ACC/AHA VALVULAR HEART DISEASE

GUIDELINES 2014

Dr.NagulaPraveen

Rick A.Nishimura,M.D.,FACC

Catherine M.Otto,MD.,FACC

Introduction

• Diagnosis and management of adults with valvular heart

disease.

• Original VHD guidelines in 1998 – revised in 2006 –

updated in 2008.

• Evidence based recommendations are made.

STAGES OF PROGRESSION OF VHD

Frequency of Echocardiogram in Asymptomatic pts with VHD

Secondary Prevention of Rheumatic fever

Duration of Secondary Prophylaxis for

Rheumatic Fever

STS PROM

• Accepted tool to predict the risk of a surgical operation.

• STS – Society of Thoracic Surgeons

• PROM – Predicted Rate Of Mortality

STS database 2000 -2010

• Frailty – ability to perform activites of daily living.

AORTIC VALVE OPERATIONS

PROM MEAN MORTALITY RATE

80% <4% 1.4%

14% 4%-8% 5.1%

6% >8% 11.1%

SEVEN FRAILTY INDICES

Katz Activities of daily living• Independence in feeding• Bathing• Dressing• Transferring• Toileting• Urinary continence

Independence in ambulation• No walking aid or

Assist required or

Walk 5 meter < 6 sec.

PROCEDURE SPECIFIC IMPEDIMENT Tracheostomy ,Heavily calcified ascending aorta,Chest deformity,arterial coronary graft adherent to chest wall,Radiation damage

MAJOR ORGAN SYSTEM COMPROMISE

• Cardiac-• Severe LV systolic

dysfunction• Severe LV diastolic

dysfunction• RV dysfunction• Fixed pulmonary HTN

• CKD stage 3 or more• Pulmonary dysfunction with

FEV1 <50%,DLCO2 <50% of predicted value

• CNS dysfunction • Dementia• Alzhemiers disease• Parkinson’s disease• CVA with persistent physical

limitation

• GI dysfunction• Crohn’s disease• UC • Serum albumin <3.0 gm/dl

• Cancer –active malignancy• Liver –cirrhosis,variceal bleed• Elevated INR

Does all patients need intervention?

• http://riskcalc.sts.org/de.aspx

NO• Life expectancy less than 1 yr.• Chance of survival with benefit <25% at 2yrs.• Improvement of NYHA by one class

- Stages of Valvular Heart DiseaseDiagnosis and follow up

Diagnostic testing – initial diagnosisDiagnostic testing – changing signs or symptomsDiagnostic testing – routine follow up Diagnostic testing – cardiac catheterisationDiagnostic testing – exercise testing

Medical therapy Timing of interventionChoice of intervention

Aortic StenosisAortic RegurgitationBicuspid Aortic valve and AortopathyMitral StenosisMitral RegurgitationTricuspid valve diseasePulmonic valve diseaseMixed valve diseaseProsthetic valves Infective EndocarditisPregnancy and VHDSurgical considerationsNon cardiac surgery in patients with VHDEvidence gaps and future directions

AORTIC STENOSIS

Stages of Valvular AS

Each of these stages is defined by

• Valve anatomy,

• Valve hemodynamics,

• The consequences of valve obstruction on left ventricle

and vasculature,

• Patient symptoms.

Hemodynamic severity is

best characterized

by the transaortic maximum velocity

or

Mean Pressure Gradient

when the transaortic volume flow rate is normal.

STAGES of VALVULAR AORTIC STENOSIS

Stages C1 and C2

Special Sub groups

• Some patients with AS have a low transaortic volume flow rate due

to either LV systolic dysfunction with a low LV ejection fraction

(LVEF) or due to a small hypertrophied left ventricle with a low

stroke volume.

• Diagnostic and management challenge.

Designated as

• D2 (with a low LV EF)

• D3 ( with a normal LVEF).

INDICATION CLASS RECOMMENDATION

ECHO I B Signs or symptoms of AS /bicuspid AV for ∆ ,cause, severity, LVsize ,function, systolicfunction, prognosis,timing of intervention.

IIa B Low dose DBS – D2AS calcified,EF<50%,1.0cm2area ,velocity <4m/sec, MPG - 40 mmHg.

Exercise testing

IIaB Asymptomatic pts >4m/sec , MPG >40 mmHg.

III B Symptomatic pts with >4m /sec , MPG>40 mmHg

Medical therapy

I B HTN in pts at risk, asymptomatic ,according to GDMT, low dose to start with

IIb C Vasodilator therapy in acute RX of decompensated severe AS with NYHA class IV HF symptoms

III A Statin therapy is not indicated for hemodynamic progression of AS in pts with mild to moderate AS calcific.

Dobutamine Stress Echocardiography

• To be done in patients with severe AS(due to small valve area) and concurrent LV systolic dysfunction.(usually have MPG <40 mmHg).

• 1.Severe AS with LV systolic dysfunction due to afterload mismatch.

• 2.Primary myocardial dysfunction with only moderate AS and reduced leaflet opening due to low flow rate.

SEVERE /MODERATE AS

CONTRACTILE RESERVE PRESENT/ABSENT. • 5 mcg/kg/min – increments of 5 ug/kg/min(max 20 ug/kg/min)• AJV,MPG,LVEF,valve area

• Pts who donot have true anatomically severe AS - increase in valve

area with only a modest increase in transaortic velocity or gradient as

transaortic stroke volume increases.

• Patients with severe AS – relatively fixed area even with an increase

in LV contractility and flow rate.

• EAE/ASE – Severe AS - >4m/sec, valve area <1.0cm2 at any point

during test protocol.

• Fail to increase in SV >20% with dobutamine – lack of Contractile

Reserve.

• Very poor prognosis with either medical or surgical therapy.

What is the rate of progression of Aortic Stenosis?

AORTIC STENOSIS PROGRESSION/EVENT FREE SURVIVAL

Severe AS (asymptomatic –sympotmatic)

Event free survival 30-50% at 2yrs

Moderate AS (3.0-3.9m/sec) 0.3m/sec/yr,7mmhg/yr,0.1cm2/yr

Aortic sclerosis 10% in 2 yrs

Progression of AS more rapid in older patients and those with more leaflet calcification

What are the symptoms in favour of AS in ExerciseTesting?

