STENOSIS MITRAL

DEFINITION Mitral stenosis is condition of pathological narrowing of mitral valve. Normal square area of mitral valve is 4-6 square cm. When it is reduced to half of it, significant hemodynamic changes take place !ig. ".#$. ETIOLOGY Commonest - %heumatic heart disease Rare causes #. &ongenital ". 'utem(acher)s syndrome *+, withcongenital or acquired mitral stenosis$. -. .nfective endocarditis with large vegetations causing o(struction. 4. /ndomyocardial fi(rosis. 0. 1urler)s syndrome. 6. Carcinoid 2malignant. 3. Methysurgide. Pathology #. ". -. &ommissural fusion is the hall mark. 4hickening of leaflets and fi(rosis. +tenosis develops after a latest period of a(out #5 years.

Fig. 2.16 Mitral valve stenosis HEMODYNAMICS OF MITRAL STENOSIS (FIG. 2.2) .. Rise in left atrial pressure: Mitral valve narrowing- (ackflow 2rise in '* pressure. ... Pulmonary venous congestion: %aised '* pressure is transmitted (ack to pulmonary veins (ecause no valves at their 7unction with '*$ thus increasing pressure in pulmonary venules and capillaries-fluid transudate into interstitial space,

alveoli and causes pulmonary edema and engorgement of lymphatics. &ongested (ronchial veins cause airway o(struction. .... Rise in pulmonary artery pressure: %ise in pulmonary venous pressure causes constriction of corresponding pulmonary arterioles eventually causing pulmonary. *rterial 14. .8. Redistribution of blood flow to upper lobes: 1igh left atrial pressure and high hydrostatic pressure affects lower lo(e vessels most. +o pulmonary arterial vasoconstriction occurs most in lower lo(es and most of (lood flow as a compensation is diverted to upper lo(e. 8. Rt ventricular failure: 9ulmonary arterial hypertension causes strain to emptying of %t.8 and eventually %t heart failure. Left Ventricular Function Remains Normal

Fig. 2.2 1emodynamics of mitral stenosis CLINICAL PICT!RE Sy"#to"$ ,evelop #5-"5 years after initial rheumatic insult. ,yspnea on e:ertion. ;rthopnea, paro:ysmal nocturnal dyspnea and symptoms of acute pulmonary edema. !atigue due to low cardiac output. 9alpitation due to *! 1emoptysis due to various mechanisms. Sig%$ .. ... .. 9eripheral &ardiovascular

Peripheral6 Mitral facies with malar flush, and small volume pulse, peripheral cyanosis.

... #. ". -. 4.

Cardiovascular6 4apping apical impulse. ,iastolic thrill may (e present at the ape:. 9arasternal heave due to %81. Auscultation !ig. ".-$ 'oud . sound at ape:. ;pening snap. Mid diastolic murmur at ape:. 9resystolic accentuation.

Mechanism and description of clinical features Loud st sound: 1igh left atrial pressure holds the mitral valve wide open until the end of diastole and ventricular systole slams it shut. Opening snap: 9roduced (y sudden (ellowing down of mitral cusps into left ventricle at the end of isometric rela:ation period. 'oud . sound and opening snap indicate that the valve is plia(le and not fi(rosed or calcified. !pening snap is a short, sharp, snapping and high pitched sound-(est heard at ape: (ut also heard over left lower parasternal area and may e:tend to cardiac (ase .

Fig. 2.& *uscultatory features of mitral stenosis Diastolic murmur 'ow pitched, descri(ed as rum(le. <egins with opening snap and has varying duration. =sually occupies mid diastole. <est heard with (ell stethoscope in left lateral position with (reath held in e:piration. =sually grade " or - (ut may (e loud or faint> =sually accentuates (efore . heart sound. Pre-systolic accentuation 9roduced (y '* contraction> may (e a(sent in *!.

