二尖瓣的病理生理学课件

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1、Alan SihoeCardiothoracic Surgery Teaching Round2nd August 2002Epidemiology 1998 in the UK:6471 first time valve replacements of which 28%MVR Numbers increasing Mitral Annulus:fibro-muscular skeleton Anchors base of valve leaflets Leaflets:conn tissue+muscle+vessels/nerves Anterior(aortic):larger;1/3

2、 of annulus Posterior(mural):2/3 of annulusAnatomyAnatomy Papillary muscles:Anterolateral Posteromedial Chordae tendinae 1st,2nd,3rd order Approx 25 major chordal trunks 100 attachments to leaflets No consensus on timing of muscle activity with cardiac cycleAnnular dynamics Annular size Increases in

3、 late systole(maximum in diastole)Contracts in pre-systole(minimum in midsystole)Annular shape More eccentric in systole Annular position Moves up towards LA in diastole Moves down towards LV apex in systoleLeaflet dynamics Opening Starts in center,moving to edges Flapping of edges at max.opening Cl

4、osing(begins in late diastole)Bulging at base/annular attachment Leaflet ascends towards LA Bulging rolls from annulus to edge Aetiology:Rheumatic Male:female ratio is 1:2-3 Acquired early(30mmHg:pulm transudation reduced lung compliance Pulm art systolic pressure 60mmHg impedes RV emptying right he

5、art failure Ultimately irreversible pulm vascular changesMS:Natural historyProgressive life-long diseaseLong latencySymptoms:i.Low cardiac output:dyspnoea,fatigueii.Pulmonary congestion/HT(orthopnea,PND)right heart failure hemoptysisiii.Atrial fibrillation/Thromboembolismiv.Cardiac cachexiaMS:Natura

6、l history Onset of symptoms to disability:10 years 10 year survival:Asymptomatic(NYHA class I)80%(progression)Symptomatic(NYHA class III)20%Causes of death:CHF 60-70%Systemic embolism 20-30%Pulmonary embolism 10%Infection 1-5%MS:Investigations CXR:LA enlargement,pulm congestion ECG:LA enlargement(no

7、tched P in II,V1)atrial arrhythmias?RVH Echo:valve area,LA/LV dimensions Doppler:measures pressure gradients TOE:better mitral/LA visualization Cardiac catheter:not essential Assocd disease;LV ventriculography&pressuresMS:Medical therapy Pharmacological Tx of mild heart failure,bronchitis,arrhythmia

8、s,hemoptysis Endocarditis prophylaxis Anticoagulation:Hx of AF/thromboembolism Balloon(or open)ValvuloplastyMS:Indications for surgerySymptomatic(NYHA class III-IV):MVR1.h long-term survival10 year survival:0-20%90%(89%at 15 yrs)2.h functional capacityValve area 1-1.5cm2 (normal 4-6 cm2)Systemic emb

9、oliMS:Indications for surgery Class I-II:controversial Risk of SCD if asymptomatic:negligible Survival not improved by MVR?role of valvotomy(pulmonary HT,AF)MVR indicated when:Valve area NYHA class II+Aetiology more diverse than MSMyxomatous degenerationLeading cause in West(30-70%)Defective fibroel

10、astic tissue floppy valveMost asymptomaticComplicated by annular dilatation,chordal rupture,endocarditisRheumatic disease next most commonMR:Carpentier classificationi.Normal leaflet motionAnnular/ventricular dilatationLeaflet disease/perforationMR:Carpentier classificationii.Excessive leaflet motio

11、n(prolapse)Chordal/papillary muscle elongation or ruptureMR:Carpentier classificationiii.Restricted leaflet/chordal motione.g.fibrosis,calcification,retraction MR:Aetiology1.Mitral AnnulusMyxomatous degenerationSenile calcificationFunctional dilatation(e.g.myocarditis)Ring abscessMarfansMR:Aetiology

12、2.Mitral leafletsRheumatic disease,endocarditis(1-30%)Unknown why some develop MS,others MRFibrocalcific leaflet thickening(without fusion)Chordae shortened,annulus dilatedalso:congenital,connective tissue diseaseMR:Aetiology3.ChordaeIschaemiaMyxomatousInfectiveConnective tissueTraumaIdiopathicMR:Ae

13、tiology4.Papillary muscle(10-25%)Dysfunction/ruptureIHD/MI:muscle&annular injuryfrank rupture rare,usually fatalesp.Posteromedial muscleAlso:abscess,sarcoid/amyloid,myocarditisMalalignmente.g.LV aneurysm,dilatation,myopathyMR:HemodynamicsAcute:J LA pressure,pulm oedemaChronic:LA/PV compliance:i pulm

14、 congestnRegurgitant volume depends on:i.Mitral orifice sizeii.LV-LA pressure gradientiii.Heart rateMedical Tx aims to control above factorsesp.decrease afterload to reduce LV dilatationMR:Cardiac adaptations LV:h preload,i afterload LV dilated,more spherical,thinned Increased SV(O2 consumption not

15、markedly h)But decompensation can gradually occur LA:h size in chronic MR h compliance Less thromboembloism,AF than MSMR:Symptoms Acute:pulmonary congestion&oedema Chronic:may be prolonged asymptomatic phase Risk of endocarditis Congestive heart failure&fatigue Right heart failureMR:Investigations C

16、XR:LA/LV enlargement ECG:normal;LVH,?AF/arrhythmias Echo:leaflet morphology&function Chamber dimensions,LV function Doppler colour mapping Cardiac catheter:assess coronaries,LV MRI:Dx,LV volumes,regurgitant fractionMR:Medical therapy Mainstay:Afterload reduction i regurgitant volume i pulm congestio

17、n i LV volume i mitral orifice but:ongoing LV volume overload 10%class I-II progress to III-IV per year Class II-III survival on medical Mx:5 year:50%10 year:25%MR:Natural history Variable aetiology difficult to predict Difficult to identify those progressing to irreversible LV damage Prognostic ind

18、icators:LV function Degree of regurgitation Underlying aetiology(esp.CAD)MR:Indications for surgeryAcute:muscle/chordal rupture with shock Immediate MVRChronic,NYHA class II-IV:MVRAim for surgery before irreversible LV changeLV dimension is a predictor of outcomeMR:Indications for surgery Chronic,asymptomatic:surveillance Surgery if LV systolic dysfunction or h LV size also:?if AF or pulmonary HT develop MVR for MR less successful than for MS Tendency for late presentation&OT Hence irreversible LV damage more likely