Prosthetic Valve Dysfunction
Shuktika Nandkeolyar
Dmitry Abramov
Helme Silvet
Purvi Parwani
INTRODUCTION
Epidemiology
The prevalence of patients with prosthetic heart valves (PHVs) is growing quickly. With the advent of transcatheter valve implantation, it is estimated that around 850,000 patients will undergo PHV implantation annually by 2050.1 Although these devices have been effective in treating native heart valve disease, they require continued evaluation and management. PHVs can be categorized as mechanical, bioprosthetic, homograft, or xenograft. Mechanical heart valves are comprised of an occluder, occluder restraint, and a sewing ring. They are bileaflet (most common), single tilting disc, or caged ball.2 Bioprosthetic valves are stented, stentless, sutureless, or the increasingly common transcatheter valves. The material for bioprosthetic valves are usually either bovine pericardial tissue or porcine valve tissue.2,3 Finally, homograft and xenograft valves are less commonly used, and typically implanted in the aortic or pulmonic position.4
There are several manifestations of PHV dysfunction, with significant implications for patient care. In this chapter, we focus on the most commonly encountered and clinically relevant complications: prosthetic valve thrombosis (PVT), pannus formation, patient-prosthesis mismatch (PPM), structural valve degeneration (SVD), endocarditis, and paravalvular leak (PVL).
Overall, the annual incidence of PHV dysfunction ranges between 0.7% and 3.5%,2,5,6,7,8,9,10 although this varies greatly between the type, location, and number of PHVs implanted.2,5,6,7,8,9,10,11,12,13,14,15 The incidence, risk factors, and pathogenesis of these PHV pathologies are important when considering their evaluation by various imaging modalities and are summarized in Table 13.1.
Risk Factors
Risk factors for developing PHV disease vary by the prosthesis used and the disease in question, with specific risk factors for each category of PHV dysfunction summarized in Table 13.1. There are also several common factors: young age, female gender, obesity, elevated calcium in end-stage renal disease or hyperparathyroidism, hypertension, pregnancy, metabolic syndrome, diabetes, and increased lipids.2,5,9,11,15,16,17,18 Valve positioning, particularly for supra-annular transcatheter valve placement of aortic PHV, is a risk factor for PVL. Risk factors for PPM include low ejection fraction, high body surface area, and a small annulus area.
PATHOGENESIS
Acute Prosthetic Heart Valve Dysfunction
There are several types of PHV dysfunction, including thrombosis and infection, which can develop over a short time and present with acute symptoms. PVT in a bioprosthetic valve occurs because of a hypercoagulable state as a reaction to recent tissue injury during surgery or an incompletely endothelialized prosthesis5; with a mechanical prosthetic valve, it occurs with inadequate anticoagulation. Slow blood flow (due to low pressure venous flow for right-sided valves, stasis in the setting of atrial fibrillation or atrial dilation for tricuspid and mitral PHV, or low ejection fraction for aortic or pulmonic PHV) can contribute to PVT.5,19 Finally, valve frame fracture, incomplete apposition, or leaflet injury may cause turbulent flow, promoting acute thrombosis formation.5
Infective endocarditis may be caused by perioperative bacterial contamination or may occur any time after valve implantation because of bacterial or fungal bloodstream infection. Endocarditis is often seen at the sewing ring and annulus in addition to valvular leaflet vegetations. It can lead to paravalvular abscess, dehiscence, pseudoaneurysms, fistulae, and conduction system block.14,19,20 Endocarditis can be a subacute process, but more commonly presents with acute valvular and paravalvular destruction, leading to prominent symptoms.
PVL occurs because of a number of mechanisms, including tissue friability, suture failure, infection, and annular or valvular calcification (for transcatheter procedures), preventing full PHV expansion, malapposition of the PHV, and underexpansion or undersizing of the PHV.2,3,15 PVLs often are seen immediately after valve implantation and most reduce or resolve over time, although PVLs can also occur from endocarditis.2,3
Chronic Prosthetic Heart Valve Dysfunction
Prosthetic valve pathology that manifests over a longer period of time includes pannus formation, valve degeneration, and PPM.