• 1.Exercise induced angina

• 2.Excessive dyspnea early in exercise

• 3.dizziness

• 4.syncope

• 5.abnormal BP response(<20 mm Hg increase)

• 6.ST-T abnormalities .

Studies on Aortic Stenosis

TRIAL NAME DRUGS USED RESULT

1 SEAS SIMVASTATIN,EZETIMIBE NO BENEFIT

2 SALTIRE HIGH DOSE ATORVASTATIN NO BENEFIT

3 ASTRONOMER ROSUVASTATIN NO BENEFIT

4 SCOPE -AS ENALAPRIL BENEFIT

SEAS study• SIMVASTATIN EZETIMIBE IN AORTIC STENOSIS• RCT ,Simvastatin 40 mg and Ezetimibe 10 mg did not reduce

aortic valve events (AVEs), while ischemic cardiovascular events (ICEs) were significantly reduced in the overall study population.

• the impact of baseline AS severity on treatment effect has not been reported.

• rates of AVEs and ICEs increased with increasing baseline severity of AS.

• Higher baseline peak aortic jet velocity predicted higher rates of AVEs and ICEs in all tertiles (all p values < 0.05) and in the total study population (p < 0.001).

Simvastatin-ezetimibe treatment was not associated with a

statistically significant reduction in AVEs in any individual tertile.

A significant quantitative interaction between the severity of AS

and simvastatin-ezetimibe treatment effect was demonstrated for

ICEs (p < 0.05) but not for AVEs (p = 0.10).

In conclusion, the SEAS study results demonstrate a strong

relation between baseline the severity of AS and the rate of

cardiovascular events but no significant effect of lipid-lowering

treatment on AVEs, even in the group with the mildest AS.

ASTRONOMER STUDY

AORTIC STENOSIS PROGRESSION OBSERVATION

MEASURING EFFECTS OF ROSUVASTATIN

(ASTRONOMER) STUDY.

• 168 patients (56 ± 13 years), AS severity was categorized based on peak velocity at baseline (Group I: 2.5-3.0 m/s; Group II: 3.1-3.5 m/s; Group III: 3.6-4.0 m/s).

• Baseline and follow-up hemodynamics, LV dimensions and diastolic functional parameters were evaluated in all three groups.

• There was increased diastolic dysfunction from baseline to follow-up in each of the placebo and rosuvastatin groups.

Conclusions

• In patients with increasing severity of AS in Groups I and II,

the lateral E' was lower and the E/E' (as an estimate of

increased LVEDP) was higher at baseline (p < 0.05).

• However, treatment with rosuvastatin did not affect the

progression of diastolic dysfunction from baseline to 3.5 year

follow-up between patients in any of the three predefined

groups.

I C

II b C

II b C

N

N

N

II b C

Choice of Surgical or Transcatheter intervention

TAVR• TAVI VIDEO• Dr Alain Cribier pioneered the first transcatheter aortic valve

implantation (TAVI) procedure in 2002

TAVRPARTNER trial.

FRANCE study.

Antegrade – Acute MR

Retrograde approaches

Transfemoral approach

Transapical approach

Transaortic surgical retrograde approach 

Two types of stent-valve devices

Balloon-expandable valves (Edwards SAPIEN and SAPIEN XT, which have replaced the Cribier-Edwards valve)

Self-expanding valve (Medtronic CoreValve) thesubclavian/axillary artery , direct aortic access via either ministernotomy or right anterior thoracotomy.

C/I for TAVR/TAVI• Bicuspid or unicuspid or noncalcified aortic valve• Severe AR (>3+)• Native aortic annulus size as measured by echo <18 mm or > the largest

annulus size for which a TAVR device is available (eg, 29 mm for the largest Medtronic CoreValve).

• HOCM. LVEF < 20 %.• Severe PAH and RV dysfunction.• Renal insufficiency (eg, creatinine >3.0 mg/dL) and/or ESRD• MRI confirmed CVA or TIA within six months (180 days) of the procedure.• Estimated life expectancy <12 months due to noncardiac comorbid

conditions.• Severe MR• Thoracic or abdominal aortic aneurysm (luminal diameter ≥5 cm), marked

tortuosity (hyperacute bend), Aortic arch atheroma (especially if >5 mm thick, protruding, or ulcerated) ,Narrowing (especially with calcification and surface irregularities) of the abdominal or thoracic aorta ,

Case scenario 1

A 50 yr old male,hypertensive since 15 yrs ,came with complaints of SOB on exertion.class III NYHA.

• On examination his pulse – 68/min, normal volume,regular ,BP 160/100 mm Hg,CVS – apex in 5th ICS left side,heaving ,S1 ,S2 normal an ESM 4/6 at right 2nd ICS heard.

• ECG- LV strain• ECHO – aortic valve calcified, valve area 1.0 cm2,AJV – 3.6m/sec ,

mean gradient 38 mm Hg, LVEF – 45%,grade I LVDD,conc LVH.

• What is the diagnosis?• What would be the next investigation in management of patient?• Finally will he be posted for surgery or not ,how, why?

• Severe Asymptomatic aortic stenosis with LV dysfunction(StageC2)

• Dobutamine stress echo• See for contractile reserve• Even if reserve absent ,Take him for surgery• Benefit is present.

Case 2 A 38 yr old male,labourer by occupation,k/c/o RHD on regular

penicillin prophylaxis was evaluated by echo on routine follow up.

• His echo showed thickened mitral valve,no MS.• Aortic valve tricuspid,thickened,calcified• Aortic valve area 0.9cm2 • AJV – 4.5m/sec,MPG – 81mmHg.• LVEF - 50%,grade I LVDD.

• What is the stage of VHD?• Plan of management?

• Asymptomatic severe AS (C1)• Exercise stress test• Look for symptoms,exercise tolerance• If present,decreased exercise tolerance • Take him for surgery.

