomatic patients with moderate
or severe MS* who have had
recurrent embolic events while
receiving adequate anticoagulation
and who have valve morphology
favorable for repair.
Class IIa
Severe MS* and severe pulmonary hypertension
(pulmonary artery systolic pressure greater than
60) with NYHA functional class I–II symptoms
who are not considered candidates for
ercutaneous mitral balloon valvotomy or surgical
MV repair

26. • I
– Symptomatic (NYHC),not BMV candidates
• IIa
– Symptomatic (PH), not BMV candidates
• IIb
– Asymtomatic, thrombus / embolic (+)
– Valve morphology
• III
– Mild MS
– Percutaneus Commissurotomy
Surgery
for Mitral Stenosis

28. Class I
Percutaneous or surgical MV commissurotomy
is indicated when anatomically possible for
treatment of severe MS, when clinically
indicated.
Rheumatic Heart Disease

29. Class IIa
1. A mechanical prosthesis is reasonable
for MV replacement in patients under
65 years of age with long-standing atrial
fibrillation.
2. A bioprosthesis is reasonable for MV
replacement in patients 65 years of age
or older.
3. A bioprosthesis is reasonable for MV
replacement in patients under 65 years
of age in sinus rhythm who elect to
receive this valve for lifestyle
considerations after detailed discussions
of the risks of anticoagulation versus
the likelihood that a second MV
replacement may be necessary in the
future.
Selection of an Mitral Valve Prosthesis
Class I
A bioprosthesis is indicated for MV
replacement in a patient who will not
take warfarin, is incapable of taking
warfarin, or has a clear contraindication
to warfarin therapy

30. Class I
1. Intraoperative transesophageal echocardiography
is recommended for valve repair surgery.
2. Intraoperative transesophageal echocardiography
is recommended for valve replacement surgery
with a stentless xenograft, homograft, or autograft
valve.
3. Intraoperative transesophageal chocardiography
is recommended for valve surgery for infective
endocarditis.
INTRAOPERATIVE ASSESSMENT
Class IIa
Intraoperative transesophageal
echocardiography is reasonable for all
patients undergoing cardiac valve surgery.

31. End Stage MS
• LV failure
• Arythmias
• Pulmonary Hypertension
Posterior Chordal Preservation
Maze
BMV

33. • PVD may occur in 5-10% of patients with untreated Septal Defect
• it does not appear to be caused solely by the magnitude of the shunt
persisting for decades.
• patients should be considered to have Eisenmenger syndrome when Septal
Defects are large and unrestrictive and when there is resting cyanosis.
• smaller Septal Defect is present in a patient with pulmonary hypertension,
other causes should be sought.
• There have been case reports of such patients being managed with
intravenous epoprostenol or oral bosentan with such success that Septal
Defects closure subsequently became possible.
Septal Defects in the Adult: Recent Progress and Overview
Gary Webb and Michael A. Gatzoulis
Circulation 2006;114;1645-1653

34. GENETIC PREDISPOSITION
BMPR-2 mutations
ALK1 mutations
5HTT polymorphism
CPS polymorphism
etc
GENETIC PREDISPOSITION
BMPR-2 mutations
ALK1 mutations
5HTT polymorphism
CPS polymorphism
etc
RISK FACTORS
HIV infection
Increased Pulmonary Flow
Portal Hypertension
Connective Tissue Disease
etc
RISK FACTORS
HIV infection
Increased Pulmonary Flow
Portal Hypertension
Connective Tissue Disease
etc
PULMONARY VASCULAR INJURYPULMONARY VASCULAR INJURY
ENDOTHELIAL
DYSFUNCTION
ENDOTHELIAL
DYSFUNCTION
SMOOTH MUSCLE
CELLS
DYSFUNCTION
SMOOTH MUSCLE
CELLS
DYSFUNCTION
MATRIX CHANGES,
PLATELETS
AND INFLAMMATORY
CELLS
ACTIVATION
MATRIX CHANGES,
PLATELETS
AND INFLAMMATORY
CELLS
ACTIVATION
VASOCONSTRICTION
VASOCONSTRICTION
THROMBOSIS
THROMBOSIS
PROLIFERATION
PROLIFERATION
INFLAMMATION
INFLAMMATION
PULMONARY HYPERTENSION VASCULAR DISEASE
INITIATION AND PROGRESSION
PULMONARY HYPERTENSION VASCULAR DISEASE
INITIATION AND PROGRESSION
PATHOBIOLOGICAL MECHANISM OF
PULMONARY HYPERTENSION

35. Risk of
Pulmonary Hypertension
• PreOperative Risk
– Elevated PVR
– Increase PBF
– Parenchimal Lung disease
• IntraOperative Risk
– CPB
• Post Operative Risk
– Pre & Intra Operative Risk
– Metabolic / Physical stress

36. Symptoms
Dyspnea
Fatigue
Leg swelling
Weakness
Palpitations
Abdominal fullness
Angina
Syncope and presyncope
Signs
Normal to low blood pressure
Jugular venous distention
Lung findings
Right ventricular lift
Pulmonic ejection click,
Systolic ejection murmur at LICS 2/3
Increased split of second heart sound
Systolic murmur at LICS 4 increasing with
inspiration (tricuspid insufficiency)
Soft diastolic decrescendo murmur of
pulmonic regurgitation in LICS 3
Hepatomegaly
Ascites
Peripheral edema
Clubbing
Cyanosis

37. Diagnosis and Treatment of Pulmonary Hypertensio
TRENTON D. NAUSER, M.D., and STEVEN W. STITES, M.D.
University of Kansas Medical Center, Kansas City, Kansas,2004

38. Echo Diagnostic of
Pulmonary Hypertension
• mPAP
• Shunt Gradient
• TV Gradient
• RV function

39. Raja SG, Basu D (2005) Pulmonary hypertension in
congenital heart disease.
19, 50, 41-49. Date of acceptance: January 25 2005.

