Echocardiographic Evaluation of Prosthetic Heart Valves Patricia Tung, M.D. February 10, 2010

Objectives Types of prostheses Prosthetic dysfunction Echocardiographic surveillance of prostheses

Types 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 thromboembolism Bioprostheses developed primarily to overcome the risk of thromboembolism and inconvenience of anticoagulation therapy. Major drawback is durability.

Mechanical Valves A, 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-cage Tilting disk - opens at an angle to the annulus plane, constrained by a strut, cage or slanted slot Bileaflet: 2 semicircular disks that form 2 large lateral openings and a smaller central opening St. 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.

Tissue Valves -3 biologic leaflets and similar anatomic structure to native aortic valve Stented valve leaflets are usually porcine or bovine/equine pericardium mounted on rigid cloth support with stent at each commissure Stentless valves use flexible fabric or tissue cuff, often attached to aortic root graft

Homograft Valves Aortic or pulmonic cadaver valve -> preserved, treated with antibiotics and frozen Usually the valve and great vessel preserved as a block; ideal when there is also aortic root pathology

Objectives Types of prostheses Prosthetic dysfunction Echocardiographic surveillance of prostheses

Mechanisms of Prosthetic Valve Dysfunction Structural failure Stenosis Regurgitation Thromboembolic complications Endocarditis Patient Prosthesis Mismatch Structural failure = failure of a prosthetic valve to open or close properly

Structural 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 calcification A – valve failure secondary to mineralization and collagen degeneration B – Cuspal tears and perforations Structural failure of current generation mechanical valves is rare; valve stenosis or regurgitation often due to thrombus or pannus ingrowth.

Cohn et al. Ann Thorac Surg, 1998. Estimates of freedom from structural valve deterioration (SVD) stratified by age. Porcine AVR Bovine pericardial AVR The rate of structural valve failure is age-dependent, and is significantly lower in patients older than 65 years (Fig. 62-49A 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.

Homograft Dysfunction Subject to severe tissue calcification Usually reserved for complex aortic root abscesses Hyperlipidemia accelerates prosthesis calcification Secondary prevention may slow this process Similar 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.

Physical Exam Findings Subtle findings especially if no baseline PE. Requires high suspicion for PV malfunction.

Echocardiographic Evaluation TTE valve area and regurgitation exclude significant obstruction Flow velocity is crucial measurement Often inadequate for infection or small structural changes (strut fracture, small vegetation, paravalvular leak) TEE inspection of valve apparatus and seating may not accurately quantify valve flow velocities Major challenges: 1. Distinguish normal from pathologic fluid dynamics of prosthetic valve 2. Acoustic shadowing from sewing rings of bioprosthetic and mechanical -> shadow and reverberations that obscure motion of valve structures and block Doppler signal TEE particularly useful for mitral valves b/c allows visualization from the LA side of valve TEE also reliably distinguishes transprosthetic from paraprosthetic regurgitation. TEE less helpful for aortic valves b/c posterior portion sewing ring shadows valve leaflets

Normal Appearance PV Left: TTE PSL of bileaflet mechanical aortic valve; leaflets obscured by shadowing from sewing ring Right: 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

Normal Doppler Clicks Normal motion of mechanical occluder or bioprosthetic leaflets creates a Doppler signal. Analogous to auscultatory click except both opening and closing create Doppler signal.

Normal Doppler Flow Patterns PSL view of stented mitral bioprosthetic valve. Left: stents protrude into ventricular chamber Right: antegrade flow into LV Bioprosthetics have flow profile similar to native Ao valve with 3 leaflets and a central orifice -> provides laminar antegrade flow with a blunt flow profile In 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.

Fluid Dynamics and Velocities Flow profiles of different valves vary substantially; none is analogous to flow across a native valve.

Normal Finding: Regurgitation Small amount regurgitation in nearly all mechanical and 30-50% of bioprosthetic prostheses Can be difficult to separate normal from pathologic regurgitation, particularly in the mitral position TEE indicated if pathologic regurgitation is suspected TEE of bileaflet mitral valve Bileaflet mechanical – 2 crisscross jets of regurgitation parallel to leaflet opening plane Tilting disk – regurg at closure line with major jet directed away from sewing ring

Pathologic Regurgitation Characterized by: An eccentric or large jet Marked variance on the color flow display A jet that originates around the valve sewing ring Visualization of a proximal flow acceleration region on the LV side of the mitral valve In 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

Prosthetic 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.

Prosthetic Valve Stenosis Pressure gradients Calculated using the Bernoulli equation (4v2) Good correlation when validated against invasive pressure measurements mechanical valves, especially bileaflet, result in overestimation of the gradient due to differing fluid dynamics Sig 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

The 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.

Prosthetic 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 area Continuity equation for aortic (and pulmonic) valves LVOT velocity recorded from apical approach with pulsed Doppler proximal to PV, avoid region of flow acceleration immediately adjacent to valve CSA LVOT = pi(D/2)2 Aortic jet veloicty recorded with CW from whichever window provides highest velocity signal LVOT 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

Prosthetic AVA: Velocity Ratio Measure velocity increase across valve Ratio of outflow tract velocity/aortic jet velocity reflects degree of stenosis Ratio = 1 if no obstruction present Given inherent stenosis, normal range is 0.35 to 0.5 for aortic prosthesis Advantages: takes volume flow rate into account; does not require outflow tract diameter measurement As stenosis increases, aortic jet velocity will increase without change in the outflow tract velocity 0.75-0.9 for normal valve

Prosthetic 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 areas Bileaflet 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

Incidence of Thromboembolic Complications Fatal Complication Non-Fatal Complication Valve Thrombosis Aortic 0.2 per 100 patient years 1.0 to 2.0 per 100 patient years 0.1 percent per year Mitral - 2.0 to 3.0 per 100 patient years 0.35 percent per year Thrombosis in tricuspid position extremely high; therefore bioprostheses preferred at this site.

Prosthetic 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 ultrasound Prosthetic valve itself is a cardiac source of embolus Infected pannus cannot be differentiated from thrombus with ultrasound.

Prosthetic Valve Endocarditis Difficult to detect with TTE Often involves sewing ring and annulus, resulting in paravalvular abscess rather than a discrete vegetation Features that increase suspicion for PV endocarditis on TTE: Regurgitation or stenosis due to infected pannus on inflow surface Valve instability or rocking Unexplained change in chamber dimensions

Prosthetic 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.

Patient Prosthesis Mismatch Size of prosthesis results in inadequate blood flow given metabolic demands Prosthesis itself functions well Indexed effective orifice area < or = 0.85cm2/m2 Predicts high transvalvular gradients, persistent LVH and increased rate of cardiac events following AVR Estimates vary between 20-70% of AVR affected PPM can result in hemodynamics consistent with stenosis even with a normally functioning prosthesis.

Objectives Types of prostheses Prosthetic dysfunction Echocardiographic surveillance of prostheses

Recommended Surveillance Baseline echocardiogram 6-8 weeks postoperatively Routine echocardiographic surveillance annually thereafter Evaluate for Regression of hypertrophy or dilation Recovery of LV systolic function Changes in PA pressures

Summary Prosthetic valve dysfunction is well detected by echocardiography Dysfunction includes Structural failure Thromboembolic complications Endocarditis PPM Distinguishing normal from pathologic function can be challenging; most useful is comparison to baseline post-prosthesis Other 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.

References Otto, 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;92:1022-1029 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.