Case 3

A 65 yr old male,hypertensive, having prostatic carcinoma been referred to cardiologist for evaluation of cardiac status.

• On evaluation ,he had aortic valve calcified,valve area 0.8cm2,AJV – 5.4m/sec, MPG – 116 mm Hg.

• LVH present.• LVEF -40%• Grade II LVDD

• What would be the plan of management?• Should he be posted for surgery or VHD corrected ?• If so ,why?

• He would have high surgical risk• He should be taken for TAVI.

Case 4 A 60 yr old male,hypertensive,diabetic,with diabetic

neuropathy culminating in lower limb loss was referred to cardiologist for evaluation of cardiac function.

• h/o CVA rt hemiparesis in the past.• Mitral annular calcification present• Aortic valve calcified,• AJV – 4.2 m/sec, mean gradient – 48 mm Hg, AVA -0.8 cm2,

• What would be the plan of management?

• He would not be benefited by surgery• Increased risk of mortality,morbidity as there are other

organ system compromise• Medical management

AORTIC REGURGITATION

Stage D AR

INDICATION CLASS RECOMMENDATION

ECHO I B Pts with symptoms of AR ,cause,severity,LV size , function, intervention timing.

I B In pts with dilated aortic sinuses,asc aorta for presence, severity of AR.

I B CMR - moderate to severe AR.

Medical therapy I B HTN (SBP > 140 mmHg) in pts with chronic AR ---- CCB,ACEI./ARBS

II a B Medical therapy with ACEI/ARBs ,BB in pts with LVD when surgery not performed.

Vasodilator therapy in AR• Effective in reducing SBP in patients with chronic AR.• Improve hemodynamic abnormalities,forward flow.

Donot alter the natural h/o of asymptomatic pts with chronic severe AR and normal LV function..

DRUG REFERENCE

Nifedipine Fioretti et al.,Am J Cardiol;1982:49:1728-32

Felodipine Sondergard L et al .,Am Heart Journal 2000;139:667-74

Enalapril vs Hydralazine J Am Coll Cardiol.1994:24:1046-53

Hydralazine Circulation.1980:62:48-55

Nifedipine JACC,1984;4;902-7.

Nifedipine vs Captopril JACC 1993

VASODILATOR THERAPY

REGURGITANT LESIONS

CHRONIC

AORTIC REGURGITATION

Treatment of hypertension (SBP>140

mmHg ) for chronic stage (Band C)with

CCBs /ACEI/ARBs

CLASS I B

Medical therapy with ACEI/ARBs in pts with severe AR and

LV dysfunction when surgery is not

performed because of comorbidities

CLASS II a B

MITRAL

Vasodilator therapy is useful to improve

hemodynamic compensation in Acute

MR

Vasodilator therapy in symptomatic pts with chronic primary MR

LVEF< 60%,in whom surgery is not preferred

Class II aB

C/ I in

asymptomatic

patients

STENOTIC LESIONS

AORTIC STENOSIS

Reasonable if used with hemodynamic monittoring in acute management of pts with severe decompensated

AS (Stage D)NYHA CLASS IV symtpoms

II b C

BICUSPID AORTIC VALVE

INDICATION CLASS RECOMMENDATION

ECHO I B Pts with bicuspid AV ,to know severity of AS/AR,shape , diameter of aortic sinuses, ascending aorta.

MRI/CT angio I B MRI,CT angio when the above cannot be assessed by echocardiography.

I B Serial evaluation is needed in BAV, aortic diameter >4.0 cm ,frequency determined by progression of dilation(annually if >4.5 cm).

Medical therapy

No proven therapies.(previously B Blockers,ARBs)

Intervention I B If diameter of aortic sinuses or Asc aorta >5.5 cm.

II a B If diameter of aortic sinuses or asc. Aorta >5.0 cm,risk for dissection present (family h/o)rate being 0.5cm/year.

IIa B Replacement of Asc aorta if pts having severe AS/AR when Asc aorta >4.5 cm

N

• Incidence of aortic dilation is higher in patients with fusion of

right or left and the non coronary cusps than the more common

phenotype of fusion of the right and left non coronary cusps.

(68% vs 40% ).

• Report of a patient with BAV – aortic measurements at the aortic

annulus,sinuses,sinotubular junction and mid –ascending aorta.

• Aortic diameters by MRI/CT typically are 1 mm to 2mm larger

than by 2d echo – inclusion of aortic wall in measurement.

• 20-30% of pts with BAV ,other family members also have

bicuspid aortic valve /aortopathy –specific gene not been

identified, patterns of inheritance variable.

• Mean rate of diameter progression was 0.5 mm/yr at the sinuses of

valsalva,0.5 mm/yr at the sinotubular junction,0.9 mm/yr at the

proximal ascending aorta.

• Previous guidelines recommended surgery when diameter >5.0cm at

any level.

• Surgery is recommended presently if diameter is 5.1-5.5 cm only if

there is a family h/o aortic dissection or rapid progression of

dilation(>0.5cm/yr). (in all others >5.5 cm).

• Does not recommend the application of formulas to adjust diameter

to body size.

• Replacement of sinuses of valsalva when considering asc aorta

replacement, is not necessary in all cases (pts with BAV and AS/AR).

Bicuspid Aortic Valve M Mode Echo

NORMAL – 1.0 -1.5BAV – 1.5-5.6

MITRAL STENOSIS

INDICATION CLASS RECOMMENDATION

ECHO I B Diagnosis, quantify hemodynamic severity , assess concomitant valvular lesions, and demonstrate valve morphology.

I B Assess the presence or absence of left atrial thrombus and to further evaluate the severity of MR.

I C Evaluate the response of the mean mitral gradient and pulmonary artery pressure in patients with MS when there is a discrepancy between resting Doppler echocardiographic findings and clinical symptoms or signs.

Medical therapy

I B Anticoagulation MS with AF,MS with prior embolic event .,MS and left atrial thrombus

II a C Heart rate control can be beneficial in patients with MS and AF and fast ventricular response.

