Prosthetic Valve Dysfunction

Prosthetic Valve Dysfunction

Shuktika Nandkeolyar

Dmitry Abramov

Helme Silvet

Purvi Parwani



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.


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

PPM is caused by a valve size or effective orifice area (EOA) that is too small to accommodate unimpeded blood flow across the valve, thereby causing a functional obstruction despite a normally functioning valve.2,18


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.

May 8, 2022 | Posted by in CARDIOLOGY | Comments Off on Prosthetic Valve Dysfunction

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