Prosthetic Heart Valves

Updated: Jan 03, 2022
Author: Kirtivardhan Vashistha, MBBS; Chief Editor: Richard A Lange, MD, MBA 

Overview

Practice Essentials

Prosthetic heart valves are increasingly being used for dysfunctional native valves requiring intervention. Broadly, they can be classified into three categories: mechanical heart valves, bioprosthetic valves, and homograft. The goal of an artificially placed valve is to function like a native one in terms of hemodynamics and with minimal side effects (low thrombogenicity).

Bioprosthetic valves (see the image below) generally offer functional properties (eg, hemodynamics, resistance to thrombosis) similar to that of native valves, but longevity is limited relative to mechanical valves. Mechanical heart valves have subpar hemodynamics with increased thrombogenicity; they also require anticoagulation but have greater long-term durability.[1]

Prosthetic Heart Valves. The Hancock M.O. II aorti Prosthetic Heart Valves. The Hancock M.O. II aortic bioprosthesis (porcine). Reproduced with permission from Medtronic, Inc.

Replacement of diseased valves with prosthetic heart valves reduces the morbidity and mortality associated with native valvular disease, but it comes at the expense of risking complications related to the implanted prosthetic device. Even when promptly recognized and treated, acute prosthetic valve failure is associated with a high mortality.

Signs and symptoms

Signs and symptoms of prosthetic heart valve malfunction depend on the type of valve, its location, and the nature of the complication. Presentations may include the following:

  • Acute prosthetic valve failure: Acute heart failure signs such as sudden onset dyspnea, syncope, precordial pain, new heart murmur, and lung crackles on auscultation

  • Subacute valvular failure: Symptoms of gradually worsening congestive heart failure

  • Embolic complications (thrombotic or infectious): Symptoms related to the site of embolization (eg, stroke, myocardial infarction [MI], signs and symptoms of visceral or peripheral embolization)

  • Anticoagulant-related hemorrhage: Site-specific hemorrhage, gastrointestinal (GI) bleed, muscle hematoma, cerebral hemorrhage

  • Prosthetic valve endocarditis: Fever, chills, fatigue, malaise, night sweats, signs and symptoms of heart failure if there is disrupted valvular integrity, dyspnea, cough, pleuritic chest pain, new or changed heart murmur, splenomegaly, septic shock, septic emboli

  • Hemolysis secondary to prosthetic valve: Symptoms secondary to anemia and/or thrombocytopenia, such as pallor, dyspnea, bleeding, and petechiae

On physical examination, normal prosthetic heart valve sounds include the following:

  • Mechanical valves: Loud, high-frequency, metallic closing sound; soft opening sound (tilting disc and bileaflet valves); low-frequency opening and closing sounds of nearly equal intensity (caged ball valves)

  • Tissue valves: Similar closing to those of native valves, low-frequency early opening sound in the mitral position

Prosthetic heart valve murmurs noted include the following:

  • Aortic prosthetic valves: Some degree of outflow obstruction with a resultant systolic ejection murmur (loudest in caged ball and small porcine valves); low-intensity diastolic murmur (tilting disc and bileaflet valves)

  • Mitral prosthetic valves: Low-grade systolic murmur (caged ball valves); short diastolic murmur (bioprostheses and, occasionally, St. Jude bileaflet valves)

Additional findings may include the following:

  • Acute valvular failure: Evidence of poor tissue perfusion; hyperdynamic precordium and right ventricular impulse (50% of cases); absence of a normal valve closure sound or presence of an abnormal regurgitant murmur

  • Subacute valvular failure: Rales and jugular venous distention; signs of right-side failure; a new regurgitant murmur or absence of normal closing sounds; a new or worsening hemolytic anemia (may be the only presenting abnormality)

See Presentation for more detail.

Diagnosis

Laboratory studies that may be useful include the following:

  • Complete blood cell (CBC) count

  • Blood urea nitrogen (BUN) and creatinine levels

  • Urinalysis

  • Blood cultures

  • Prothrombin time (PT) or international normalized ratio (INR)

  • Peripheral smear

  • Lactate dehydrogenase (LDH) and haptoglobin

  • Liver function tests

Imaging studies that may be helpful include the following:

  • Chest radiography: This modality can help in delineating the valvular morphology and determining whether the valve and occluder are intact; each of the most commonly used valve types has its own characteristic radiographic appearance

  • Echocardiography (transthoracic Doppler, transesophageal [the study of choice for a suspected prosthetic valve complication])

  • Cinefluorography: This study may detect impaired occluder movement but often cannot readily determine the etiology

  • Computed tomography (CT) scanning: The Society of Cardiovascular Computed Tomography (SCCT) states that CT scanning should be performed as part of the evaluation of all patients being considered for transcatheter aortic valve implantation (TAVI)/transcatheter aortic valve replacement (TAVR), except those in whom CT is contraindicated.[2, 3]  CT images should be interpreted with a member of the TAVI/TAVR team or reviewed with the operator before the procedure.

See Workup for more detail.

Management

In patients with acute valvular failure, diagnostic studies must be performed simultaneously with resuscitative efforts.

Treatment approaches to primary valve failure include the following:

  • Emergency valve replacement

  • Concomitant adjunctive therapy

  • Afterload reduction and inotropic support

  • In selected cases, intra-aortic balloon counterpulsation

Treatment approaches to prosthetic valve endocarditis (PVE) include the following:

  • Administration of intravenous (IV) antibiotics as soon as two sets of blood cultures are drawn

  • Cessation of warfarin until central nervous system involvement is ruled out and invasive procedures are determined to be unnecessary[4]

  • Consideration of IV heparin instead of oral anticoagulation in the acute setting

  • Consideration of emergency surgery in patients with large, mobile vegetations; persistence of septicemia for more than 2 days after being on an effective antibiotic treatment; moderate to severe heart failure; or with an unstable prosthesis noted on echocardiography or fluoroscopy

Treatment approaches to thromboembolic complications include the following:

  • Anticoagulation (if it has not already been initiated or if the patient has a subtherapeutic INR)

  • Assessment of valve function

Treatment approaches to prosthetic valve thrombosis include the following:

  • Surgery (historically the mainstay of treatment but associated with a high mortality)

  • Thrombolytic therapy (appropriate for selected patients with thrombosed prosthetic valves): Should always be performed in conjunction with cardiovascular surgical consultation

  • In cases of major anticoagulant-related hemorrhage, reversal of anticoagulation

See Treatment and Medication for more detail.

Background

Implantation of prosthetic cardiac valves to treat hemodynamically significant valvular disease has become an increasingly common procedure. According to a study by iData Research, it is estimated that 180,000 patients undergo heart valve replacement in the United States every year,[5] and the numbers are expected to increase further with the advent of newer modalities and with growing evidence of appropriate clinical indications for heart valve replacement. For example, indications for transcatheter aortic valve replacement (TAVR) have been expanded several times since the initial Food and Drug Administration (FDA) approval for prohibitive-risk surgical patients in 2011.[6]  In 2019, following the results of the Placement of Aortic Transcatheter Valves (PARTNER)-3 trial, the FDA further expanded the indication for TAVR valves to include low-risk patients with severe aortic stenosis.[7, 8]

Broadly, these devices can be classified into three categories: mechanical heart valves, bioprosthetic valves, and homograft. The goal of an artificial valve is to function like a native one in terms of hemodynamics, with minimal side effects (low thrombogenicity). Bioprosthetic valves generally offer functional properties (eg, hemodynamics, resistance to thrombosis) similar to those of native valves, but they are at risk of structural damage and thus limiting their long-term usage. Mechanical heart valves have subpar hemodynamics and an increased level of thrombogenicity that requires anticoagulation, but they usually have long-term durability.[1]

Replacement of diseased valves reduces the morbidity and mortality associated with native valvular disease, but this comes at the expense of risking complications related to the implanted prosthetic device. These complications include primary valve failure, prosthetic valve endocarditis (PVE), prosthetic valve thrombosis (PVT), thromboembolism, and mechanical hemolytic anemia. In addition, because many of the affected patients require long-term anticoagulation, anticoagulant-related hemorrhage may occur.