II b B Heart rate control may be considered for patients with MS in normal sinus rhythm and symptoms associated with exercise

• Definition of severe MS is based on the severity at which

symptoms occur as well as the severity at which intervention will

improve symptoms.(MVA <1.5cm2 is considered severe).

• Transmitral gradient of >5-10 mm Hg at normal heart rate.

• DPHT is dependent not only on mitral obstruction,also on

compliance of LA,LV.

• Doppler hemodynamics (apical 4 C view)- peak and mean TVG

–averaged from 3-5 beats in SR,5-10 in AF.

• Heart rate should always to be included in the report.

• RVSP >60-70mm Hg on exercise.

• 30-40% pts with MS will develop AF.

• A reduction in the diastolic interval from 604 milliseconds to

219 msec as heart rate increased from 60-120 bpm,indicating a

63% reduction in total diastolic time.for maintaining same

cardiac output a 38% increase in mean flow rate during

diastole ,which by bernoulli equation ,requires an increase in

mean mitral gradient by 90%.

• Moderate to severe MS – 0.09cm2/yr.

•

Congenital MS

• Usually takes the form of a parachute mitral valve(mitral chordae are attached to a single or dominant papillary muscle

Form a component of shone complex

Includes• Supramitral rings• Valvular or subvalvular AS• Aortic coarctation

MITRAL REGURGITATION

MITRAL REGURGITATION

PRIMARY

ACUTE CHRONIC

SECONDARY

CHRONIC

Why does murmur of acute MR not holosystolic

• The rapid systolic rise in LA pressure with a concomitant fall in LV systolic pressure limits the pressure gradient driving MR to early systole. – short and unimpressive MR.

• Torrential MR – no murmur – rapid equalisation of LA and LV pressures.

• Vasodilator therapy • IABP –by lowering systolic aortic pressure,decreases LV

afterload,increases forward output• Increases diastolic mean aortic pressure –systemic circulation• Chordae tendinae –repair

TTE I B LV size and function, RV function and left atrial size,PAP, severity of primary MR (stages A to D)

CMR I B Assess LV and RV volumes, function, or MR severity when not satisfactorily addressed by TTE

TEE I B Establish the anatomic basis for chronic primary MR (stages Cand D) and to guide repair

I C When noninvasive imaging provides nondiagnostic information about severity of MR, mechanism of MR, and/or status of LV function.

EST II a B

Exercise hemodynamics reasonable in symptomatic patients with chronic primary MR ,in discrepancy between symptoms and the severity of MR at rest

II a C

Exercise treadmill testing can be useful in patients with chronic primary MR to establish symptom status and exercise tolerance

RX II a B

Medical therapy for systolic dysfunction is reasonable in symptomatic patients with chronic primary MR (stage D) and LVEF less than 60% in whom surgery is not contemplated.

III B Vasodilator therapy is not indicated for normotensive asymptomatic patients with chronic primary MR (stages B and C1) and normal systolic LV function

Mitra clip

MITRACLIP VIDEO

Described by Alfieri Originally for MR with MVPEVEREST II trial

TRICUSPID VALVE DISEASE

TTE I C

PAP ,PVR invasive I C

CMR ,3D echo IIb C

Exercise testing IIb C

diuretics IIa C

Reduce PAP (functional TR) IIb C

CLASS RECOMMENDATION

TTE I C Assess the anatomy,evaluate severity,associated regurgitation,left sided valve disease

Invasive hemodynamics

II b C Symptoms and noninvasive data are discordant

Medical therapy Loop diruetics

Intervention I C Severe TS at the time of operation for left sided valve disease

I C Isolated symptomatic severeTS

II b C PBTV in absence of TR

PULMONIC VALVE DISEASE

• ..\Documents\Transcutaneous Pulmonary Valve implantation.mp4

PROSTHETIC VALVE DISEASE

CLASS RECOMMENDATIONS

TTE I B Evaluation of valve hemodynamics after implantation(6 weeks to 3 months)

Repeat TTE I C change in symptoms

TEE I C Prosthetic valve dysfuncton(accurate for mitral valve dysfunction)

Annual TTE II a C Bioprosthetic valves after the first 10 years

PROSTHETIC VALVE DYSFUNCTION

BIOPROSTHETIC VALVE

DYSFUNCTION

INSIDIOUS ONSET

Exterional dyspnea,

Louder systolic murmur

New diastolic murmur

ABRUPT ONSET

Valve endocarditis

Degenerative rupture of a valve cusp

MECHANICAL VALVE

DYSFUNCTION

Present with HF symptoms

Systemic thromboembolism

Hemolysis

Often acute/subacute

Acute or chronic paravalvular

regurgitation –IE,suture

dehiscence

Earlier evaluation may be prudent in selected patients at risk of early bioprosthetic valve degeneration –

• Renal impairement• Diabetes mellitus• Abnormal calcium metabolism• Systemic inflammatory disease• Patients <60 yrs of age.

• Patients are usually asymptomatic until valve dysfunction is severe.

Rahimtoola et al,J Am Coll Cardiol.2010;55:2413-26

Kappetein et al,J Thorac Cardiovasc Surg,2009;137:881-5

IIa C

65 yrs

• Patient – prosthetic mismatch. • Aortic annular enlarging procedures.• Risk of need for reoperation with a bioprosthetic valve is

inversely related to the patient’s age at the time of implantation.

20 yrs of age at the time of implantation

70 yrs of age at time of implantation

90%

10%

Rate of structural deterioration 15-20 yrs after implantation

Pibarot et al,Circulation 2009;119:1034-48Pibarot et al,Circulation2006;92:1022-29

Bioprosthetic valve vs Mechanical valve

• Prospective randomized study , 1977 and 1982• 575 pts • Older generation mechanical vs bioprosthetic valve

replacement (Bjork-Shiley spherical disc mechanical prosthesis or a Hancock porcine bioprosthetic valve).

