Timing and indications of surgery in stenotic and regurgitant valvular lesions

Timing and indications of surgery in stenotic and regurgitant valvular lesionsDr.Deepak RajuAortic stenosisPathophysiologyAssessment of severityNatural historyManagement strategyRole of exercise test,EBCTRecommendations

Concept of afterload mismatchTerm coined by Ross et al (1976)Increasing aortic pressure increased LV contractility,LV volume and mass kept constantAt a particular level contractility started decreasing-mismatch b/w afterload and contractile state

AS-pathophysiologyIncreasing severity of AS-matched by increasing LV mass and contractilityCompensation by hypertrophy fails to sustain afterload Clinical afterload mismatch occursLV utilizes preload reserve-mechanism by which stroke volume is maintained by increasing preloadPreload reserve is not a good compensatory mechanism in AS(LV on steep portion of diastolic pressure volume loop)Systolic pump function fails once preload reserve is no longer adequateEarliest stage of LV dysfunction in severe AS LV systolic dysfunctionAfterload mismatch and/or impaired contractilityLV diastolic dysfunctionLaplace equationStress =pressure .radius/2.wall thicknessIncreased wall thickness compensates for pressure overloadImpaired relaxation&altered compliance-Diastolic dysfunctionAtrial booster pump maintains LV filling

Assessment of severityJet velocity-reproducible,strongest predictor of clinical outcomeAortic valve area-continuity equationVelocity ratio-suboptimal image of LVOTeffectively indexed for BSARatio 26% predictive of probability of cardiac death or AVREnergy loss indexCalculated from aortic valve area and area of aorta at sinotubular junctionSevere AS 4.5 mmHg/ml/m2 (Zeineb et al JACC 2009)9

Natural historyProlonged latent periodRate of progression of stenosis of moderate severityJet velocity 0.3 m/s/yrGradient 7 mmHg/yrArea 0.1 cm2/yr

Asymptomatic adult-AS

Pellikka et al .circulation 2005,622 pts,mean follow up 5.4 yrOther findings(Pellikka et al )Patients with jet velocity >4.5 m/s had greater likelihood of develpoing symptoms(relative risk 1.34)Incidence of sudden cardiac death was 1% /yrAsymptomatic patient-ASPatients with asymptomatic severe AS require frequent monitoring for devt.of symptomsIn a meta analysis of seven studies the risk of sudden cardiac death was found to be 0.4%/yr(375 pts,mean follow up 2.1 yr)Follow upClinicalfrequent monitoring for devt of symptomsevery year for mild6 mth for moderate and severeTTEEvery year for severe AS1-2 year for moderate AS 3-5 year for mild ASPatient education regarding devt of symptoms

Exercise testingMay be considered in asymptomatic patients with unclear symptoms to elicit(IIb)limited exercise capacityexercise induced symptomsAbnormal BP responseAmato et al 2001,Heart 200166pts,14 mth follow upPositive stress restHorizontal or downsloping ST dep>1 mm (men ) &2mm (women)or upsloping ST>3mm in menAngina ,near syncopeVentricular arrhythmia SBP fails to rise by 20 mmHgGrp with Abnormal exercise response19% symptom free survival at 2 yrsNormal85% symptom free survival at 2 yrs6% experienced SCD;all had positive stress test

Das P et al, Eur Heart J,2005125 pts,12 mth follow upPositive testLimiting symptoms(chest tightness,breathlessness,dizziness)Abnormal BP response(BP at peak exercise same or below baseline)ST dep >2mmExercise limiting symptoms independent predictor of outcome Exercise brought out symptoms in 37% ptsIn this group spontaneous symptoms developed in 51% compared to 11% in others

