2Objectives Types of prostheses Prosthetic dysfunction Echocardiographic surveillance of prostheses
3Types of Prostheses Mechanical valves Tissue valves Homograft valves Major differences related to risk of thromboembolism (higher for mechanical) and risk of deterioration (higher for bioprosthetic).Durability of mechanical valves unsurpassed but inherent risks of thromboembolismBioprostheses developed primarily to overcome the risk of thromboembolism and inconvenience of anticoagulation therapy. Major drawback is durability.
4Mechanical ValvesA, The Starr-Edwards caged-ball valve. B, The Omniscience valve. C, The Medtronic-Hall valve. D, The St. Jude bileaflet valve. E, The CarboMedics bileaflet valve.3 main categories: tilting disk, bileaflet, and ball-cageTilting disk - opens at an angle to the annulus plane, constrained by a strut, cage or slanted slotBileaflet: 2 semicircular disks that form 2 large lateral openings and a smaller central openingSt. Jude’s: 1. Does not require supporting struts and 2. has favorable flow characteristics ->causes lower transvalvular pressure gradient at any outer diameter and cardiac output than caged-ball or tilting disc valves. Therefore favorable hemodynamics in smaller sizes; ideal for children.
5Tissue Valves-3 biologic leaflets and similar anatomic structure to native aortic valveStented valve leaflets are usually porcine or bovine/equine pericardium mounted on rigid cloth support with stent at each commissureStentless valves use flexible fabric or tissue cuff, often attached to aortic root graft
6Homograft ValvesAortic or pulmonic cadaver valve -> preserved, treated with antibiotics and frozenUsually the valve and great vessel preserved as a block; ideal when there is also aortic root pathology
7Objectives Types of prostheses Prosthetic dysfunction Echocardiographic surveillance of prostheses
8Mechanisms of Prosthetic Valve Dysfunction Structural failureStenosisRegurgitationThromboembolic complicationsEndocarditisPatient Prosthesis MismatchStructural failure = failure of a prosthetic valve to open or close properly
9Structural Failure Bioprosthetics Structural failure result from progressive tissue degeneration. Fibrocalcific changes to leaflets -> 1. increased resistance to opening (stenosis) or failure to coapt (regurgitation)Usually occurs 10 or more years after implantation; acute stenosis rare. Acute regurgitation can occur with a leaflet tear; often adjacent to an area of calcificationA – valve failure secondary to mineralization and collagen degenerationB – Cuspal tears and perforationsStructural failure of current generation mechanical valves is rare; valve stenosis or regurgitation often due to thrombus or pannus ingrowth.
10Cohn et al. Ann Thorac Surg, 1998. Estimates of freedom from structural valve deterioration (SVD) stratified by age.Porcine AVRBovine pericardial AVRThe rate of structural valve failure is age-dependent, and is significantly lower in patients older than 65 years (Fig A Braunwald).In patients over 65 undergoing AVR with a porcine bioprosthesis, the rate of structural deterioration is less than 10 percent at 10 years.Valve failure is prohibitively rapid in children and in adults under 35 to 40 years of age; bioprostheses are avoided unless circumstances dictate.Cohn et al.Ann Thorac Surg,1998.
11Homograft Dysfunction Subject to severe tissue calcificationUsually reserved for complex aortic root abscessesHyperlipidemia accelerates prosthesis calcificationSecondary prevention may slow this processSimilar progressive deterioration as tissue valves.Nollert G, Miksch J, Kreuzer E, et al: Risk factors for atherosclerosis and the degeneration of pericardial valves after aortic valve replacement. J Thorac Cardiovasc Surg 2003; 126:965.Farivar RS, Cohn LS: Hypercholesterolemia is a risk factor for bioprosthetic valve calcification and explantation. J Thorac Cardiovasc Surg 2003; 126:969.
12Physical Exam Findings Subtle findings especially if no baseline PE. Requires high suspicion for PV malfunction.
13Echocardiographic Evaluation TTEvalve area and regurgitationexclude significant obstructionFlow velocity is crucial measurementOften inadequate for infection or small structural changes (strut fracture, small vegetation, paravalvular leak)TEEinspection of valve apparatus and seatingmay not accurately quantify valve flow velocitiesMajor challenges:1. Distinguish normal from pathologic fluid dynamics of prosthetic valve2. Acoustic shadowing from sewing rings of bioprosthetic and mechanical -> shadow and reverberations that obscure motion of valve structures and block Doppler signalTEE particularly useful for mitral valves b/c allows visualization from the LA side of valveTEE also reliably distinguishes transprosthetic from paraprosthetic regurgitation.TEE less helpful for aortic valves b/c posterior portion sewing ring shadows valve leaflets
14Normal Appearance PVLeft: TTE PSL of bileaflet mechanical aortic valve; leaflets obscured by shadowing from sewing ringRight: TEE bileaflet mechanical mitral valve a) diastole – sewing ring and 2 open leaflets; b) systole shadowing from sewing ring and reverb from leaflets obscures LV side of valve
15Normal Doppler ClicksNormal motion of mechanical occluder or bioprosthetic leaflets creates a Doppler signal.Analogous to auscultatory click except both opening and closing create Doppler signal.