• Overall survival was similar at 15 yrs in both groups.PRIMARY

VALVE FAILURE

BIOPROSTHETIC VALVE

MECHANICAL VALVE

P VALUE

AGE <65 yrs

AVR 26% 0% 0.0001

MVR 44% 4 %

VETERANS AFFAIRS randomized trial. J Am Coll Cardiol2000;36:1152-8.

50 yrs40 yrs

30 yrs20 yrs

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

40%

55%

75%

90%

structural deterioration and reoperation

Age at the time of implantation and primary structural deterioration in

BIOPROSTHETIC VALVE IMPLANTATION

RahimtoolaSH et al ,J Am Coll Cardiol .2010;55:2413-26

Edinburgh Heart Valve Study

• Outcomes are similar with implantation of either a bioprosthetic or mechanical valve for patients between 60 -70 yrs of age.

• 533 pts • Mean age 54.4 +/-10.4 yrs.• Bjork Shiley mechanical prosthesis or a porcine prosthesis• No difference in long term survival(p=0.39)

Wheatley DJ et al,Heart 2003;89:715-21

Italian study

• 310 pts• 55-70 yrs of age • No difference in overall survival at 13 yrs • Thromboembolism,bleeding,IE,and major adverse prosthesis

related events were no different between the two valve types.

• Valve failures (p= 0.0001) ,reoperations were more frequent in the bioprosthetic group (p=0.0003)

Banbury MK,et al Long-term results of the Carpentier-Edwards pericardial aortic valvee: a 12 year follow-up. Ann Thorac Surg 1998;66Suppl:73– 6.

Society for Cardiothoracic Surgery in the Great Britain and Ireland

National Database

• 2004-2009,Bioprosthesis at the time of valve replacement• 41,227 pts

60-65 yrs 65-70 yrs >70 yrs0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

37%

62%

87%

55%

78%

96%

initialfinal

Dunning et al,J Thorac Cardiovascular Surg 2011;142:776-82

Ross procedure

Replacement of the aortic valve with a pulmonary autograft,

Replacing the pulmonary valve with a homograft.• Requires an experienced surgical team

Failure is most often due to regurgitation of the pulmonary autograft (the neoaortic valve ) in the second decade after the operation.

• Regurgitation is typically due to• leaflet prolapse ( if implanted in the subcoronary position )• Aortic sinus dilation (if implanted starting at the aortic sinuses)

• Placing the pulmonary valve within a dacron conduit.• Neoaortic valve in subcoronary position with a reinforced native

aorta.

ANTITHROMBOTIC THERAPY FOR PROSTHETIC VALVES

Anticoagulation with a VKA and INR monitoring is recommended in pts with a mechanical prosthetic valve

CLASS I A

Anticoagulation with VKA to achieve INR 2.5 is recommended in mechanical AVR ,no riskfactors for thromboembolism

CLASS I B

VKA ,INR -3.0 in pts with mechanical AVR ,additional risk factors for thromboembolism,older generation mechanical AVR

CLASS I B

VKA,INR -3.0 in mitral mechanical valve pts CLASS I B

Aspirin 75-100 mg in addition to VKA in mechanical prosthesis pts CLASS I A

Aspirin 75-100 mg in all pts with bioprosthetic aortic or mitral valve CLASS II a B

Anticoagulation with VKA – INR 2.5 reasonable in bioprosthetic MVR or repair ,first 3 months

CLASS II a C

Anticoagulation with VKA – INR 2.5 reasonable after bioprosthetic AVR

CLASS II b B

Clopidogrel 75 mg daily may be reasonable for first 6 months after TAVR in addition to life long aspirin 75-100mg daily

CLASS II b C

Anticoagulation with oral direct thrombin inhibitors or anti Xa agents should not be used in mechanical prosthesis patients

CLASS IIIHARMIII HARM

B

Strive to attain the single INR value.

• It is preferable to specify a single INR target in each patient,

recognizing that the acceptable range is 0.5 INR units on each

side of this target, this is preferable because it avoids patients

having INR values consistently near the upper or lower edge of

the range.

• Fluctuations in INR are assosciated with increased incidence of

complications in pts with prosthetic valves.

Mechanical valves

Thrombogenecity of prosthetic material

intravascularly

Zones of low flow

Platelet activation

Areas of high shear stress

Effects of mechanical valve

Valve thrombosisEmbolic events

• Rate of thromboembolism in patients with bileaflet mechanical AVR on VKA and antiplatelet regimen in 0.53% per patient year over the INR range of 2.0 -4.5.

LOWERING –IT trial ,Am H J 2010;160:171-8

Adverse events increased if INR was >4.0.• New generation AVR ,without other risk factors for thromboembolism

, risk of thromboembolism was similar,

risk of hemorrhage is lower in group with an INR of 2.0 -3.0 vs INR 3.0- 4.5(p<0.01) Chest 2005;127:53-9.

• INR 1.5-2.5 vs INR 2.0 -3.0 – noninferior ,quality of evidence was low.

AREVA trial ,Circulation,1996;94:2107-12

• Preferred INR is 2.5 – bileaflet and single tilting disc in aortic position (low thromboembolic risk pts)

Preferred target INR

CONDITION INR RANGE

AVR bileaflet ,current generation single tilting disc (Medtronic hall)

2.5 2.0 -3.0

Additional risk factors for thromboembolism (AF,LVD,prev.TE,hypercoagulability)

3.0 2.5-3.5

Ball in cage valve (Starr Edwards valve) 3.0 2.5-3.5

MVR All types of mechanical valves 3.0 2.5-3.5

GELIA trial

G erman Experience with Low Intensity Anticoagulation • Mechanical mitral prosthesis (St Jude Medical valve)• Low INR (2.0 -3.5) was assosciated with lower survival rates

than a higher target INR range (2.5-4.5) in those with a mechanical valve.

• Patient compliance is challenging with higher INR goals

INR WITHIN RANGE

2.0 -3.5 74.5%

3.0 -4.5 44.5%

CHEST ,2005:127:53-9.

Role of Aspirin• Aspirin is recommended in all patients with prosthetic heart

valves (incl. mechanical valves with VKA therapy)• Risk of thromboembolism with VKA – 1 -2%/yr.