More than 80 models of artificial valves have been introduced since 1950. In day-to-day clinical practice, however, it is necessary to be familiar with a few basic types. Prosthetic valves are either created from synthetic material (mechanical prosthesis) or fashioned from biological tissue (bioprosthesis). The choice of prosthesis is determined by the anticipated longevity of the patient and his/her ability to tolerate anticoagulation.[9]

Selecting the best prosthetic heart valve for a patient can be difficult owing to the lack of industry standards on the sizing, placement, and hemodynamic and structural performance of these devices. In October 2020, the European Association for Cardio-Thoracic Surgery (EACTS), the Society of Thoracic Surgeons (STS), and the American Association for Thoracic Surgery (AATS) Valve Labelling Task Force released their recommendations for providing surgical heart valve physical dimensions, intended implant position, and hemodynamic performance in a transparent, consistent manner.[10] The task force also advocates for a standardized chart to assess the probability of prosthesis–patient mismatch and calls for manufacturers to provide essential information required for valve choice on standardized charts.

Design Features

Mechanical valves

Three main designs of mechanical valves exist: caged ball valve, tilting disc (single leaflet) valve, and bileaflet valve. The only Food and Drug Administration (FDA)–approved caged ball valve is the Starr-Edwards valve (see the image below).

Prosthetic Heart Valves. Starr-Edwards Silastic ba Prosthetic Heart Valves. Starr-Edwards Silastic ball valve mitral Model 6120. Reproduced with permission from Baxter International, Inc.

Tilting disc (single leaflet) valves

Tilting disc valve models include the Medtronic Hall valve (see the image below), Omnicarbon (Medical CV) valves, Monostrut (Alliance Medical Technologies), and the discontinued Bjork-Shiley valves (Shiley Laboratories).

Prosthetic Heart Valves. Medtronic Hall mitral val Prosthetic Heart Valves. Medtronic Hall mitral valve. Reproduced with permission from Medtronic, Inc.

Bileaflet valves

Bileaflet valves include the St. Jude (St. Jude Medical) (see the following image), the most commonly implanted valve in the United States; CarboMedics valves (Sulzer CarboMedics); ATS Open Pivot valves (ATS Medical); and On-X and Conform-X valves (CryoLife).

Prosthetic Heart Valves. St. Jude Medical mechanic Prosthetic Heart Valves. St. Jude Medical mechanical heart valve. Photograph courtesy of St. Jude Medical, Inc. All rights reserved. St. Jude Medical is a registered trademark of St. Jude Medical, Inc.

Bioprosthetic valve

Bioprosthetic (xenograft) valves are made from porcine valves or bovine pericardium. Porcine models include the Carpentier-Edwards valves (Edwards Lifesciences) and Hancock II and Mosaic valves (Medtronic). See the images below.

Prosthetic Heart Valves. Carpentier-Edwards Durale Prosthetic Heart Valves. Carpentier-Edwards Duralex mitral bioprosthesis (porcine). Reproduced with permission from Baxter International, Inc.
Prosthetic Heart Valves. The Hancock M.O. II aorti Prosthetic Heart Valves. The Hancock M.O. II aortic bioprosthesis (porcine). Reproduced with permission from Medtronic, Inc.

Pericardial valves include the Perimount series valves (Edwards LifeSciences). Ionescu-Shiley pericardial valves have been discontinued. Stentless porcine valves have also come into use; they offer improved hemodynamics with a decreased transvalvular pressure gradient when compared to older stented models. Stentless models include the Edwards Prima Plus, Medtronic Freestyle, and Toronto SPV valve (St. Jude Medical).[11]

Indications for Heart Valve Surgery

Aortic stenosis

The 2020 American College of Cardiology/American Heart Association (ACC/AHA) recommendations for aortic valve replacement in patients with valvular aortic stenosis (AS) are summarized below.[12] In most adults with symptomatic severe AS, aortic valve replacement (AVR) is the surgical treatment of choice. If concomitant coronary disease is present, AVR and coronary artery bypass graft (CABG) surgery should be performed simultaneously.

Successful AVR produces substantial clinical and hemodynamic improvement in patients with AS, including octogenarians. AVR should be performed in all symptomatic patients with severe AS regardless of left ventricular (LV) function, as survival is better with surgical treatment than with medical treatment.

ACC/AHA recommendations for AVR in AS are as follows[12] :

  • Symptomatic patients (by history or on exercise) with severe high-gradient AS (class I)

  • Patients with asymptomatic severe AS and LV ejection fraction (LVEF) below 50% (class I)

  • Patients with severe AS undergoing other cardiac surgery (class I)

  • Asymptomatic patients with very severe AS and low surgical risk or decreased exercise tolerance or hypotension on exercise (class IIa)

  • Symptomatic patients with low-flow/low-gradient severe AS with reduced LVEF and results of a low-dose dobutamine stress study showing aortic velocity ≥4 m/s or a mean pressure gradient ≥40 mmHg with a valve area ≤1.0 cm2 (class IIa)

  • Patients with moderate AS undergoing CABG surgery or surgery on the aorta or other heart valves (class IIa)

  • Asymptomatic patients with severe AS and rapid progression with low surgical risk (class IIb)

The class recommendations indicated above are defined as follows[12] :

  • Class I: Conditions for which there is evidence and/or general agreement that the procedure or treatment is beneficial, useful, and effective

  • Class II: Conditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment

  • Class IIa: Weight of evidence/opinion is in favor of usefulness/efficacy

  • Class IIb: Usefulness/efficacy is less well established by evidence/opinion

  • Class III: Conditions for which there is evidence and/or general agreement that the procedure/treatment is not useful/effective and in some cases may be harmful

Choice of intervention AS include the following[12] :

  • Symptomatic patients with severe AS with low to intermediate surgical risk: Surgical AVR (SAVR) is preferred (class I)

  • Symptomatic patients with severe AS and high surgical risk, SAVR or transcatheter aortic valve replacement (TAVR) is offered on a case-by-case basis with evaluation of patient-specific risk and preferences (class I)

  • Symptomatic patients with severe AS and prohibitive risk for SAVR should undergo TAVR (class I)

  • TAVR is a reasonable alternative for symptomatic patients with severe AS and intermediate surgical risk (class IIa)

  • Percutaneous balloon aortic valvuloplasty (BAV) can be used as a bridge to AVR in patients with hemodynamic instability due to severe AS (class IIb)

Aortic regurgitation

Under the 2020 ACC/AHA guidelines, aortic valve surgery is recommended for patients with chronic, severe aortic regurgitation (AR) when the patient is symptomatic.[12] It is also recommended in the asymptomatic patient with chronic, severe AR who has a resting EF of 50% or less or LV dilatation. Additional circumstances in which aortic valve surgery may be reasonable are listed below.[12] Surgical treatment of AR usually requires replacement of the diseased valve with a prosthetic valve, although valve-sparing repair is increasingly possible with advances in surgical technique and technology.