16Normal Doppler Flow Patterns PSL view of stented mitral bioprosthetic valve.Left: stents protrude into ventricular chamberRight: antegrade flow into LVBioprosthetics have flow profile similar to native Ao valve with 3 leaflets and a central orifice -> provides laminar antegrade flow with a blunt flow profileIn the mitral position, orientation of bioprosthesis results in anteromedially directed inflow toward the septum instead of toward the apex (as for normal valves). This causes a reversed vortex of blood flow in mid-diastole as seen in an apical 4C view.
17Fluid Dynamics and Velocities Flow profiles of different valves vary substantially; none is analogous to flow across a native valve.
18Normal Finding: Regurgitation Small amount regurgitation in nearly all mechanical and 30-50% of bioprosthetic prosthesesCan be difficult to separate normal from pathologic regurgitation, particularly in the mitral positionTEE indicated if pathologic regurgitation is suspectedTEE of bileaflet mitral valveBileaflet mechanical – 2 crisscross jets of regurgitation parallel to leaflet opening planeTilting disk – regurg at closure line with major jet directed away from sewing ring
19Pathologic Regurgitation Characterized by:An eccentric or large jetMarked variance on the color flow displayA jet that originates around the valve sewing ringVisualization of a proximal flow acceleration region on the LV side of the mitral valveIn addition to Doppler eval of regurgitation- Shape, origin, and orientation of the regurgitant jet- Vena contracta diameter- Intensity and shape of the continuous wave Doppler signal- Evidence of distal flow reversal- LV size, hypertrophy, and systolic function
20Prosthetic Valve Regurgitation For aortic valves, TTE color flow imaging in parasternal and apical views can be helpful b/c the Doppler signal reaches the LVOT w/o intercepting the valve prosthesis (no shadowing).For mitral valves, parasternal can be helpful if view can be obtained where the LA side is not shadowed by prosthesis.
21Prosthetic Valve Stenosis Pressure gradientsCalculated using the Bernoulli equation (4v2)Good correlation when validated against invasive pressure measurementsmechanical valves, especially bileaflet, result in overestimation of the gradient due to differing fluid dynamicsSig variation in normal prosthetic valve velocities, gradients and areas. However, all prostheses are inherently stenotic compared to a native valve.Mitral prostheses have lower velocities and gradients than aortic prostheses 2/2 passive flow at lower pressures; generally true for larger vs smaller prostheses.Although max velocity across PV > native, shape of velocity curve is triangular vs rounded for native stenosis. Therefore, mean gradient PV usu less than native valve with SAME max antegrade velocity
22The most complex fluid dynamics are from bileaflet mechanical valves - Flow velocity profile shows three peaks corresponding to each opening, with higher velocities in the center of the orifice- Local high pressure gradient in the central orifice that is often significantly greater than the overall pressure gradient across the valve.Within narrow central stream, acceleration forces result in localized high pressure gradient and velocity with pressure recovery distal to the valve (i.e. pressure difference b/t upstream to valve > valve to downstream. Because CW Doppler records highest velocity along a length of the beam, the higher upstream velocity is recorded. Whereas gradient of interest is the upstream to downstream gradient.Because of pressure recovery, Doppler overestimates transvalvular gradient, especially in bileaflet valves.