42. differential diagnosis
• Pulmonary embolism
• Cardiac Tamponade
• Tension Pneumothorax
• Eisenmenger's Syndrome
• Chronic obstructive and restrictive lung diseases
• Severe valve disease with pulmonary hypertension

43. PVR
• Pulmonary vasculature
– Smooth muscle
– Endothelial
• NeuroHormonal involvement
– Mech ventilation
– CPB
– Lung disease
– Pulmonary venous hypertension

44. Management of
Pulmonary Hypertension
• Pre Operative Management
• Intra Operative Management
• Post Operative Management

45. Pre Operative Management
• Oxygen delivery
• Medical treatment
• Risk factor
Low PVR High PVR

46. Intra Operative Management
• During Inductie
• PFO creation
• CPB
– Atelectasis
– Acute lung injuryRisk : lung hypoxia,lung edema,elevated PAP
Cause : humoral inflamatory mediator
Manifestation : acute lung edema,acutebroncospasm
Prevention : PA vent,hemodilusi,membran oxygenator
blood filtrasion, medical
Risk : smoking. Lung edema
Cause : static lung
Prevention : gradual CPAP

47. Post Operative Management
• Ventilation
– Fi O2
– PEEP
• Hemodinamic
– Coronary perfusion
– Cardiac Output
• pH
• Metabolism
• Medical management

48. Strategies
to treat acute PH
• Reduce Sympathetic Stimulation
– Analgesia & sedation
– Muscle relaxant
– Treat hypo & hyperthermia
– Low doses of vasoconstrictive agent if
possible
• Lower PVR
– Gas exchange
• Increase alveolar O2 tension
• Treat acidosis
• Hypocapnia
– Mechanical Ventilation
• Avoid hyper/hypo inflation
• Low intra thoracic pressure
– Vasodilating drugs
• Specific : NO
• Non specific :
– Nitroprusside
– Glycerol trinitrate
– PDE3 inhibitor
– Isoproterenol
– Prostacyclin I2
– Prostaglandin E1

49. Strategies
to treat chronic PH

50. Evidence-Based Treatment AlgorithmEvidence-Based Treatment Algorithm
World Symposium on PAH, Venice, Italy, June 23 – 25, 2003World Symposium on PAH, Venice, Italy, June 23 – 25, 2003
Combination?
ACCP Evidence-based Clinical Practice Guidelines
Euro Heart J 2004; 25: 2243 – 2278 and Chest 2004; 126: 35S – 62S

51. Evaluation of
Suspected
Pulmonary Hypertension
Diagnosis and Treatment
of Pulmonary Hypertension
TRENTON D. NAUSER, M.D., and
STEVEN W. STITES, M.D.
University of Kansas Medical Center
F:JOBxDiagnosis and Treatment of Pulmonary Hypertension
May 1, 2001 - American Family Physician.htm

53. Strategies
to treat acute PH
• Reduce Sympathetic Stimulation
– Analgesia & sedation
– Muscle relaxant
– Treat hypo & hyperthermia
– Low doses of vasoconstrictive agent if
possible
• Lower PVR
– Gas exchange
• Increase alveolar O2 tension
• Treat acidosis
• Hypocapnia
– Mechanical Ventilation
• Avoid hyper/hypo inflation
• Low intra thoracic pressure
– Vasodilating drugs
• Spesific : NO
• Non specific :
– Nitroprusside
– Glycerol trinitrate
– PDE3 inhibitor
– Isoproterenol
– Prostacyclin I2
– Prostaglandin E1

55. Atrial hypertrophy and dilatation may be
either a cause or a consequence of
persistent AF,
- Hemodynamic Consq
- Thrombus formation
- Risk for Ischemic Stroke
-Prev stroke/TIA
-Hypertension
-CHF
-Advanced age
-DM
-CAD
Decreased HRV in mitral stenosis patients with sinus rhythm suggests increased
sympathetic activity in patients prone to atrial fibrillation. The evaluation of HRV
may be a useful tool for the identification of patients predisposed to AF.
Ann Saudi Med 2002;22(3-4):143-148.
HEART RATE VARIABILITY IN PATIENTS WITH MITRAL
STENOSIS: A STUDY OF 20 CASES FROM KING
ABDULAZIZ UNIVERSITY HOSPITAL
Awdah Al-Hazimi, PhD; Nabil Al-Ama, MRCP; Moustafa Marouf, PhD

56. Therapy
• Objective
– Prevent Thromboemblism
– Prevent HF
– Relieve of Symptom
• Rate / Rhythm controle
• Cardioversion
• Anti Coagulant

60. Thank YouThank You