ACC/AHA recommendations for AVR in AR are as follows[12] :

  • Symptomatic patients with severe AR, irrespective of LV systolic function (class I)

  • Asymptomatic patients with chronic severe AR and LV systolic dysfunction (EF < 50%) at rest (class I)

  • Patients with chronic severe AR while undergoing CABG or surgery on the aorta or other heart valves (class I)

  • Asymptomatic patients with severe AR with normal LV systolic function (EF >50%) but with severe LV dilatation (end-diastolic dimension [EDD] >65 mm or end-systolic dimension [ESD] >50 mm) (class IIa)

  • Patients with moderate AR while undergoing surgery on the ascending aorta (class IIa)

  • Patients with moderate AR while undergoing CABG (class IIa)

  • Asymptomatic patients with severe AR and normal LV systolic function at rest (EF >50%) when the degree of LV dilatation exceeds an EDD of 70 mm or ESD of 50 mm, when there is evidence of progressive LV dilatation, declining exercise tolerance, or abnormal hemodynamic responses to exercise (class IIb)

  • Asymptomatic patients with mild, moderate, or severe AR and normal LV systolic function at rest (EF >50%) when degree of dilatation is not moderate or severe (EDD < 70 mm, ESD < 50 mm) (class III)

Mitral stenosis

Valve replacement for mitral stenosis (MS) may be considered in patients who are candidates for surgical therapy when the valve is not suitable for valvotomy (either surgical or percutaneous). The recommendations for surgery in patients with mitral stenosis, according to the 2020 ACC/AHA guidelines, are described below.[12]

1. Mitral valve surgery (repair if possible) is indicated in patients with symptomatic (New York Heart Association [NYHA] functional class III–IV) severe MS (mitral valve area [MVA] ≤1.5 cm2) under any of the following circumstances (class I):

  • Percutaneous mitral balloon valvotomy is unavailable

  • Percutaneous mitral balloon valvotomy is contraindicated because of left atrial thrombus despite anticoagulation or because concomitant moderate to severe mitral regurgitation (MR) is present

  • The valve morphology is not favorable for percutaneous mitral balloon valvotomy based on a Wilkins score in a patient with acceptable operative risk

2. Patients with severe MS (MVA ≤1.5 cm2) undergoing other cardiac surgery (class I)

3. Severely symptomatic patients (NYHA III/IV) with severe MS (MVA ≤1.5 cm2) with other operative indications (class IIa)

4. Patients with moderate MS (MVA of 1.6-2.0 cm2) undergoing other cardiac surgery (class IIb)

5. Patients with severe MS (MVA ≤1.5 cm2) with recurrent embolic events while on adequate anticoagulation are candidates for mitral valve surgery and excision of the left atrial appendage (class IIb)

Mitral regurgitation

Chronic primary MR

Although more technically demanding, mitral valve repair is recommended over mitral valve replacement (MVR) in most patients with severe, chronic mitral regurgitation (MR) who require surgery. Such patients should be referred to surgical centers experienced with mitral valve repair. If mitral valve repair is not feasible, MVR with preservation of the chordal apparatus is preferred, as this preserves LV function and enhances postoperative survival.[12] Note the following ACC/AHA recommendations for surgery in patients with MR[12] :

  • Mitral valve surgery is recommended in symptomatic severe MR, irrespective of LV systolic function (class Ib).

  • Mitral valve surgery is indicated in asymptomatic patients with chronic severe primary MR and an LVEF < 60% and an LVESD ≥ 40 mm (class Ib).

  • In patients with chronic severe primary MR limited to the posterior leaflet, mitral valve repair is preferred over MVR (class I).

  • In patients with chronic severe primary MR involving the anterior leaflet or both leaflets when a successful and durable repair can be accomplished, mitral valve repair is preferred over MVR (class I).

  • In patients with chronic severe primary MR undergoing other cardiac surgery, mitral valve repair or MVR is indicated (class I).

Chronic severe secondary MR

In patients with chronic severe secondary MR undergoing CABG or AVR, mitral vlave surgery is reasonable (class IIa).

In severely symptomatic patients (NYHA III-IV) despite being on goal-directed medical therapy who have chronic severe secondary MR, mitral valve surgery can be considered (class IIb).

Tricuspid regurgitation

Valve replacement is required in both tricuspid regurgitation (TR) and tricuspid stenosis (TS) if the anatomic characteristics of the leaflet are not amenable to repair. Note the following:

  • In patients with severe TR undergoing left-sided valve surgery, tricuspid valve (TV) surgery is indicated (class I).

  • In symptomatic patients with severe primary TR unresponsive to medical therapy, TV surgery can be beneficial (class IIa).

  • In asymptomatic or minimally symptomatic patients with severe primary TR and progressive right ventricular systolic dysfunction and/or dilatation, TV surgery can considered (class IIb).

Tricuspid stenosis

TV surgery is indicated in the following (all class I)[12] :

  • Patients with severe TS undergoing left-sided valve surgery
  • Patients with isolated, symptomatic severe TS

Clinical Implementation of Bioprosthetic Valves

Factors involved in decision making for the type of valve prosthesis (mechanical or bioprosthetic) to use include the following:

  • Age: Mechanical valves, given their longer durability, are indicated in younger patients (age < 50 y). In older patients (age >65 y), bioprosthetic valves are favored due to the higher risk of anticoagulation complications in this population.

  • Risk of thrombogenicity: Mechanical valves have a high risk of thrombogenicity and patients who receive these valves require lifelong anticoagulation, thus making such valves unsuitable for anyone with contraindications to anticoagulation. Bioprosthetic valves are used in clinical scenarios where warfarin is contraindicated or if the patient is at a higher risk of bleeding.

  • Compliance with regular internation normalized ratio (INR) monitoring: Consistent INR monitoring is required in patients receiving warfarin therapy for a mechanical valve.

  • Other indications for long-term anticoagulation: Consider using mechanical valves in patients with a high risk of thromboembolism who many benefit from anticoagulation (eg, atrial fibrillation).

  • Specific anatomic considerations: For example, a valve-in-valve procedure is relatively contraindicated in individuals with a small aortic root size.

  • Patient preference: Religious values, lifestyle choices, inconvenience of long-term anticoagulation, and/or the risk of reintervention may influence a patient's preference of the valve type.

ACC/AHA recommendations for selection of a prosthetic aortic valve include the following[12] :

  • A mechanical prosthesis is recommended for aortic valve replacement (AVR) in patients with a mechanical valve in the mitral or tricuspid position (class I).

  • A bioprosthesis is recommended for AVR in patients of any age who will not take warfarin or who have major medical contraindications to warfarin therapy (class I).

  • A bioprosthesis is reasonable for AVR in patients aged 70 years or older who do not have risk factors for thromboembolism (class IIa).

  • AV re-replacement with a homograft is reasonable for patients with active prosthetic valve endocarditis (class IIa).

  • A bioprosthesis might be considered for AVR in a woman of childbearing age (class IIb).

  • A mechanical prosthesis is reasonable in younger patients (age < 50 y) with no contraindications to anticoagulation therapy (class IIa).

ACC/AHA recommendations for selection of a prosthetic mitral valve include the following[12] :

  • A mechanical prosthesis is recommended for mitral valve replacement (MVR) in patients with a mechanical valve in the mitral or tricuspid position (class I).

  • A mechanical prosthesis is reasonable for MVR in patients younger than 50 years who have long-standing atrial fibrillation (class IIa).

  • A bioprosthesis is reasonable for MVR in patients aged 65 years or older (class IIa).