23Prosthetic Aortic Valve Area Velocities across PVs vary with volume flow rate for a given orifice area. Therefore, normally functioning prosthesis may have high velocities and gradients secondary to increased CO (sepsis, pregnancy) OR a low transvalvular velocity with depressed CO.Therefore, a flow independent measure of PV function is more useful clinically > valve areaContinuity equation for aortic (and pulmonic) valvesLVOT velocity recorded from apical approach with pulsed Doppler proximal to PV, avoid region of flow acceleration immediately adjacent to valveCSA LVOT = pi(D/2)2Aortic jet veloicty recorded with CW from whichever window provides highest velocity signalLVOT diameter PSL midsystole immed adjacent to Ao valve\*****direct measurement of outflow tract preferred to valve size since size relates to external diameter of sewing ring, not effective diameter of subvalvular flow region
24Prosthetic AVA: Velocity Ratio Measure velocity increase across valveRatio of outflow tract velocity/aortic jet velocity reflects degree of stenosisRatio = 1 if no obstruction presentGiven inherent stenosis, normal range is 0.35 to 0.5 for aortic prosthesisAdvantages: takes volume flow rate into account; does not require outflow tract diameter measurementAs stenosis increases, aortic jet velocity will increase without change in the outflow tract velocityfor normal valve
25Prosthetic Mitral Valve Area Can be estimated using the pressure half-time approach as for native mitral valve stenosis.The expected half-time for a PV is longer than with a native valve.Pressure half time for mitral and tricuspid valve areasBileaflet valves affect accuracy of pressure gradient but the T1/2 less affected b/c depends on time course of velocity decline rather than absolute velocity itself
26Incidence of Thromboembolic Complications Fatal ComplicationNon-Fatal ComplicationValve ThrombosisAortic0.2 per 100 patient years1.0 to 2.0 per 100 patient years0.1 percent per yearMitral-2.0 to 3.0 per 100 patient years0.35 percent per yearThrombosis in tricuspid position extremely high; therefore bioprostheses preferred at this site.
27Prosthetic Valve Thrombosis TEE is often negative if the thrombi are small or if new thrombus has not formed since the initial embolic event.Thus an embolic event in a patient with a prosthetic valve (esp mechanical) must be presumed to be related to the PV even if the TEE is negative.Echo evaluation, especially in mechanical valves, is limited due to shadowing and reverberations unless very large thrombus. Echo cannot definitively exclude thrombus.Clinical events often occur with clots smaller than the detection limit for ultrasoundProsthetic valve itself is a cardiac source of embolusInfected pannus cannot be differentiated from thrombus with ultrasound.
28Prosthetic Valve Endocarditis Difficult to detect with TTEOften involves sewing ring and annulus, resulting in paravalvular abscess rather than a discrete vegetationFeatures that increase suspicion for PV endocarditis on TTE:Regurgitation or stenosis due to infected pannus on inflow surfaceValve instability or rockingUnexplained change in chamber dimensions
29Prosthetic Valve Endocarditis Often involves the sewing ring and annulus resulting in formation of a paravalvular abscess rather than the typical vegetation.TTE – LA masked by valve from parasternal and apical windows. TEE generally required.
30Patient Prosthesis Mismatch Size of prosthesis results in inadequate blood flow given metabolic demandsProsthesis itself functions wellIndexed effective orifice area < or = 0.85cm2/m2Predicts high transvalvular gradients, persistent LVH and increased rate of cardiac events following AVREstimates vary between 20-70% of AVR affectedPPM can result in hemodynamics consistent with stenosis even with a normally functioning prosthesis.
31Objectives Types of prostheses Prosthetic dysfunction Echocardiographic surveillance of prostheses
32Recommended Surveillance Baseline echocardiogram 6-8 weeks postoperativelyRoutine echocardiographic surveillance annually thereafterEvaluate forRegression of hypertrophy or dilationRecovery of LV systolic functionChanges in PA pressures
34SummaryProsthetic valve dysfunction is well detected by echocardiographyDysfunction includesStructural failureThromboembolic complicationsEndocarditisPPMDistinguishing normal from pathologic function can be challenging; most useful is comparison to baseline post-prosthesisOther means of assessing prosthetic valve function include:Fluoroscopy - useful with mechanical valves. Good for assessing mechanical leaflet motion due to outstanding spatial and temporal resolution and stability of valve ring with the cardiac cycle (i.e. rocking of the base).MRI - safely in all valves except Starr-Edwards (early 60’s). Can visualize mechanical valves, but lacks the temporal resolution and Doppler capabilities of echocardiography. Shows gross valve position, function, and regurgitation.Cardiac catheterization - Aortogram/LV gram can evaluate regurgitation.
35ReferencesOtto, C. Textbook of Clinical Echocardiography, Fourth Edition 2009.Libby et al. Braunwald’s Heart Disease. Eighth Edition 2008.Pibarot, P and Dumesnil JG. Prosthesis-patient mismatch: definition, clinical impact, and prevention. Heart 2006;92:Bonow RO, Carabello BA, Chatterjee K, et al: ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to revise the 1998 Guidelines for the Management of Patients with Valvular Heart Disease): Developed in collaboration with the Society of Cardiovascular Anesthesiologists: endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. Circulation 2006; 114:e84.