16_43_20_Mitral_stenosis valvular heart disease

Valvular heart disease

1. MITRAL STENOSISMITRAL STENOSIS
Dr R SchulenburgDr R Schulenburg
Division of Adult Cardiac Surgery, Division of Adult Cardiac Surgery,
Universitas Hospital, BFNUniversitas Hospital, BFN

2. Etiology and Essential PathologyEtiology and Essential Pathology
Predominately post-inflammatory Predominately post-inflammatory
scarring(other malignant carcinoid, SLE)scarring(other malignant carcinoid, SLE)
Fibroreactive transformation of the valveFibroreactive transformation of the valve
Affecting all segments of the valvular Affecting all segments of the valvular
apparatusapparatus
Calcifications at commisural edges lead to Calcifications at commisural edges lead to
classic ‘fish-mouth’ appearanceclassic ‘fish-mouth’ appearance
Only 25% have pure MSOnly 25% have pure MS

3. PathophysiologyPathophysiology
Reduction in MVA with a rise in Reduction in MVA with a rise in
atrioventricular gradientatrioventricular gradient
LA hypertrophy and imposes a pressure LA hypertrophy and imposes a pressure
load on the RV through the development of load on the RV through the development of
pulmonary hypertensionpulmonary hypertension
Increases in RV end-diastolic pressure and Increases in RV end-diastolic pressure and
volume cause RV dilatation which may volume cause RV dilatation which may
result in funtional TVR(annular dilatation)result in funtional TVR(annular dilatation)

4. PathophysiologyPathophysiology
LV diastolic function is usually preserved LV diastolic function is usually preserved
although there may be(25%) dysfunction in although there may be(25%) dysfunction in
patients with severe, chronic MS(chronic patients with severe, chronic MS(chronic
preload reduction and/or extension of preload reduction and/or extension of
scarring from the valve to adjacent scarring from the valve to adjacent
myocardium)myocardium)
Systemic effects of severe TVRSystemic effects of severe TVR

5. Classification and Natural HistoryClassification and Natural History
Mild(MVA>1.5, MG<5mmHg, Mild(MVA>1.5, MG<5mmHg,
PASP<30mmHg)PASP<30mmHg)
Moderate(MVA 1-1.5, MG 5-10mmHg, Moderate(MVA 1-1.5, MG 5-10mmHg,
PASP 30-50mmHg)PASP 30-50mmHg)
Severe(MVA<1, MG>10mmHg, Severe(MVA<1, MG>10mmHg,
PASP>50mmHg)PASP>50mmHg)

6. Natural HistoryNatural History
MV>1.5 usually does not produce symptoms MV>1.5 usually does not produce symptoms
at restat rest
Symptoms develop when the LAP Symptoms develop when the LAP
increases(Dyspnoea) >5mmHgincreases(Dyspnoea) >5mmHg
Occurs when there is an increase in Occurs when there is an increase in
transmitral flow or a decrease in diastolic transmitral flow or a decrease in diastolic
filling time(exercise, emotional stress, filling time(exercise, emotional stress,
infection, pregnancy, AF with a rapid infection, pregnancy, AF with a rapid
ventricular response)ventricular response)

7. Nutural HistoryNutural History
MS is a continuous, progressive, life-long disease, MS is a continuous, progressive, life-long disease,
usually consisting of a slow, stable course in the usually consisting of a slow, stable course in the
early years followed by a progressive acceleration early years followed by a progressive acceleration
in later lifein later life
Once symptoms develop, there is another period Once symptoms develop, there is another period
of almost a decade before symptoms become of almost a decade before symptoms become
disableingdisableing
Asymptomatic/minimally symptomatic: survival is Asymptomatic/minimally symptomatic: survival is
80% at 10yrs but once significant limiting 80% at 10yrs but once significant limiting
symptoms develop, there is a dismal 0-15% 1-year symptoms develop, there is a dismal 0-15% 1-year
survival ratesurvival rate

8. Natural HistoryNatural History
When severe pulmonary HPT develops , When severe pulmonary HPT develops ,
mean survival drops to <3yrsmean survival drops to <3yrs
60-70%-progressive pulmonary and 60-70%-progressive pulmonary and
systemic congestionsystemic congestion
20-30%-systemic embolism20-30%-systemic embolism
10%-pulmonary embolism10%-pulmonary embolism
1-5%-infection1-5%-infection

9. DiagnosisDiagnosis
History: slow, indolent increase in dyspnoea and History: slow, indolent increase in dyspnoea and
general fatigue(any sudden change in symptom general fatigue(any sudden change in symptom
complex should raise suspicion!)complex should raise suspicion!)
Clinical:RV heave, Apex beat, Diastolic rumble, Clinical:RV heave, Apex beat, Diastolic rumble,
Opening snapOpening snap
ECGECG
CXR:Cardiac chamber enlargement, Pulmonary CXR:Cardiac chamber enlargement, Pulmonary
venous hypertension, Pulmonary arterial venous hypertension, Pulmonary arterial
hypertensionhypertension
ECCHO/TEEECCHO/TEE
Cardiac cathCardiac cath

10. ManagementManagement
Medical: AB prophylaxis, diuretics, negetive Medical: AB prophylaxis, diuretics, negetive
chronotropic drugs, atrial fibrillationchronotropic drugs, atrial fibrillation
Interventional: Percutaneous balloon Interventional: Percutaneous balloon
valvotomyvalvotomy
Surgical: Cosed/open commissurotomy, Surgical: Cosed/open commissurotomy,
MVRMVR