EVENTS VKA VKA plus aspirin p value

Major embolism/death

8.5% 1.9% < 0.001

Stroke rate 4.2% 1.3% <0.027

Overall mortality 7.4% 2.8% <0.01

Risk of minor bleeding (epistaxis,bruising)

increased

Major bleeding 6.6% 8.5% 0.43

LIWACAP study ,Clin Appl Thrombo hemostst 2007;13:241-8.

The risk of GI irritation and hemorrhage with Aspirin

is

dose dependent over the range of 100mg-1,000 mg /day,

but the antiplatelet effects

are

independent of dose over this range.

LIWACAP study;Clin Appl Thromb Hemost.2007;13:241-8

• Risk of clinical thromboembolism –average 0.7%/yr in pts with biological valves in sinus rhythm.

• Mitral > Aortic (2.4% vs 1.9%)

• St JUDE MEDICAL EPIC heart valve bioprosthesis(AVR)• Incidence of thromboembolic events,bleeding,death was

similar between those who received aspirin or warfarin.

• No studies examining the long term effects of antiplatelet agents in patients with bioprosthetic MVR or mitral valve repair.

WoA epic pilot trial.J Heart Valve Disease 2007;16:667-71

Risk of stroke after all types of mitral valve surgery

30 days 180 days 5 years0%

1%

2%

3%

4%

5%

6%

7%

8%

9%

2%

3%

8%

% stroke

Eur J Thoracic Surg1995;615-9

Risk of ischemic strokeSurgery Within 30 days at 5 yrs P value

Mitral valve repair 1.5% 6.1% 0.9% <0.0001

Bioprosthetic 4.6% 8.0% 2.1%

Mechanical 1.3% 16.1%2.7% <0.001

Anticoagulation with a VKA in bioprosthetic AVR

Anticoagulation with an INR target of 2.5 may be reasonable for atleast 3 months and perhaps as long as 6 months after bioprosthetic AVR

Not treated with VKA Treated with VKA

Strokes per 100 person years

7.00 2.69

CV event rate at 6 months

6.50 2.08

Antiplatelet therapy after TAVR

• Small prospective RCT• Single center study• 79 pts with self expanding TAVR

Clopidogrel +Aspirin

Aspirin P value

Events at 30 days 13% 15% 0.71

6 months 18% 15% 0.85

RE ALIGN trial

• Randomized ,Phase II Study to Evaluate the Safety and Pharmacokinetics of Oral Dabigatran Etexilate in Patients after Heart Valve Replacement

• Stopped prematurely for excessive thrombotic complications in dabigatran arm.

• 252 pts

DABIGATRAN WARFARIN

Ischemic stroke 9 pts (5%) nil

Composite end point of stroke,TIA,systemic embolism,MI

15 pts (9%) 4 pts (5%)

Major bleeding episode 7 pts( 4%) 2 pts (2%)

Bleeding of any type 45 pts (27%) 10 pts (12%)

Am Heart J,2012;163:931-7.

Bridging therapy for prosthetic valves Medical therapy

VKA anticoagulation with INR in range in pts with mechanical valves.

I C Minor procedures (dental extractions ,cataract surgery,surgeries on skin,dental caries)

Temporary interruption in VKA anticoagulation,INR being subtherapeutic,without bridging in bileaflet mechanical AVR

I C Invasive or surgical procedureINR <1.5 (stop warfarin 2-4 days before procedure)

Bridging anticoagulationMechanical AVR + thrombotic risk factor, older generation AVR, tricuspid valve,mechanical MVR

I C Invasive or surgical procedure

FFP or IV prothrombin complex

II a C Emergency noncardiac surgery

BRIDGING THERAPY

• Usually UFH ,or SC LMWH used• Stop warfarin 2-4 days before surgery (INR<1.5),start 24

hrs after surgery.• Start IV UFH (48 hrs before surgery )and stopped 4-6 hrs

(IVUFH)or 12 hrs (for SC LMWH )before the procedure.

• For procedures with a low bleeding risk,such as coronary

angiography from the radial approach,only slight

modification in VKA dosing is needed.

• With interventional procedures at higher risk,many prefer to

stop VKA anticoagulation and use bridging therapy as is

done for other surgical procedures.

ACCP ,Evidence based guidelines for thrombotic management,CHEST april 2012

Excessive anticoagualtion and serious bleeding

• INR >5.0 –risk of hemorrhage.• Rapid decrease in INR below therapuetic range – risk of

thromboembolism.• High dose vitamin K not given routinely,creates a

hypercoagulable condition.• 5-10 INR ,withold VKA,serial INR• INR>10 ,not bleeding – 1-2.5 mg oral vitamin K1

(phytonadione) in addition to witholding VKA therapy.• Emergency conditions –FFP,prothrombin complex –

CLASS IIaB

THROMBOEMBOLIC EVENTS

• Mechanical valve 1-2%• Bioprosthetic valve 0.7%• Embolic events do occur even when in therapeutic range.• AVR 2.5• AVR+RISK FACTORS

(AF,previous TE, hypercoagulable condition ,older gen ,LVSD,

>1 mechanical valve ) 3.0• MVR 3.0

• Time in therapuetic range is only 60-70%• Increase INR 2.53.0 in AVR,

3.0 4.0 in MVR

Management

• Optimal anticoagulation

• Antiplatelet therapy.

• Improve patient compliance

• Surgical intervention is rarely needed.

• Replacement of prosthetic valve –

stenosed/regurgitation/degenerated.

PROSTHETIC VALVE THROMBOSIS

• Mechanical PVT – prevalence is 0.3% to 1.3% per pt yr in developed

countries.

• 6.1% per patient year in developing countries.

• TEE more sensitive for detection of valve thrombosis, mitral valve.

• Prior history of stroke,thrombosis area by TEE are independent

predictors of complications after thrombolysis.

• A thrombus area <0.8cm2 – lower risk of complications from

thrombolysis irrespective of NYHA classification.

• Fluoroscopy,CT imaging for prosthetic aortic valves.