Pannus formation is caused by an autoimmune reaction between the host and prosthesis, creating a fibrous ingrowth (either on mechanical or bioprosthetic PHVs, leading to impaired movement of the PHV leaflets.2,6
SVD predominantly affects bioprosthetic PHV. The three primary mechanisms are calcification or degradation of the valve tissue, immune response to residual xenoantigens, or lipid-mediated inflammation.2,11 Calcification or degradation
is thought to occur because of a coating of glutaraldehyde on the bioprosthetic valves. Although the coating decreases thromboembolic risk and decreases immune response against porcine and bovine tissues, it also attracts calcium deposits that ultimately lead to stenosis from limitation of leaflet motion or regurgitation from disruption of the connective tissue matrix.2,11
is thought to occur because of a coating of glutaraldehyde on the bioprosthetic valves. Although the coating decreases thromboembolic risk and decreases immune response against porcine and bovine tissues, it also attracts calcium deposits that ultimately lead to stenosis from limitation of leaflet motion or regurgitation from disruption of the connective tissue matrix.2,11
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CLINICAL PRESENTATION
Common Signs and Symptoms
The clinical presentation of acute PHV diseases includes a new murmur, embolic phenomena, or decompensated heart failure including cardiogenic shock. Chronic PHV pathology can present with more indolent symptoms that can be difficult to recognize, such as progressive dyspnea and fatigue. Development of new symptoms in a patient with a PHV requires a high index of suspicion on the part of the clinician to recognize, diagnose, and treat PHV diseases in a timely manner.
Symptoms commonly seen with each type of PHV disorder are summarized in Table 13.1.19 PVT is suggested when a patient with known mechanical PHV presents with interruption in anticoagulation and new acute heart failure, thromboembolism, and absence or diminution of the “click” on routine examination of the valve.5,19 PPM or pannus may present with progressive shortness of breath and fatigue, or incomplete resolution of symptoms post initial PHV placement.2,19 In addition to these symptoms common to all PHV diseases, endocarditis can present with fatigue, fever, conduction disease, chills, and cutaneous immunologic or septic thrombotic signs (ie, Osler nodes, splinter hemorrhages, petechiae, and Janeway lesions),15,19 whereas PVL can present with pallor, fatigue, petechiae, or jaundice consistent with hemolytic anemia.
Differential Diagnosis
The differential diagnosis of PHV dysfunction can be categorized by obstruction and regurgitation. Although manifestations
of various etiologies of PHV dysfunction can overlap, typical causes of obstruction include SVD, PVT, pannus, and PPM, whereas typical causes of regurgitation include PVL, SVD, and endocarditis. Symptoms mimicking valve dysfunction also need to be differentiated from other cardiac or noncardiac conditions that can have similar presentations.
of various etiologies of PHV dysfunction can overlap, typical causes of obstruction include SVD, PVT, pannus, and PPM, whereas typical causes of regurgitation include PVL, SVD, and endocarditis. Symptoms mimicking valve dysfunction also need to be differentiated from other cardiac or noncardiac conditions that can have similar presentations.
DIAGNOSIS
Initial Evaluation of Suspected Prosthetic Heart Valve Dysfunction
PHV dysfunction can be suspected on the basis of the signs and symptoms, as shown in Table 13.1. Typical first-line evaluation modality is transthoracic echocardiogram (TTE) or transesophageal echocardiogram (TEE), although other modalities including fluoroscopy, cardiac computed tomography (CCT), cardiac magnetic resonance (CMR) imaging, and positron emission tomography/computed tomography (PET/CT) may play an important role in the diagnosis depending on the patient presentation and clinical suspicion (Algorithms 13.1 and 13.2). Although PHV dysfunction can present with a wide range of pathologic findings on imaging, the presentation commonly includes imaging findings of valve flow obstruction, flow regurgitation, or endocarditis-related changes.