Clinical Trial Evidence for Bioprosthetic Valves

In a Veterans Affairs (VA) study comparing bioprosthetic valves with mechanical valves, all-cause mortality at 15 years after aortic valve replacement (AVR) was lower in patients who received a mechanical valve than in those who received a bioprosthetic valve (66% vs 79%, respectively).[13] In the study, 575 patients at 13 VA medical centers undergoing single AVR (n = 394) or single mitral valve replacement (MVR) (n = 181) were randomized to receive a Hancock porcine valve or a Bjork-Shiley spherical disc valve. Long-term survival and valve-related complications were compared. No significant difference in all-cause mortality was seen between the two MVR valve type groups.[13]

There was a higher reoperation rate after AVR with the bioprosthetic valve than with the mechanical valve (29 ± 5% vs 10 ± 3%).[13] Valve-related deaths after AVR accounted for 41% of all deaths in the bioprosthetic group and 37% in the mechanical valve group; valve-related deaths after MVR were 57% of all deaths in the bioprosthetic group and 44% in the mechanical valve group. Primary valve failure was significantly greater with bioprosthetic valves for AVR (bioprosthetic vs mechanical, 23 ± 5% vs 0 ± 0%) and for MVR (44 ± 8% vs 5 ± 4%).[13]

Almost all the primary valve failures were in patients younger than 65 years (18 of 20 patients in the AVR group; 20 of 21 patients in the MVR group).[13] Bleeding occurred more frequently in patients with a mechanical valve than in those with a bioprosthesis (AVR, 51 ± 4% vs 30 ± 4%; MVR, 53 ± 7% vs 31 ± 6%). However, no statistically significant differences were seen between the two valve groups for systemic embolism, infective endocarditis, or valve thrombosis.[13]

Similar results were seen in an Edinburgh heart valve trial, in which 533 patients (AVR, n = 211; MVR, n = 261; double valve replacement, n = 61) were randomized to receive a Bjork-Shiley 60° spherical tilting disc valve (n = 267) or a porcine bioprosthesis (Hancock, n = 107; Carpentier-Edwards, n = 159).[14] Long-term survival at 20 years were not significantly different between the two valve groups (mechanical 25.0 ± 2.7%, porcine 22.6 ± 2.7%), but major bleeding was more common in the Bjork-Shiley group than in the bioprosthesis group (40.7 ± 5.4% vs 27.9 ± 8.4%, respectively). No significant differences were seen in major embolism or endocarditis.[14]

Pathophysiology

Valve failure

Primary valve failure, although rare, is an important complication in patients with prosthetic heart valves, and it is a major cause of morbidity and mortality. As noted earlier, bioprostheses are less thrombogenic than mechanical valves, but this advantage is balanced by their diminished durability when compared with mechanical valves. Although 30-35% of bioprostheses will fail within 10-15 years, it can be anticipated that most mechanical valves will remain functional for 20-30 years.

Bioprosthetic valve failure can be secondary to structural degeneration due to thickening, calcification, valve dehiscence/tearing/disruption, or it may develop from nonstructural causes such as patient-prosthesis mismatch, prosthesis malposition, paravalvular regurgitation, thrombosis, and pannus formation. It results in either obstruction or incompetence of the underlying valve, causing hemodynamic changes.

Due to the excellent durability of mechanical valves, structural valve deterioration is extremely rare; primary valve failure in patients who receive these valves may be secondary to suture line dehiscence, thrombus formation, or breakage or separation of the valve components. Acute valvular regurgitation or embolization of the valve fragments may also result.

When the mitral valve acutely fails, rapid left atrial (LA) volume overload causes increased LA pressure. Pulmonary venous congestion and, ultimately, pulmonary edema occur. Cardiac output is decreased because a portion of the left ventricular (LV) output is being regurgitated into the LA. The compensatory mechanism of increased sympathetic tone increases the heart rate and the systemic vascular resistance (SVR). This may worsen the situation by decreasing diastolic filling time and impeding LV outflow, thereby increasing the regurgitation.

Acute failure of a prosthetic aortic valve causes a rapidly progressive LV volume overload. Increased LV diastolic pressure results in pulmonary congestion and edema. The cardiac output is reduced substantially. The compensatory mechanism of an increased heart rate and a positive inotropic state, mediated by increased sympathetic tone, partly helps to maintain output. However, this is hampered by an increase in SVR, which impedes forward flow. Increased systolic wall tension causes a rise in myocardial oxygen consumption. Myocardial ischemia in acute aortic regurgitation may occur, even in the absence of coronary artery disease.

Biological prosthetic valves often degenerate slowly over time, become calcified, or suffer from thrombus formation. These events result in the slow progressive failure of the valve. The clinical presentation is usually that of gradually worsening congestive heart failure, with increasing dyspnea. Alternatively, patients may present with unstable angina or systemic embolization, or they may be entirely asymptomatic.

The first transcatheter aortic valve implantation (TAVI) device for use in the United States was approved in November 2011. Subsequently, not enough time has passed yet to gather data concerning longevity and use. Vascular complications and strokes related to the procedure are falling with improved delivery techniques and equipment. Complications related to the conduction system requiring permanent pacemaker implantation occur in 14% of patients. This risk is increased with the use of the CoreValve prosthesis.[15]

Prosthetic valve endocarditis

Even with antibiotic prophylaxis, the yearly incidence of prosthetic valve endocarditis (PVE) is around 0.5%. PVE occurring within 1 year of implantation (early PVE) is usually due to perioperative contamination or hematogenous spread.[16]  PVE occurring after 1 year (late PVE) is usually caused by hematogenous spread.

The pathologic hallmark of PVE in mechanical valves is ring abscesses. Ring abscesses may lead to valve dehiscence and perivalvular leakage. Local extension results in the formation of myocardial abscesses. Further extension to the conduction system often results in a new atrioventricular block. Valve stenosis and purulent pericarditis occur less frequently.

Bioprosthetic valve PVE usually causes leaflet tears or perforations. Valve stenosis is more common with bioprosthetic valves than with mechanical valves. Ring abscess, purulent pericarditis, and myocardial abscesses are much less frequent in bioprosthetic valve PVE.

Finally, glomerulonephritis, mycotic aneurysms, systemic embolization, and metastatic abscesses also may complicate PVE.

Prosthetic valve thrombosis

Prosthetic valve thrombosis is a major complication of mechanical heart valves although the newer generation valves have lower thrombogenic risks. Bioprosthetic heart valve thrombosis although rare, if present, is usually seen within 3 months of placement of the valve and requires anticoagulation for that time period (time period required for appropriate endothelization). The pathophysiology involves increased thrombogenicity of the valve material, interaction between the prosthesis material and the suture zone, localized regions of turbulent flow, and location of the valve itself. For example, tricuspid mechanical prostheses are known to be more thrombogenic than others. Low cardiac output can favor thrombosis and other factors such as subtherapeutic anticoagulation; other risk factors of thrombosis may contribute as well. Sometimes, overgrowth of granulation tissue, called pannus formation, can mimic prosthetic valve thrombosis; it is thought to be secondary to increased levels of cytokines, resulting in excess fibrosis and scar tissue formation at the periannular tissue.[2, 3, 4]

 

Etiology

Prosthetic valve endocarditis (PVE) has been divided into two subcategories. These reflect differences in clinical features, microbial patterns, and mortality. Early PVE occurs within the first year of valve insertion, whereas late PVE occurs after the first year.

Early PVE is usually the result of perioperative contamination. Causative organisms include Staphylococcus epidermidis (25-30%), Staphylococcus aureus (15-20%), gram-negative aerobes (20%), fungi (10-12%), streptococci (5-10%), and diphtheroids (8-10%).

Late PVE is usually the result of transient bacteremia from dental or genitourinary sources, gastrointestinal manipulation, or intravenous drug abuse. The causative organisms are similar to those that cause native valve endocarditis, includinf Streptococcus viridans (25-30%), S epidermidis (23-38%), S aureus (10-12%), gram-negative bacilli (10-12%), group D streptococci (10-12%), fungi (5-8%), and diphtheroids (4-5%). An increase in cases of PVE due to methicillin-resistant S aureus (MRSA) has been observed.