Not always a(sent in *!> persists in short diastole due to high velocity$. "ow to demonstrate diastolic murmur in sub clinical #$% *fter e:ercising the patient put him in left lateral and auscultate. Pulmonary area When pulmonary hypertension develops? .. heart sound splits, 9" (ecomes loud, %arely @raham +teell murmur of pulmonary insufficiency occurs- caused (y dilatation of pulmonary artery. All auscultatory features of pulmonary hypertension are listed below: 'oud 9", .. heart sound split narrowly. 9ulmonary e7ection click. /7ection systolic murmur increasing with inspiration. @raham +teell murmur early diastolic murmur at pulmonary area. Murmur of tricuspid incompetence. %t atrial @allop. 4ypes of pulmonary hypertension occurring in mitral stenosis6 #. 9assive. ". *ctive ? -. ;rganic o(literation of pulmonary vasculature$ 8aria(ility in auscultatory features- that may occur6 +oft . sound- rigid Acacific valve. .n severe M+, M,M may (e a(sentAsoft. 9+M a(sent when dominant mitral regargitation is pressure +ilent M+-4ight M+ with large %8 displacing '8 posteriorly and so masking the murmur. Diag%o$ti' F(at)*($ 'oud . sound at ape: ;pening snap 'ow pitched rum(ling mid diastolic murmur with presystolicaccentuation6 (est heard, with patient in left lateral position with (reath held in e:piration. Di++(*(%tial Diag%o$i$ +o* Cli%i'al Pi't)*( o+ Mit*al St(%o$i$ #. '* my:oma, ". <all valve throm(us, -. &or triatriatum. 'eft atrial my:oma - murmur varies with posture. Di++(*(%tial Diag%o$i$,Fo* Mi- Dia$toli' M)*")* #. Mitral stenosis ". 4ricuspid stenosis murmur accentuating with inspiration$

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!low murmurs caused (y increased (lood flow across the mitral or tricuspid valve during diastole in the following$ Mitral regurgitation 4ricuspid regurgitation *+, 8+, 9,* 4. Carey coomb&s murmur: .n acute rheumatic mitral valvulitis 2 functional murmur 0. Austin Flint murmur: ;ccurs in free aortic incompetence> functional murmur mid diastolic murmur at ape: see !ig. 6.-$. !ther Conditions Causing Loud $ound #. 4achycardia. ". 1yperdynamic states valve remains open at end diastole and is forci(ly closed (y hyper contractile '8$. !ther Conditions Causing !pening $nap 4ricuspid stenosis, my:oma. A$$($$"(%t$ i% Mit*al St(%o$i$ #. ,egree of stenosis severity$ ". 4he mo(ility of mitral valve -. 9ulmonary hypertension 4. 9resence of other lesions and dominance. *. #. ". -. 4. <. #. ". -. Degree of stenosis is assessed (y6 +" 2 ;+ interval which is inversely proportional to severity =sual range of +"- ;+ interval is 5.5B 2 5.#" sec> 5.56 and less in severe. ,uration of murmur6 .t is directly proportional to severity6 longer the duration severe the stenosis. ,egree of '* enlargement in C-ray and /&@ and (y /cho. 9resence of pulmonary hypertension in pure M+. Mobility of valve is denoted (y6 9resence of loud . sound ;pening snap *(sence of valve calcification.

.n com(ined mitral lesion factors which denote dominant #$ are6 9resence of opening snap 'oud . sound 9resystolic accentuation *(sence of ... ht sound Which mitral lesion causes gaint '*? Mitral regurgitation$.

Co"#li'atio%$ o+ "it*al $t(%o$i$ .. &omplications of pulmonary venous congestion ... &omplications of enlarged left atrium .... &omplications at valve level. Complications of Pulmonary Venous Congestio 9aro:ysmal nocturnal dyspnea *cute pulmonary edema 1emoptysis 9ulmonary arterial hypertension %ight heart failure 9recipitants of pulmonary edema6 *!, pregnancy, e:ercise, emotion, chest infection, anesthesia. Complications of 'nlarged Left Atrium *trial fi(rillation 2deteriorates the condition suddenly. '* throm(us formation with throm(oem(olic signs &ere(ral %enal &oronary 9eripheral 'eriche)s syndrome 9ressure on esophagus causing dysphagia 9ressure on '. recurrent laryngeal nerve causing hoarseness of voice ;rtner)s syndrome 'ifting up of ' main (ronchus 2 causing emphysema. Complications at Valve Level .nfective endocarditis 2 rare. Causes of hemoptysis6 %upture of (ronchial vein, pulmonary edema pulmonary infarct, (ronchitis, 914. IN.ESTIGATIONS /0*ay Ch($t +hows features of mitralisation of heart6 #. +traightening of left (order of the heart hypoplastic aorta, prominent M9*, enlarged left atrial appendage, all these -, come in line with '8 (order and so straightening$. ". !eatures of pulmonary hypertension6 ,ialated main pulmonary artey, narrowing of peripheral pulmonary arteries. -. !eaturers of pulmonary venous congestion6 4hin short horiDontal lines 7ust a(ove costophrenic angle representing interlo(ar septae