Management strategyIn most asymptomatic patients with aortic stenosis,risk of surgery(3-4% for AVR-STS database) is higher than risk of watchful waitingEarly surgeryolder pts to higher mortality(8.8% in >65 yr, US medicare data)Younger pts-morbidity and mortality of prosthetic valveEarly AVR may be considered Severe valve calcificationRapid progressionIncrease in jet velocity >0.3 m/s/yrDecrease in valve area >0.1 cm2 /yrExpected delays in surgery

Symptomatic ASCritical point in natural history of ASAverage survival is 2-3 yearsHigh risk of sudden cardiac death AVR improves symptoms and survival

Ross J Jr, Braunwald E: Aortic stenosis. Circulation 38:61, 1968Low flow low gradient aortic stenosisDobutamine stress echocardiography(IIa)Transvalvular PG,valve area calculated in baseline and low dose dobutamine stressSevere AS-fixed valve area,increase in stroke volume and gradientAS not severe-valve area increases >0.2 cm2 ,increase stroke volume ,no change in gradientLack of contractile reserve-increase in stroke volume 60 mmHgAsymptomatic,PSG >50mmHg,with ST or T wave changes in left precordial leads at rest or with exerciseClass II aAsymptomatic,PSG > 50mmHg,wants to play competitive sports or planning pregnancyWhen possible BAV preferred over surgery in adolescent or young adult

AR-PathophysiologyAR volume overload and pressure overloadVolume overload EDV chamber complianceCombination concentric and eccentric hypertrophyPressure overload chamber size- wall stress-elevates afterloadPreload reserve and compensatory hypertrophy maintain ejection performance-asymptomatic patient

Latent phase of AR, like AS, may last decadesDecompensation Preload reserve exhaustedHypertrophy inadequateImpaired contractilityLV systolic dysfunction-initially reversible-afterload excessImpaired contractility predominates later-irreversibleChamber enlargementSpherical geometryLV systolic function and ESD-most important predictors of postoperative survival and recovery of LV function

Natural historyAsymptomatic patient with normal LV function9 published studies,593 patients,mean follow up of 6.6 yrs25% of patients who die or develop LV dysfunction do so before the onset of symptomsQuantitative evaluation of LV function indispensable

Natural history

End systolic dimension in relation to devt of symptoms,LV Dysfunction or deathBonow et al,circulation 1991ESD>50mm-19% /yrESD 40-50 mm-6% /yrESD 55mm)Class II bAsymptomatic severe AR with borderline LV dilatation(EDD 70-75,ESD 50-55)abnormal hemodynamic response to exerciseprogressive LV dilatationDeclining exercise toleranceModerate AR undergoing CABG or aortic surgery

Bicuspid aortic valve with dilated ascending aortaClass ISurgery to repair aortic root or replacement of ascending aortaDiameter of ascending aorta or root >5cmRate of increase in size >0.5 cm/yrDiameter>4.5 cm undergoing AVR Mitral stenosisNarrowing of valve area to < 2.5 cm2 occurs before devt.of symptomsSymptoms at rest occur when valve area 60 mmHg with exerciseClass IIaSymptomatic (III,IV) moderate or severe MS,non pliable calcified valve if not candidates for surgeryClass II bAsymptomatic moderate MS when new AFSymptomatic mild MS,exercise PASP >60 mmHg,PAWP>25mmHg,Mean grad >15 mmHg

Indications for surgeryCLASS ISymptomatic(III or IV),moderate or severe MSPMBV unavailable or contraindicatedValve morphology not favourableModerate MRCLASS II aMV replacement in severe MS,class I or II symptoms,PASP>60 mmHg and not considered for PMBV

Event free survival after BMV-50-65% at 3-7 yrs Survival higher (80%) in pts with favourable MV morphology MS in young adults,adolescentsClass ISymptomatic(III,IV) with MV mean gradient >10 mmHgClass IIaMV gradient >10mmHg withMild symptomsAsymptomatic with PASP>50 mmHgType of surgeryParachute MV-creation of fenestration among fused chordaeAnnulus enlarging operation-hypoplastic mitral annulusBallon dilatation in congenital MS-usefulness limited