Multiple negative blood culture results are unusual with common pathogens, but they are seen more commonly with infections by the Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae (HACEK) group; Serratia and Rickettsia species; as well as Aspergillus, Histoplasma, and Candida species.

Rarely, Brucella can cause PVE.[17]

Epidemiology

Prosthetic valve thrombosis is more common in mechanical valves. With proper anticoagulation, the rate of thrombosis in all valves is within the range of 0.1-5.7% per patient-year. Caged ball valves have the highest rate of thromboembolic complications, whereas bileaflet valves have the lowest. Valve thrombosis is increased with valves in the mitral position and in patients with subtherapeutic anticoagulation; it is also known to be increased in tricuspid mechanical protheses relative to left-side mechanical valves.

Anticoagulant-related hemorrhagic complications of mechanical valves include major hemorrhage in 1-3% of patients per year and minor hemorrhage in 4-8% of patients per year.

Low-grade hemolytic anemia occurs in 70% of prosthetic heart valve recipients, and severe hemolytic anemia occurs in 3%. The incidence is increased with caged ball valves and in those with perivalvular leaks.

Primary valve failure occurs in 3-4% of patients with bioprostheses within 5 years of implantation and in up to 35% of patients within 15 years. Mechanical valves have a much lower incidence of primary failure.

Prosthetic valve endocarditis (PVE) occurs in 2-4% of patients. The incidence is 3% in the first postoperative year, then 0.5% for subsequent years. The incidence is higher when valve surgery is performed in patients with active native valve endocarditis, and it is higher in mitral valves. Mechanical and biological valves are equally susceptible to early PVE, but the incidence of late PVE is higher for bioprostheses. Despite improvements in surgical techniques, no appreciable change in the incidence has been observed.[18]

Age

In children, bioprostheses rapidly calcify and, therefore, undergo rapid degeneration and valve dysfunction. The incidence of bioprosthetic failure is much higher in patients younger than 40 years. The incidence of having any prosthetic valve complication decreases with age.

Prognosis

In a retrospective cohort analysis of 4253 patients who underwent primary isolated aortic-valve replacement, 15-year survival and stroke rates were equivalent with bioprosthetic and mechanical valves.[1, 19]  For bioprosthetic valves, the risk of repeat surgery was greater, but the incidence of major bleeding was lower.

In propensity-matched comparisons, actuarial 15-year mortality was 60.6% with the bioprosthetic aortic valve and 62.1% with the mechanical valve.[1, 19]  Cumulative 15-year stroke rates were 7.7% and 8.6% in the two groups, respectively. Reoperation was 12.1% in the bioprosthetic valve group at 15 years and 6.9% in the mechanical valve group, whereas major bleeding occurred in 6.6% of bioprosthesis patients and in 13.0% of the mechanical-valve group.[1, 19]

Morbidity/mortality

Acute failure of a prosthetic aortic valve usually leads to sudden or near-sudden death. Prompt recognition and treatment of acute prosthetic mitral valve failure can be lifesaving.[16]

Prosthetic valve endocarditis (PVE) has an overall mortality of 50%. In early PVE, it is 74%, whereas in late PVE, mortality is 43%. With a fungal etiology, mortality is 93%; mortality for staphylococcal infections is 86%. PVE due to Staphylococcus has a 25-40% mortality.[16, 18]

Fatal anticoagulant-induced hemorrhage occurs in 0.5% of patients per year.

Complications

Complications of prosthetic valves include primary valve failure, PVE, prosthetic valve thrombosis, thromboembolism, and mechanical hemolytic anemia. In addition, anticoagulant-related hemorrhage may occur.

Primary valve failure may occur abruptly from the tearing or breakage of components, or from a thrombus suddenly impinging on leaflet mobility. More commonly, valve failure presents gradually from calcifications or thrombus formation. Bioprostheses are less thrombogenic than mechanical valves, but this advantage is balanced by their diminished durability when compared with mechanical valves. Primary valve failure occurs in 3-4% of patients with bioprostheses within 5 years of implantation and in up to 35% of patients within 15 years. In contrast, it is anticipated that most mechanical valves will remain functional for 20-30 years.

When the mitral valve fails acutely, rapid left atrial (LA) volume overload causes increased LA pressure. Pulmonary venous congestion and, ultimately, pulmonary edema ensue. Cardiac output is decreased because a portion of the left ventricular (LV) output is regurgitated into the LA. The compensatory mechanism of increased sympathetic tone increases the heart rate and the systemic vascular resistance (SVR), which may worsen the situation by decreasing diastolic filling time and impeding LV outflow, thereby increasing the regurgitation.

Acute failure of a prosthetic aortic valve causes a rapidly progressive LV volume overload. Increased LV diastolic pressure results in pulmonary congestion and edema. The cardiac output is reduced substantially. The compensatory mechanism of an increased heart rate and a positive inotropic state, mediated by increased sympathetic tone, partly helps to maintain output. However, this is hampered by an increase in SVR, which impedes forward flow. Increased systolic wall tension causes a rise in myocardial oxygen consumption. Myocardial ischemia may follow acute aortic regurgitation, even in the absence of coronary artery disease.

Stenosis or incompetence of prosthetic valves may develop as a result of a tear or perforation of the valve cusp, valvular thrombosis, pannus formation, valve calcification, or stiffening of the leaflets.

PVE occurs in 2-4% of patients. The incidence is 3% in the first postoperative year, then 0.5% for subsequent years, and it is higher in mitral valves. Mechanical and biological valves are equally susceptible. PVE occurring within 60 days of implantation (early PVE) is usually due to perioperative contamination or hematogenous spread. PVE occurring after 60 days (late PVE) is usually caused by hematogenous spread. Glomerulonephritis, congestive heart failure, mycotic aneurysms, and metastatic abscesses may complicate PVE.

Bioprosthetic valve endocarditis usually causes leaflet tears or perforations. Valve stenosis is more common with bioprosthetic valves than with mechanical valves. Ring abscess, purulent pericarditis, and myocardial abscesses are much less frequent in bioprosthetic valve endocarditis.

 

Presentation

History

In patients with malfunctioning prosthetic heart valves, symptoms are dependent on the type of valve, its location, and the nature of the complication. With valvular breakage or dehiscence, failure often occurs acutely with rapid hemodynamic deterioration. Failure occurs more gradually with valve thrombosis, calcification, or degeneration.

Note the following:

  • Information about the type of valve is important; the potential for complications depends on valve type and position. Sources include a wallet-sized identification card (typically given to the patient at the time of surgery) and/or a review of the patient's medical records.

  • Review of the operative report may be useful. If the native valve annulus is described as being heavily calcified or infected, the chance of a perivalvular leak is greater.

  • Patients with acute prosthetic valve failure often present in extremis, with sudden onset of dyspnea, syncope, or precordial pain.

  • Patients with acute aortic valve failure often experience sudden death. Survivors have acute severe dyspnea, sometimes accompanied by precordial pain, or syncope.

  • Patients with subacute valvular failure present with symptoms of gradually worsening congestive heart failure. This includes increasing dyspnea with exertion, orthopnea, paroxysmal nocturnal dyspnea, and fatigue. They also may present with unstable angina or, at times, be entirely asymptomatic.

  • Patients with embolic complications have symptoms related to the site of the embolization. Stroke syndromes are the most common presentation, although patients may present with myocardial infarction, sudden death, or symptoms of visceral or peripheral embolization.

  • Symptoms due to anticoagulant-related hemorrhage are related to the site of the hemorrhage.

  • A history of fever should raise clinical suspicion of the possibility of prosthetic valve endocarditis: Be alert to fever, chills, fatigue, malaise, night sweats, signs and symptoms of heart failure, dyspnea, cough, pleuritic chest pain, new or changed heart murmur on auscultation, splenomegaly, septic shock or primary valvular failure, and/or septic emboli.

