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MITRAL VALVE DISEASE

Incidence of Rheumatic fever has dramatically

decreased in developed countries.

Remains endemic in developing world.

Increase in life expectancy explains in crease in

prevalence of degenerative Mitral valve disease.


MITRAL STENOSIS
Aetiology
Rheumatic fever
• Fusion of commissures
• Thickening of leaflets
• Thickening of subvalvular apparatus
Degenerative mitral stenosis
• Elderly patients
• Extensive calcification
congenital mitral stenosis
• Rare
Pathophysiology
Stenotic MV causes a diastolic gradient between
LA and LV.
Increases LA, capillary wedge and pulmonary
arterial pressure – more pronounced with high
CO and tachycardia.
LA enlargement AF
Stasis of blood in LA thrombo embolism
Clinical Features
Progressive dyspnoea pulmonary
oedema.
Palpitation AF.
Systemic embolism.
Loud 1st heart sound.
Opening snap in early diastole.
Mid – diastolic murmur.
Signs of PHT.
Signs of RHF.
Investigations
ECG
• AF
• LA enlargement
• RVH
Chest Radiography
• LA enlargement
• Dilatation of pulmonary artery
• Interstitial oedema / pulmonary oedema.
ECHO (TTE and TOE)
• Most important investigation to confirm the
diagnosis and guide management.
• MS confirmed by 2D Echo showing leaflet
thickening and restricted movement.
• Severity of MS assessed by transvalve gradient
using Doppler technique / trace MVA by
planimetry.
• Valve anatomy – commissural fusion, leaflet
thickening, calcification and subvalvular
involvement.
cardiac catheterization and haemodynamic
studies
• Rarely needed.
MANAGEMENT
Medical Therapy
Symptom relief
• ß blocker - heart rate, prolong diastole,
increase ventricular filling, reduce
transmitral gradient.
• Diuretics.
Anticoagulation
• All patients with MS and AF
• Patients with sinus rhythm
• Previous embolic events.
• Thrombus in LA / LAA.
• LA > 5 cm.
• Target INR 2 – 3.
Intervention / Surgery
PTMC
• Symptomatic patients with severe MS.
• Safe procedure when performed by experienced team.
• Good immediate and long – term results.
• Non – calcified valve.
• pregnancy
• Contraindications.
• Massive bicommissural calcification.
• LA /LAA thrombus.
• Significant MR.
• Severe associated AV disease.
Surgery
• MVR
• Open and closed Mitral valvotomy.
• MVR carries a higher risk than PTMC and is
associated with long – term prosthesis – related
complications.
• Generally considered when valves are
anatomically unsuitable for balloon dilatation.
Percutaneous mitral commissurotomy
using an Inoue balloon.
Follow – up

Moderate MS with no symptoms.


• Echo every 1 – 2 years / new symptoms.

• Annual Echo after PTMC – risk of restenosis.


MITRAL REGURGITATION
Aetiology
Rheumatic MR – thickening and retraction of the
posterior leaflet.
Ischaemic MR – acute or chronic ischaemia.
• Acute MR due to papillary muscle ischaemia
or rupture complicating AMI (usually inferior)
pulmonary oedema.
• Chronic Ischaemic MR is more common and
associated ventricular remodeling.
Degenerative MR.
Mitral valve Prolapse and regurgitation.
• Leaflets are pliable and elongation or rupture of chordae
leads to prolapse of one or both leaflets into LA.
Endocarditis causing MR
• Leaflet perforation.
• Chordal rupture.
Functional / secondary Mitral regurgitation.
• Dilated cardiomyopathy.
• Modification of movement of subvalvular
apparatus.
MR secondary to inflammatory disease,
endomyocardial fibrosis, and HOCM
Pathophysiology
Acute MR abrupt rise of LA pressure
pulmonary oedema.
Chronic well tolerated with a moderate rise
in LA pressure. Long term MR LV
dilatation with irreversible myocardial damage
and dysfunction.
Clinical Features
Asymptomatic for many years
Dyspnoea.
Pansystolic murmur.
Third heart sound – severe MR.
.
Investigation
ECG
• LA enlargement.
• Rarely AF.
Chest Radiography
• Enlarged LA / LV.
• Pulmonary oedema.
Echo
• Key examination to confirm diagnosis, quantify
regurgitation and assess underlying mechanism.
• CW or color Doppler – detect systolic
regurgitant flow.
• Quantification of regurgitant volume.
.
• Mechanism and cause of MR – TTE and TOE
assessment of leaflet structure, and movement,
features of subvalvular apparatus and the
dimensions of Mitral annulus.
• Consequences of MR – PHT, LA dilation, LV
dialatation and dysfunction
LV angiography
• Semiquantitative assessment of MR.
• LV dilatation and EF.
Management

Medical Management

• ACEI reduces volume of chronic severe MR

and may palliate LV dysfunction.

• Anticoagulation is mandatory in AF.


Surgery
• Severe acute MR requires early surgery.
• Chronic MR – timing of surgery.
• Symptomatic patients.
• Asymptomatic patients with LV dysfunction
or LVESD > 45 mm.
• Valve repair or MVR.
Follow – up

Asymptomatic patients with moderate MR.

Followed up annually and Echo every 2-3 years.

Severe MR and PHT / AF / LV dysfunction

should be followed-up more frequently.

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