RECOMMENDATIONS

CLASS II a B Fibrinolytic therapy is reasonable for patients with a thrombosed left sided prosthetic heart valve ,recent onset (<14 days) of NYHA class I –II symptoms and a small thrombus <0.8cm2

CLASS II a B Fibrinolytic therapy is reasonable for right sided prosthetic heart valves

CLASS I B Emergency surgery is recommended in pts with a thrombosed left sided prosthetic heart valve with NYHA III-IV symptoms

CLASS IIa B Emergency surgery is reasonable for patients with a thrombosed left sided prosthetic heart valve with a mobile or large thrombus >0.8cm2

Factors that predict adverse outcomes from fibrinolytic therapy

• Active internal bleeding• History of hemorrhagic stroke• Recent cranial trauma/neoplasm• Diabetic hemorrhagic retinopathy• Large thrombi• Mobile thrombi• Systemic hypertension (>200/120 mm Hg)• Hypotension/shock• NYHA III/IV

• Fibrinolytic therapy of a left sided obstructed prosthetic valve is

assosciated with an overall rate of thromboembolism and

bleeding of 17.8%,the degree of risk is directly proportional

to thrombus size.

• A mobile thrombus or a length of >5 -10 mm – increased

embolic risk.

• >1.0 cm or 0.8cm2 area – 2.4 fold increase in embolism risk per

1.0cm2 increase in size.

Fibrinolytic agent

rTPA 10 mg IV bolus – 90 mg infused IV over 2 hours.Heparin,GPIIb/IIIa held,aspirin continued

20 mg IV bolus – 10 mg per hour for 3 hours

STREPTOKINASE 5,00,000 IU in 20 minutes – 15,00,000 IU over 10 hours.i.e.,1,50,000 U/hr

UROKINASE Less effective

If fibrinolytic therapy is successful ,it is followed by IV UFH

until VKA achieves an INR of 3.0 -4.0 for aortic prosthetic

valves and 3.5-4.5 for mitral prosthetic valves

J Am Coll Cardiol 1997;30:1521-6

Surgery vs fibrinolytic therapy in patients with left sided PHVT

• Success rate - 90% with surgery.

70%.-fibrinolytic therapy

No difference in mortality between two groups.

SURGERY FIBRINOLYTIC THERAPY

THROMBOEMBOLISM 1.6% 16%

MAJOR BLEEDING 1.4% 5%

RECURRENT PVT 7.1% 25.4%

RESTORING NORMAL VALVE FUNCTION

90% 70%

Karthikeyan et al,Eur Heart Journal,2013:34:1557-66

• Mortality rate was 17.6% pts with NYHA class IV, 4.7% in pts with NYHA class I –III.

• Mortality was similar for removing the thrombus or replacing the entire prosthetic valve.

• In pts with recent hemorrhagic stroke,surgery is a better option.

Guidelines for management of left sided prosthetic valve thrombosis,JACC,1997;30:1521-6

PROSTHETIC VALVE STENOSIS

• Mechanical valve - chronic thrombus or pannus• Bioprosthetic valve ----- leaflet fibrosis ,calcification• Patient –prosthesis mismatch – prosthesis functions normally.

Indexed effective orifice area <0.85cm2 for AV prosthesis.

Severe patient –prosthesis mismatch - <0.65cm2/m2

Detrimental in pts with low LVEF.

Can be avoided by adequate indexed orifice area (pts body size,annular dimension)

• No medical therapy for prevention• Valve in valve approach.(not fully validated)• For mechanical valve – consider bioprosthetic valve at reoperation,if

noncompliant is the cause

PROSTHETIC VALVE REGURGITATION

• TEE –clear images of the LA side of mitral prosthesis,delineation,severity of paravalvular MR.

• No medical therapies.• Intractable hemolysis or HF due to severe mechanical

Prosthetic/paraprosthetic valve regurgitation - surgery indicated (I B)

• Severe symptomatic or asymptomatic bioprosthetic regurgitation – (II a C)

• Catheter based approaches in high risk for surgery -II a B

Success -80-85%

Complications -9%

Procedural death <2%

INFECTIVE ENDOCARDITIS

• In hospital mortality rate - 15-20%

• 1 yr mortality rate - 40%

• Overall incidence of IE – 3-10/100,000 pt –yrs

• Higher prevalence in older patients.

• IE associated with prosthetic,intracardiac – 50 times more

compared to general population.

Class I C At least 2 sets of blood culture should be obtained in patients at risk of IE ,who have unexplained fever for more than 48 hours,pts with a new diagnosis of left sided valve regurgitation

Class I B Modified duke criteria for evaluation of pt with suspected IE.

Class I B Intraoperative TEE in pts undergoing valve surgery for IE

Class II a B TEE to diagnose IE in pts with Staph.aureus bacteremia without a known source.

Class II a B TEE in pts with prosthetic valve ,fever ,no murmur,no bacteremia

Class II a B Cardiac CT when echo not conclusive

Class II a B Temporarily discontinue anticoagulation in pts with IE who develop CNS compatible with embolism/stroke regardless of indications for anticoagulation

Class I B Early surgery in pts with HF

Class I B Early surgery n left sided IE by S.aureus,fungal

Class I B Early surgery if there is heart block,annular or aortic abscess

Class IB Early surgery if persistent fever >5-7 days despite antibiotics

• In patients with chronic (subacute ) – 3 sets of blood culture.

• Blood cultures are positive 90% of pts with IE.• 10% - serology.• 3/4ths of pts with IE are diagnosed within 30 days of onset

of infection- classic features are absent.

In hospital mortality 15-20%

1 yr mortality rate 40%

Stroke 16.9%

Embolization other than stroke 22.6%

HF 32.3%

Intracardiac abscess 14.4%

Need for surgical therapy 48.2%

Arch Internal Med2009;169:463-73.