4. 0. 6. 3. B.

thickened (y edema and fi(rosis-Eerley ( lines near costophrenic angle> perpendicular to pleural surface. Pulmonary edema: 9erihilar congestion, haDiness spreading from hilum to periphery-F(at)s wing appearanceG and nodular opacities. '* enlargement seen as opacity within %* opacity. %edistri(ution of (lood from the (ase to the ape: causing enlarged upper lo(e (ronchial veins. 'eft upper lo(e (ronchus elevated causing compensatory emphysema. 1emosiderosis consequent feature of repeated pulmonary congestion

1a*i)" S2allo2 /nlarged '* causes esophageal indentation in right o(lique view. C-ray and (arium swallow contraindicated in pregnancy. ECG 9 pulmonaleA9 mitral> %81 with %t a:is deviation, atrial fi(rillation> (iphasic 9 wave. P mitrale: 9 wave duration H#"5 ms> prominent notched 9 P pulmonale: 9eaked 9 waves, amplitude H".05 m 8. ECHO &onfirms the diagnosis6 *sseses the severity +hows presence or a(sence of throm(usAcalcification +hows other associated lesions if any. *lso indicates mitral valve area( mitral valve morphology) /chocardiographic mitral morphology score is derived from following features6 #. 'eaflet rigidity, ". 'eaflet thickening, -. 8alvular calcification, and 4. +u(valvular disease each graded as #I to 4I> score HB fare (adly. Do##l(* +hows #$pressure gradient across mitral valve and "$ pulmonary artery pressure. TEE 4ransesophageal echocardiogram6 +hows '* throm(us, endocarditis. Cath(t(*i3atio% #. +hows pressure gradient (etween '* and '8> measures 9*, '*, '8 diastolic pressures 2 &atheteriDation is indicated when clinical and echoA,oppler data are discordant. ". 1elps to assess #R severity in those posted for (alloon valvotomy especially when clinical and other data are discordant.

#ultislice C*: * new modality to assess mitral valve area. TREATMENT #edical: 4reatment of cardiac failure 4reatment of arrhythmia-atrial fi(rillation 4reatment of pulmonary edema 9rophyla:isAtreatment of infective endocarditis +econdary prophyla:is for rheumatic fever. Avoid: *nemia, tachyarrhythmia and vigorous e:ercise which can precipitate cardiac failure. INTER.ENTION #. *iming+mildAmoderate symptoms ". M8area J# cm"Am" -. ,elay worsens prognosis. 4. .f patient is symptomatic despite medical treatment. Mit*al 1alloo% .al4)lo#la$ty ndications for6 +ignificant symptoms class ..-.8 .solated mitral stenosis No or trivial mitral regurgitation No calcification or rigidity of the valve-valve must (e mo(ile 'eft atrium- free of throm(us 9ulmonary hypertension 05-65 mm of 1g 8alve area of,J#sq cm. T('h%i5)( o+ 1alloo% .al4)lo#la$ty 8alvotomy is done (y inflating a (alloon mounted on a cardiac catheter, 8ia rt femoral vein (alloon mounted catheter is passed trans septally> *dvanced into '* over a curly guide wire, now the distal portion of (alloon is inflated slightly and (alloon is advanced up to ape: of '8. 4hen (alloon is gradually withdrawn, until positioned across mitral valve. *t this position the (alloon is inflated procedurally, splitting the commissural adhesions. 8alvuloplasty only requires light sedation, like for cardiac catheteriDation. *fter 3-#5 years of valvuloplasty, valve usually restenoses and mitral valve replacement is indicated. Complications of ,alloon Valvuloplasty Mitral regurgitation 'eft to %t shunt 4hrom(oem(olism 9ericardial tamponade