  • Hemolysis secondary to prosthetic valve: Note symptoms secondary to anemia and/or thrombocytopenia, such as pallor, dyspnea, bleeding and petechiae.

Physical Examination

Normal prosthetic heart valve sounds

Mechanical valves

Tilting disc and bileaflet valves have a loud, high-frequency, metallic closing sound. This frequently can be heard without a stethoscope. Absence of this distinct closing sound is abnormal and implies valve dysfunction. These valves may also have a soft opening sound.

Caged ball valves (Starr-Edwards) have low-frequency opening and closing sounds of nearly equal intensity.

Tissue valves

Closing sounds of tissue valves are similar to those of native valves. A low-frequency early opening sound may present in the mitral position.

Valve failure/thrombosis

Muffled or absent normal prosthetic heart sounds may be a clue to valve failure or thrombosis.

Prosthetic heart valve murmurs

Aortic prosthetic valves

Because of their smaller orifice size, all aortic valves often produce some degree of outflow obstruction with a resultant systolic ejection murmur. Caged ball and small porcine valves produce the loudest murmurs. The intensity of the murmur increases with rising cardiac output.

Tilting disc valves and bileaflet valves do not occlude their outflow tract completely when closed, allowing some back flow. This causes a low-intensity diastolic murmur. Suspect prosthetic aortic valve failure in a patient with a greater than 2/6 diastolic murmur.

Caged ball and tissue valves cause no diastolic murmur because they completely occlude their outflow tract in the closed position. Consider any degree of diastolic murmur in these patients pathologic until proven otherwise.

Mitral prosthetic valves

Caged ball valves may cause a low-grade systolic murmur due to the turbulent flow caused by the cage projecting into the left ventricle. Consider any holosystolic murmur greater than 2/6 pathologic in a patient with an artificial mitral valve. Short diastolic murmurs may be heard with bioprostheses and, occasionally, with the St. Jude bileaflet valve. These are best heard at the apex with the patient in the left lateral decubitus position.

Acute valvular failure

Patients with acute valvular failure present with cardiogenic shock and severe hypotension. Note the following:

  • Evidence of poor tissue perfusion is present, including diminished peripheral pulses, cool or mottled extremities, confusion or unresponsiveness, and decreased urine output.

  • A hyperdynamic precordium and right ventricular impulse is present in 50% of patients with acute valvular failure.

  • Absence of a normal valve closure sound or the presence of an abnormal regurgitant murmur is an important clue to the presence of prosthetic valvular failure.

Subacute valvular failure

Patients with subacute valvular failure often present with signs of gradually worsening left-sided congestive heart failure, including the following:

  • Rales and jugular venous distention may be present.

  • Signs of right-sided failure, including hepatic congestion and lower extremity edema, may also be present.

  • Patients with subacute valvular failure may present with a new regurgitant murmur or absence of normal closing sounds.

  • A new or worsening hemolytic anemia may be the only presenting abnormality in patients with subacute valvular failure.

Prosthetic valve endocarditis (PVE) manifestations

The clinical manifestations of PVE are often obscure. Note the following:

  • Fever occurs in 97% of patients with PVE.

  • A new or changing murmur is present in 56% of patients. Absence of a murmur does not exclude the diagnosis. Valvular dehiscence, stenosis, or perforation causes the murmur. They may not occur early in the course of the illness.

  • Signs considered classic for native valve endocarditis, including petechiae, Roth spots, Osler nodes, and Janeway lesions, are often absent in PVE.

  • Splenomegaly supports the diagnosis of PVE, but it is present in only 26% of early PVE cases and in 44% of late PVE cases.

  • PVE may present as congestive heart failure, septic shock, or primary valvular failure.

  • Systemic emboli may be the presenting symptom in 7-33% of cases of PVE. This is more common with fungal etiologies.

Thromboembolic complications

Patients with complications related to embolization present with signs related to the site of embolization. Stroke syndromes are the most common; however, patients may present with myocardial infarction, sudden death, or visceral or peripheral embolization. Systemic embolization should alert the clinician to suspect valve thrombosis or PVE.

Anticoagulant-related hemorrhage: Signs due to anticoagulant-related hemorrhage depend on the site of hemorrhage.[20, 21]

 

DDx

Diagnostic Considerations

Other conditions to consider in patients with prosthetic heart valves include the following:

  • Hemolytic anemia

  • Thromboembolic disease

  • Cardiac conduction disturbances

Prepare patients with acute primary valve failure and severe hemodynamic compromise for surgery as quickly as possible. Delays in surgery to pursue diagnostic testing result in increased mortality.

Consider prosthetic valve endocarditis (PVE) in any patient with a prosthetic valve and a fever.

Pregnancy

Women with mechanical heart valves are considered very high risk for maternal mortality and morbidity in the setting of pregnancy, even classified by the World Health Organization as risk category III. One should consider a preconception transthoracic echocardiogram (TTE) to assess valvular function, ventricular function, and pulmonary artery pressures. If abnormalities are found, then preconception interventions may be beneficial to reduce risks during pregnancy.[12]

Pregnant women are at higher risk of valvular thrombosis due to being in a hypercoagulable state. It is important to discuss with the patient the risks and benefits of the anticoagulation strategies in pregnancy to determine the best strategy moving forward.[12]

For women with mechanical prosthetic valves, anticoagulation is recommended with frequent monitoring throughout the pregnancy. If therapeutic anticoagulation cannot be achieved or maintained, these women should be counseled against pregnancy. Vitamin K antagonists (VKAs), such as warfarin, are associated with the lowest maternal complications but the highest risk of miscarriage, fetal death, and congenital abnormalities, particularly when taken during the first trimester. Although low molecular-weight heparin (LMWH) is not teratogenic, it is associated with an increased risk of maternal thrombotic events.[12]

There is no perfect strategy for anticoagulation in pregnant women with mechanical prosthetic valves. The therapy strategies are as follows: continue warfarin throughout the pregnancy, switch to LMWH and use throughout the pregnancy, or use LMWH during the first trimester and warfarin during the second and third trimesters.[12]

At least 1 week before planned delivery, pregnant women on a VKA should be switched to twice daily dosing of LMWH or intravenous unfractionated heparin (UFH). Pregnant women should be switched off LMWH to UFH 36 hours before planned vaginal delivery. UFH should be stopped at least 6 hours prior to vaginal delivery. If labor occurs while the woman is therapeutic on a VKA, reversal of VKA prior to cesarean delivery is important.[12]

Differential Diagnoses

 

Workup

Approach Considerations

 

 

Laboratory Studies

Complete blood cell count

Hemolysis may cause anemia; in this case, microscopic evidence of hemolysis should be present. A sudden increase in hemolysis may signal a perivalvular leak.[22]

A hematocrit lower than 34% is present in 74% of patients with prosthetic valve endocarditis (PVE); this is the most common hematologic finding.

A white blood cell (WBC) count lower than 12,000/μL is present in as many as 54% of patients with PVE.

Blood urea nitrogen/creatinine levels

Glomerulonephritis and acute renal failure may complicate PVE.

Urinalysis

Hematuria is present in 57% of patients with PVE.

Blood cultures

Multiple blood cultures should be taken, and they should be held for 3 weeks. Blood culture results are positive in multiple samples in 97% of patients with PVE.

Prothrombin time (PT)/international normalized ratio (INR)

Recommendations vary regarding the target INR. The following information is offered as a general guideline, but remember that therapy must be individualized.

Bioprosthetic valves

INR of 2-3 for 3 months following implantation; anticoagulation may then be discontinued unless the patient has another indication, such as atrial fibrillation or the development of prosthetic valve thrombosis.