NVE PVE

TTE sensitivity 50-90% 36-69%

specificity >90%

TEE sensitivity 90-100% lower

specificity

PPV 90% 90%

TTE TEE

1.Anterior aspect of a prosthetic aortic valve

2.Aortic transvalvular gradient

3.Vegetations and perivalvular complications

4.Active and healed vegetations

5.Thickened valves or valvular nodules and vegetations

differentiation

Most vegetations 83.8% remain constant in size under therapy and this does not worsen prognosis

Right sided pacemaker leads IE – intracardiac echo

S.Aureus

bacteremia

Neurological complications

30%

Paravalvular cardiac abscesses

30-40%

HF

20-50%Mortality 19%-65%

Systemic embolization

40%

• PVE – less incidence of vegetations(mechanical) ,higher incidence of annular abscess and other paravalvular complications.

• 15-35% of all pts with IE develop clinically evident emboli.(CMR - >30%)

• MC cause of stroke in pts with IE – septic embolus resulting in ischemia –with hemorrhagic transformation later -11 days later also.

• Death may occur suddenly in pts with endocarditis induced HF ,if aortic valve is involved.

ICE –PCS IE pts with HF Rx with surgery Medical Rx

inhospital mortality 21% 45%

1 yr mortality 29.1% 58.4%

In complicated left heart NVE -4 baseline featureshave been independently assosciated with 6 month mortalityAbnormal mental statusModerate –to severe HF Bacterial etiology other than viridansMedical therapy alone

Reinfection is more common in injectable drug users (5-10% pts)Repair better than replacement

PVEEARLY <60 days of surgery Health care acquired

infection - S. aureus

INTERMEDIATE 60-365 days after surgery Health care +community acquired – coagulase

negative staphylococcus

2/3 cases of PVE

LATE >1 yr after surgery Resembles NVE

INJECTABLE DRUG USERS MORTALITY

Staphylococcus <5% *right sided 20-30%*left sided

Enterococcus 15-25%

Pseudomonas aeruginosa

Enterobacteriaciae >50%

Embolism

• 20-40% pts with IE.

• Incidence decreases to 9-21% on antibiotic use

• New embolic event occurs if vegetation >10 mm,anterior mitral

leaflet vegetations.

• Risk of embolism is highest during the first days after initiation

of antibiotic treatment and decreases after 2 weeks.

• Surgical intervention is needed in case of staphylococcal PVE.

PREGNANCY AND

VALVULAR HEART DISEASE

NATIVE VALVE STENOSIS

Medical therapy I C MS WITH AF

II a C Bblockers for rate control in AF(metoprolol)

II b C Diuretics in MS and HF

III ACEI/ARBS not to be given in pts with valve stenosis

Intervention I C Before pregnancy ,Severe symptomatic AS

I C Before pregnancy ,Severe symptomatic MS

I C

IIa B

Before pregnancy ,PBMV in asymptomatic severe MS.

For pregnant pts ,with MS ,in HF despite medical therapy

II a C Before pregnancy ,Severe asymptomatic AS

III Valve operation in absence of HF symptoms

AORTIC STENOSIS MITRAL STENOSIS

MATERNAL MORTALITY RATE

17% uncommon

FETAL,NEONATAL MORTALITY RATE

32% 30%

HF 10-44% 75%

Risk of arrhythmia 25% 75%

increased incidence of HTN emergencies

Valve operation 30-40% fetal mortalityMaternal -9%No ideal time

High pump flows and normothermic perfusion

NATIVE VALVE REGURGITATION

• Symptomatic pts - High risk of HF during pregnancy• Valve repair is ideal.• Threshold to be higher

CLASS I C Valve repair or replacement before pregnancy for symptomatic women with severe valvular regurgitation

CLASS II a C Valve operation for pregnant with severe valvular regurgitation only if there are refractory NYHA class IV HF symptoms

CLASS IIb C Valve repair Before pregnancy may be considered in asymptomatic pts with severe MR

CLASS III Not to be performed in pregnancy in absence of HF symtpoms (NYHA CLASS III/IV)

• Risk of embryopathy is dose dependent • <3% - <5 mg/day• >8% - >5mg/day

CONCOMITANT PROCEDURES

INTERVENTION FOR AF

Class II a C A concomitant MAZE procedure at time of MV repair/replacement for Rx of chronic persistent AF.

Class II a B A full biatrial MAZE procedure

Class II b C Concomitant maze or pulmonary vein isolation in patients with paroxsymal AF with h/o embolism on anticoagulation

Class II b C Concomitant maze or pulmonary vein isolation at time of other cardiac surgeries with paroxysmal AF

Class III Catheter ablation in pts with severe MR in place of combined maze procedure plus mitral repair.

MAZE PROCEDURE

MAZE I - initial incisons deep into the atrial wall,open sternotomy,CP bypass

MAZE II -

MAZE III – cut and sew (1992)

MAZE IV – cryoablative /radiofrequency

"Maze" refers to the series of incisions arranged in a maze -like pattern in the atria. Today, various methods of minimally invasive maze procedures, collectively named mini maze procedures, are used.James Cox in 1987.Mini mazeWolf maze

Non cardiac surgery in HVD• Rate of cardiac complications in undiagnosed severe AS

undergoing noncardiac surgery is 10-30%.• 30 day mortality high for pts with AS 2.1%• HIGH risk of post operative MI in AS pts.• Tachycardia to be avoided in AS. DC shock for conversiob in

acute setting.• CCB s for HTN• Phenylephrine is useful.• High dilution neuraxial local anaesthetic • MS – IV fluids cautious• Regional anaesthesia in AR/MR• Preload to be maintained• 48-72 hrs post op

CLASS IIa B Moderate risk elective noncardiac surgery, asymptomatic severe AS.

CLASS II a C Moderate risk elective noncardiac surgery, asymptomatic severeMR

CLASS II a C Moderate risk elective non cardiac surgery asymtpomatic sevvere AR,normal LVEF

CLASS II b C Moderate risk in pts with asymptomatic severe MS ,not favourable for PBMV

EVIDENCE GAPS AND FUTURE DIRECTIONS

• Vaccine development• At risk of calcific aortic stenosis – therapies to prevent

progression.• Values of measures of LV size,volumes,myocardial structure

immediately after intervention.• TAVI