MR -pathophysiologyIncreased preload,reduced or normal afterloadEccentric cardiac hypertrophyIncreased LVEDV-compensated phaseProlonged hemodynamic overload ultimately leads to myocardial decompensationEjection phase indices are initially higher in c/c MR due to reduced afterloadOnce decompensation occurs start decreasing Values in low normal range reflect impaired myocardial function Mitral regurgitationMild to moderate MR asymptomatic for yearsSevere MR-asymtomatic for years-compensated phase Natural history of severe MR due to flail leaflet-Sarano et al,1996At 10 years 90% required MVR or deadMortality -6-7% /yr in MR by flail leaflets in pts with symptoms(class III,IV) or LV dysfunction(EF40 mm2 had 4% /yr risk of cardiac death(198 pts follow up 2.7 yr)Rosenhek et al ,2006132 pts ,5 yr follow upIndications of surgery were symptoms,LVD ,LV dilatation,devt of PAH or AFOne cardiac death in a patient who refused surgery

Surgery for asymptomatic patient with normal LV function only considered if >90% likelihood of successful MV repairRate of reoperation similar in MVR or MV repair(7% to 10%) at 10 yrsOperative mortality 2% for MV repair,6% for MVR(STS database)Indications for surgeryClass I Symptomatic a/c severe MRSymptomatic c/c severe MR(class II to IV) in the absence of severe LVD(EF55mm)Asymptomatic c/c severe MR with mild to moderate LVD(EF 30% to 60% and/or ESD >40mm) MV repair recommended over MVR

64Class II aAsymptomatic severe MR with normal LV fn(EF >60% AND ESD50 mmHg at rest or >60 mmHg with exercise) Symptomatic severe MR with severe LVD,if MV repair likelyClass II bc/c severe MR secondary to severe LVD,persistent symptoms despite optimal therapy for heart failure

Tricuspid valve diseaseSevere TR poor long term outcome due to RV dysfunction&systemic venous congestionManagement strategy depends on clinical status and cause of tricuspid valve abnormalityTR a/w dilatation of tricuspid annulus should be repairedTricuspid dilatation is an ongoing processAnnuloplasty improves functional status independent of degree of TR

Tricuspid valve and chordal reconstruction can be attempted in some cases(endocarditis,trauma)TVR- when leaflets themselves are diseased,abnormal or destroyed-bioprosthesis preferredTR should be addressed along with left sided valve surgery when annulus is dilated >70 mm peroperatively or >3.5 cm in TTE(Bianchi et al,2009)

Indications for tricuspid valve surgery Class ITricuspid valve repair for severe TR in patients with mitral valve d/s requiring mitral valve surgeryClass II aTVR or annuloplasty for severe primary TR when symptomaticTVR for severe TR when not amenable to repair or annuloplastyClass II bTricuspid annuloplasty for less than severe TR in patients undergoing mitral valve surgery when there is pulmonary hypertension or annular dilatationPulmonary stenosisNHCHD study 564 pts Medical management-46%(mild or moderate)Pressure gradients stable in majority14% had significant increase of gradient40 mmHg4% chance of increase gradients in other pts surgery moderate to severe diseasegradient decreased to insignificant levels in 90%No recurrence in follow up 14 yrs22 yr follow up of same cohort(1993)Pts with initial gradient 30 mmHgAsymptomatic patient with PSG>40 mmHgClass II bAsymptomatic patient with PSG>30-39 mmHgLong term follow up of BPV similar to surgery with no recurrence (10 yr follow up ,Mc Crindle et al,circulation 1994 )Surgery still required for dysplastic pulmonary valve Pulmonary regurgitationConsequence of BPV or surgical valvotomy or TOF repairRV systolic dysfunction-9%Pulmonary valve replacement indicated in symptomatic patients(class III or IV) with severe PRAsymptomatic patients-before RV function deteriorates 73 THANK YOU