 ALGORITHM 13.1 Diagnosis of prosthetic heart valve dysfunction* *References 2-4 CCT, cardiac computed tomography; CMR, cardiac magnetic resonance imaging; 18F-FDG PET, 18F-fluorodeoxyglucose positron emission tomography; INR, international normalized ratio; PPM, patient prosthesis mismatch; PVL, paravalvular leak; SVD, structural valve dysfunction; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography. |
Echocardiography (Transthoracic Echocardiogram and Transesophageal Echocardiogram)
Two-Dimensional Imaging/Three-Dimensional Visual Appearance
Stenotic Lesions: Use of echocardiography (TTE and/or TEE) is a class I indication if there is suspicion of PHV dysfunction, and is generally the first diagnostic study ordered.21,22 TEE may be required for PHV evaluations, especially those in the mitral position, because of acoustic shadowing.2,4 A complete echocardiographic assessment of suspected PHV disease should include visualization of leaflet mobility, calcification, thickening, or vegetation, as well as thrombus and pannus. Thrombus generally begins at the valve ring and expands inward, obstructing leaflet mobility, with a soft echogenicity and smooth contour (Case Studies 13.1 and 13.2).5 Pannus generally appears more dense than does thrombus on echocardiography, although the differentiation between the two by echocardiography can be
challenging in clinical practice.2 SVD-related stenosis is diagnosed by visualization of decreased leaflet mobility with calcification and/or fusion of the valve leaflets (Case Studies 13.3 and 13.4,
Video 13.3).2,19 In addition to two-dimensional (2D) imaging, three-dimensional (3D) echocardiography is helpful in visualizing components of the PHV and presence of pannus or thrombus that are not well seen on 2D imaging because of acoustic shadowing.4
challenging in clinical practice.2 SVD-related stenosis is diagnosed by visualization of decreased leaflet mobility with calcification and/or fusion of the valve leaflets (Case Studies 13.3 and 13.4,
Video 13.3).2,19 In addition to two-dimensional (2D) imaging, three-dimensional (3D) echocardiography is helpful in visualizing components of the PHV and presence of pannus or thrombus that are not well seen on 2D imaging because of acoustic shadowing.4 ALGORITHM 13.2 Management of prosthetic heart valve dysfunction.(19, 21, 37) AR, aortic regurgitation; AS, aortic stenosis; CCT, cardiac computed tomography; CMR, cardiac magnetic resonance;18F-FDG PET, 18F-fluorodeoxyglucose positron emission tomography; LA, left atrium; LVOT, left ventricular outflow tract; NYHA, New York Heart Association; PHV, prosthetic heart valve; TEE, transesophageal echocardiogram; TTE, transthoacic echocardiogram. |
Regurgitant Lesions: A complete 2D or 3D echocardiographic study evaluates for the presence of perivalvular abscess, abnormal rocking motion of the valve, and dehiscence at the sewing ring. SVD-related regurgitation is caused by torn or flail leaflets, and usually causes central or eccentric valvular regurgitation.2,3 Infective endocarditis can cause paravalvular or valvular regurgitation depending on the site, and can lead to destruction of the surrounding paravalvular areas, including abscess formation. Vegetations are generally irregularly shaped, independently mobile structures of low echogenicity, although imaging cannot easily distinguish infected vegetations from noninfected echodensities such as thrombi.2 Idiopathic PVL due to malposition or malapposition of the PHV may not be immediately evident on 2D or 3D imaging, and may require the addition of color Doppler.
Patient-Prosthesis Mismatch (PPM): The 2D appearance of the valve in the case of PPM may be normal because PPM is a functional obstruction without mechanical dysfunction of the valve itself.2 The physiologic relationship between the flow, valve area, and transvalvular gradient can be explained by the formula: gradient = Q2/K × EOA2, where Q = flow, K is a constant, and EOA = effective orifice area.2 For the gradient to remain normal, the EOA must be proportionate to flow. The flow can be disproportionately increased (leading to an elevated gradient) in patients with high cardiac output states such as anemia, thyrotoxicosis, pregnancy, and infection; hence, these etiologies must be ruled out before a diagnosis of PPM is made.19 If no other etiology for an elevated gradient is discovered, then PPM can be diagnosed,2,19 implying that valve area is too small for the patient’s body size during normal flow conditions.
Chamber Quantification and Volumes
Chamber quantification of all chambers and both left ventricular outflow tract (LVOT) and right ventricular outflow tract (RVOT) measurements should be obtained to diagnose PHV dysfunction optimally.2 Dilation of atrial or ventricular chambers may indicate or support the presence or progression of PHV dysfunction. Accurate outflow tract measurements are important in calculations including Doppler velocity index (DVI) or regurgitant volume.
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