Mechanical valves

Aortic valve INR is 2-3; mitral valve INR is 2.5-3.5. Patients with atrial fibrillation should be kept at the higher end of these ranges.[4] In patients with low hemorrhage risk, low-dose aspirin is recommended in addition to warfarin.[4]

Nontherapeutic values should raise the suspicion of valve thrombosis or systemic embolization.

Procedures

Certain procedures may cause bacteremia and thereby raise the risk of prosthetic valve endocarditis (PVE). Emergency physicians and other clinicians must be up to date with the latest prophylaxis guidelines. See Prevention.

Chest Radiography

An overpenetrated anteroposterior chest radiograph helps to delineate the valvular morphology and whether or not the valve and occluder are intact. In more clinically stable patients, a lateral chest film helps identify the valve position and type.

The following sections contain descriptions of the radiographic appearance of the more commonly seen valves.

Starr-Edwards caged ball valve

The base ring is radiopaque, as is the cage.

There are three struts for the aortic valve, and there are four struts for the mitral or tricuspid valve

The silastic ball is impregnated with barium that is mildly radiopaque (but not in all models).

Bjork-Shiley tilting disc valve

Although the Bjork-Shiley tilting disc valve has been discontinued, many patients still have these valves implanted.

The base ring and struts are radiopaque. Two U-shaped struts project into the base ring.

The edge of the occluder disc is also radiopaque.

Medtronic-Hall tilting disc valve

The base ring is radiopaque.

Three small radiopaque struts and one large hook-shaped strut project into the base ring.

The occluder disc is mildly opaque, but it often cannot be seen.

Alliance Monostrut valve

The occluder has a radiopaque rim; the base ring and two struts are radiopaque.

St. Jude medical bileaflet valve

The mildly radiopaque leaflets are best seen when viewed on end. They appear as radiopaque lines when the leaflets are fully open.

The base ring is not visualized on most models. The valve may not be visualized on some radiographs.

CarboMedics bileaflet valve

The valve housing and leaflets are radiopaque and easily visible.

Carpentier-Edwards porcine valve

The tall serpiginous wire support is the only visualized portion.

Hancock porcine valve

The radiopaque base ring is the only visible part in some models.

Other models have radiopaque stent markers with or without a visible base ring.

Ionescu-Shiley bovine pericardial valve

The base ring and wide fenestrated stents are one piece.

Echocardiography

Two-dimensional (2D) transthoracic echocardiography (TTE) is the examination of choice as a first-line imaging study when assessing prosthetic heart valves.[11] Its ease of use and ability to assess ventricular function and size as well as pulmonary pressures make it an effective first-line imaging study. TTE is also the image of choice when assessing valvular abnormalities with Doppler signal recordings; it is able to demonstrate perivalvular leaks, vegetations, and inadequate valve/occluder movement. TTE with Doppler can also detect the presence of acute valvular regurgitation and grade its severity.

Drawbacks with TTE include limited windows, which can be further affected by body habitus, dependency on angles for Doppler accuracy, and acoustic shadowing from the prosthetic valve.[23]  Acoustic shadowing originating from the components of the prosthetic valve can severely limit the image of the valve itself as well as any pathologic process such as regurgitant streams, vegetations, and thrombosis. This is especially true with valves in the mitral position.

Transesophageal echocardiography (TEE) has emerged as the imaging study of choice to further evaluate a patient with prosthetic heart valves after initial assessment with TTE, particularly when there is a suspicion for prosthetic valve complications. Its advantages relative to TTEs include higher resolution, better visualization of the atrial side of prosthetic mitral valves and the posterior aspect of the prosthetic aortic valve, and better evaluation of any periannular complications. TEE has similar drawbacks as TTE, with imaging limited by acoustic shadowing of the prosthetic valve and dependency on angles for Doppler accuracy.[23]

Cinefluorography

Cinefluorography is an easy and noninvasive imaging study that uses fluoroscopy to evaluate mechanical prosthetic heart valves. Its ease of use paired with its ability to evaluate prosthetic heart valves function and to detect calcium on the leaflets make it another imaging study that can be used in prosthetic valve assessment. What cinefluorography fails to do is provide any assessment on hemodynamics as well as the etiologies for the prosthetic valve dysfunction.[23]

Electrocardiography

An atrioventricular (AV) block may indicate the presence of a myocardial abscess. A fever and new AV block is considered prosthetic valve endocarditis (PVE) until proven otherwise.

AV block may also complicate transcatheter aortic valve implantation (TAVI), although this usually occurs early in the postoperative period.

Atrial fibrillation is common in mitral valve replacement and may cause hemodynamic compromise.

Computed Tomography Scanning

In the current era of transcatheter device therapy, the prevalence of prosthetic aortic valves and their associated complications is increasing.

Although echocardiography remains the first-line imaging investigation for the assessment of prosthetic valve complications, it often fails to identify the underlying mechanism of prosthesis failure. Cardiac computed tomography (CT) scanning provides better anatomical delineation and excellent isotropic spatial resolution but no hemodynamic assessment. 

Cardiac CT scanning, although not typically used for routine evaluation of prosthetic valves, can provide information when valvular dysfunction or other complications are suspected. Unlike transthoracic echocardiography (TTE), it is not limited by body habitus and has excellent spatial imaging. It is great for aortic pathologies, has a high sensitivity to detect calcifications, and allows for the detection and differentiation of thrombi. Limitations of the cardiac CT scan include radiation exposure, contrast exposure, and disrupted images from metallic artifacts. Patients with renal disease or contrast allergies are typically unable to have this study.[23]

Relatively recently, cardiac CT imaging has emerged as an imaging technique capable of providing high isotropic spatial resolution of the prosthetic valve, and its utility can provide important complementary diagnostic information. Retrospective gating may be used to visualize leaflet excursion throughout the cardiac cycle. Valvular and nonvalvular complications can be readily assessed (eg, pseudoaneurysm, valvular thrombus, pannus formations, patient prosthesis mismatch, valve dysfunction). Moreover, differentiation of pannus versus thrombus can be discriminated by Hounsfield units (HU), with a thrombus having less than 90 HU and a pannus having over 145 HU.[24]

Magnetic Resonance Imaging

Cardiac magnetic resonance imaging (CMRI) can be used in patients with prosthetic heart valves when trying to rule out concomitant aortic pathology. It allows for visualization of the aortic valve even without contrast medium. There is no radiation associated with this study, and it allows for better characterization of the myocardium as well as for volumetric and flow assessments. There remain limited data on its use in assessing prosthetic valves, however, and imaging can be hampered by artifacts from metallic objects.[23]

CMRI in the evaluation of valvular prosthesis is limited. The data are not as comprehensive as that of echocardiography and cardiac computed tomography scanning. The presence of a metallic stent scaffold and metallic leaflets limit leaflet visualization due to susceptibility artifact.

Quantitative assessment of regurgitation by phase velocity mapping can offer another layer of assessment in addition to that of echocardiography. Recent guidelines identify specific indications for appropriate use of CMRI in evaluation of patients. CMRI is a class I indication for patients with moderate to severe aortic regurgitation who have poor echocardiographic images for left ventricular function, volume, and severity assessment. Remodeling secondary to chronic valve dysfunction can be assessed via chamber size, function, and myocardial tissue characterization.[23]

Nuclear Imaging

Nuclear imaging modalities are not often used for assessing prosthetic valves as data are limited for their use except in the setting of infective endocarditis. Positron emission tomography (PET) scanning using fluorodeoxyglucose (FDG) uptake can suggest infectious or metabolic activity.[23]

 

Treatment

Approach Considerations

In patients with acute valvular failure, diagnostic studies must be performed simultaneously with resuscitative efforts.