Myocardial infarction. S)*g(*y +o* Mit*al St(%o$i$ #itral Valvotomy +urgical separation of fused commissures *dhesions that cause the mitral orifice to (e narrowed, are lysed mechanically (y hand or (y dilator$. 8alvotomy can (e closed or open. 8alvotomy is done if facilities or e:pertise for (alloon valvuloplasty is not available) Closed Valvotomy 9rerequisite6 !le:i(le, non-calcified valves with no '* throm(us. 9erformed through a left thoracotomy without a (ypass. &ontraindication are same as for (alloon valvuloplasty and additional. &ontraindications are chest deformity, severe lung disease and elderly frail patients. &losed valvotomy is rarely performed now a days in developed countries. !pen Valvotomy 9rerequisite6 !le:i(le, non-calcified valves. 9erformed on a cardiopulmonary (ypass through a mid sternotomy. .ndications6 !ailure of (alloon valvulopastyAclosed commissurotomy. *ssociated mild M%, '* throm(us. After valvuloplasty or valvotomy*nti(iotic prophyla:is for endocarditis is a must and yearly follow up for restenosis is done. MITRAL .AL.E REPLACEMENT I%-i'atio%$ #. %estenosis ". +evere advanced M+ 8alve area J #sq cm <ut patient must have good '8 function$. -. &lass .., ..., .8 symptoms. 4. +evere M+ unfit for valvotomy or valvuloplasty6 calcified, rigid valve 0. +evere associated M%, thickened fused chordae 6. 9ulmonary artery systolic pressure of H 65-B5 mm of 1g. 3. %ecurrent throm(o em(olic manifestations. Ty#($ o+ P*o$th(ti' .al4($ (Fig. 2.6) #. <ioprosthetic valve ". Mechanical prosthetic valve.

Fig. 2.6 9rosthetic valves M('ha%i'al Caged ,all valve: e.g. +tarr-/dward valve6 *dvantage-@ood dura(ility ,isadvantage-<ulky and space occupying. Co"#li'atio%$ 9eriprosthetic mitral regurgitation 1emolytic anemia Kaundice 4hrom(oem(olism 'ife long anticoagulation needed .nfective endocarditis 9aravalvular ring a(scess. *ilting disc valve: e.g. +t. Kude valve, <7Lrk-+hiley valve not (eing used now$ ,ioprosthetic valve: *utograft6 from patient)s pericardium *dvantage2anticoagulant)s not so much necessary6 disadvantage2not dura(le6 7ust #5 years or less 9orcine tissue2throm(oem(olism less. Following valve replacement long term anticoagulant therapy is indicated. 9atient with prosthetic valve replacement 2put on warfarin for rest of their life. <ut :enograft porcine$ or homograft cadaver$ do not require anticoagulation, e:cept in presence of large '* and *!. Note: 9atients after valvuloplastyAvalvotomy require prophyla:is for inf.endocarditis. Co"#li'atio%$ o+ .al4( R(#la'("(%t %estenosis 4hrom(oem(olic phenomenon 1emolytic anemia Mechanical or material defects of valve itself.

e.g., failure of closure or openingAdetachment partial Afull. S!MMARY i. .n most case of M+6 ,alloon valvotomy is successful. ii. .f valve anatomy is unfavoura(le for valvotomy6 valve replacement *iming of valve replacement6 a. NM1* functional class - or 4. (. 9ulmonary hypertension pulmonary arterial systolic pressure J05 mm 1g$ ,ioprosthetic valve can degenerate within a decade and necessitatereoperation with attendant increased surgical risk. iii. .n young women who wish to (ear children6 .f in these women (alloon valvuloplasty is not feasi(le, valve replacement is advised (ut it is complicated6 Mechanical valve needs anticoagulation> warfarin causes 1igh incidence of fetal malformation> heparin has (een shown to have +erious complication. Ma%ag("(%t o+ Mit*al St(%o$i$ P*o'(-)*( #. 9ercutaneou s (alloon mitral vavotomy ". Mitral valve repair for M+. &losed or open mitral valvotomy I%-i'atio%$ +ymptomatic NM1* class .., ..., .8 Mitral valve area J# cm" With no M%, no '* throm(us, no calcification NM1* &lass ...-.8 Mitral valve area J# cm" .f (alloon valvotomy is not availa(le 8alve morphology favoura(le for repair with no M%, no calcification, no '* throm(us. NM1* &lass ...-.8 ModerateAsevere M+ with valve area J# cm" who are unfit for valvotomy or repair -4hose with '* clot or mitral calcification or rigid mitral valvecom(ined M+ and M% Mitral valve restenosis.

-. replacement for M+

Mitral valve

Not( .n addition to factors mentioned a(ove, various parameters like /!, '8/,,, 914, *!, 8alve morphology and others have to (e considered in details in deciding a(out surgery.