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

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

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

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

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

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

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

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

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

10. Management
Medical: AB prophylaxis, diuretics, negetive chronotropic drugs, atrial fibrillation
Interventional: Percutaneous balloon valvotomy
Surgical: Cosed/open commissurotomy, MVR