Initiate arrangements for transfer to a center with cardiac surgical capabilities in patients presenting with moderate-to-severe hemodynamic compromise if these services are not readily available.

Mortality in patients with acute prosthetic valvular failure is directly related to delay of surgical correction.

Emergency Department Care

Primary valve failure

Patients with valvular failure due to breakage or abrupt tearing of the components usually present with acute hemodynamic deterioration. These patients require emergent valve replacement. Adjunctive therapy may be initiated while such arrangements are being made. A less dramatic presentation of valvular failure may be seen in patients with valve thrombosis or in those with more gradual deterioration of bioprosthetic valves (see "Thromboembolic complications," below).

Depending on which prosthetic valve has failed will determine which treatment strategy to pursue. Inotropes are helpful in the setting of depressed left ventricular ejection fraction or right ventricular dysfunction in the setting of left-sided acute valve failure. Dobutamine can be used for inotropic properties, but keep in mind there is an increased risk of arrhythmias. Norepinephrine can also be used for hemodynamic support and has some inotropic properties as well; however, it comes with the drawback of increasing afterload. In all left-sided valve failures, afterload reduction can be achieved medically with nitroprusside.[25]  Begin afterload reduction and inotropic support to reduce the impedance to forward flow and improve peripheral perfusion. If the mean arterial pressure is higher than 70 mmHg, sodium nitroprusside may be used. If the mean arterial pressure is lower than 70 mmHg, inotropes may be used.

Avoid inotropic agents with vasoconstricting properties.

Intra-aortic balloon pumps are particularly helpful in the setting of acute mitral regurgitation and can mechanically assist with afterload reduction. These devices can also be used for afterload reduction in aortic stenosis. Note that intra-aortic balloon pumps are contraindicated in the setting of aortic regurgitation.[25]

Prosthetic valve endocarditis

The standard to diagnose infective endocarditis relies on the Modified Duke Criteria, which incorporates clinical, imaging, and bacteriological criteria.[12]

Administer intravenous antibiotics as soon as two sets of blood cultures are drawn. Vancomycin and gentamicin may be used empirically pending blood culture results and the determination of methicillin resistance.

Patients taking a vitamin K antagonist (VKA), such as warfarin, who develop prosthetic valve endocarditis (PVE) should stop taking the VKA until central nervous system (CNS) involvement is ruled out and invasive procedures are determined to be unnecessary.[4]

Consider anticoagulation in PVE, as the incidence of systemic embolization is as high as 40%.

Consider emergency surgery in patients with moderate-to-severe heart failure or in patients with an unstable prosthesis noted on echocardiography or fluoroscopy.

Thromboembolic complications

Patients presenting with embolization need to be anticoagulated if they are not already taking anticoagulants or have a subtherapeutic international normalized ratio (INR). It is important to document the type of anticoagulant therapy used and the duration on treatment spent in the therapeutic range. It is also important to rule out other potential causes of embolization, such as infective endocarditis, new-onset atrial fibrillation, and excluding other hypercoagulable states, if clinically suspicious.[12]

Assessment of valve function is needed when prosthetic thrombosis is suspected. Urgent evaluations with transthoracic echocardiography (TTE), transesophageal echocardiography (TEE), fluoroscopy, cardiac computed tomography (CT) scanning, or cardiac magnetic resonance imaging (CMRI) is necessary to assess valve function, leaflet motion, and the presence of the thrombosis as well as its extent.[12]

The RE-ALIGN trial (Randomized, Phase II Study to Evaluate the Safety and Pharmacokinetics of Oral Dabigatran Etexilate in Patients after Heart Valve Replacement) evaluated the safety and efficacy of dabigatran in patients with bileaflet mechanical prosthetic heart valves (recently implanted or implanted >3 months prior to enrollment) who were randomized to dose-adjusted warfarin or dabigatran 150, 220, or 300 mg twice daily. The study was terminated early due to the occurrence of significantly more thromboembolic events and excessive major bleeding with dabigatran compared with warfarin. These data resulted in revision of the US dabigatran prescribing information to include a contraindication in patients with mechanical prosthetic valves.[26]

Prosthetic valve thrombosis

Note the following:

  • Surgery had historically been the mainstay of treatment of prosthetic valve thrombosis, but it is associated with a high mortality rate.

  • Mortality of 18% has been reported in those with New York Heart Association (NYHA) class IV undergoing surgery for left-sided prosthetic valve thrombosis.

  • Thrombolytic therapy may be used to treat select patients with thrombosed prosthetic valves.

  • Thrombolytic therapy is currently recommended over surgery for right-sided prosthetic valve thrombosis.[4]

  • Thrombolytic therapy is recommended over surgery for small left-sided prosthetic valve thrombosis (thrombus area < 0.8 cm2). The use of heparin and serial echocardiography is also recommended in these cases to documents improvement and thrombus resolution.[4]

  • Thrombolytic therapy is recommended in large (=0.8 cm2) left-sided prosthetic valve thrombosis when contraindications to surgery are present.[4]

  • Contraindications to thrombolysis of left-sided prosthetic valve thrombosis include the presence of a large left atrial thrombus, ischemic CVA between 4 hours and 4-6 weeks ago, and very early postoperative state (< 4 d).[27]

  • Thrombolytic therapy should always be done in conjunction with cardiovascular surgical consultation.

  • Patients with major anticoagulant-related hemorrhage require reversal of their anticoagulation with fresh frozen plasma and vitamin K.

  • The time off anticoagulants should be as short as possible to avoid valve thrombosis.

  • Recombinant factor VIIa or prothrombin complex concentrate should not be used to reverse excessive anticoagulation in patients with prosthetic heart valves.

Based on findings from a retrospective study of 778 patients, Yaffee et al recommend extending established guidelines for blood conservation strategy (BCS) in routine cardiac surgeries to aortic valve replacement.[28, 29] The investigators reported that implementing BCS (eg, limits on intraoperative hemodilution, tolerance of perioperative anemia, blood management education of the cardiac surgery team) may reduce the use of red blood cells (RBCs) during surgery—without increasing mortality or morbidity.[28, 29]

In their study, implementation of the strategy resulted in a 2.7-fold reduction in RBC transfusions as well as a 1.7-fold reduction in the incidence of major complications (eg, sepsis, respiratory failure, renal failure, death).[28, 29] The incidence of RBC transfusion fell significantly from 82.9% before use of BCS to 68.0% after implementation of the strategy.

Transfusion of 2 or more units of RBC on the day of surgery was associated with mortality, prolonged intubation, postoperative renal failure, and an increased incidence of any complication. Factors that affected the risk of RBC transfusion included the following[28, 29] :

  • Decreased risk: Isolated aortic valve replacement, minimally invasive approach, BCS

  • Increased risk: Older age, previous cardiac procedure, female sex, smaller body surface area

Consultations

In patients presenting with any degree of prosthetic valvular failure, early consultation with a cardiologist is recommended to perform and interpret a echocardiography.

Consult a cardiothoracic surgeon early in cases of severe hemodynamic compromise.

Prevention

Provide antibiotic prophylaxis to patients undergoing procedures that may result in bacteremia. The following list, although not exhaustive, includes most inpatient and outpatient procedures performed in the emergency department that may result in bacteremia and, therefore, may lead to prosthetic valve endocarditis (PVE)[30] :

  • Dental and oral procedures

  • Respiratory procedures, particularly those which involve disruption of the respiratory mucosal surface, or when a known infection is present. If a known infection caused by Staphylococcus aureus is present, prophylaxis with an anti-staphylococcal penicillin, cephalosporin, or vancomycin should be given. In cases of known or suspected methicillin-resistant S aureus (MRSA), prophylaxis with vancomycin should be given.

  • Sclerotherapy of bleeding esophageal varices

  • Routine prophylaxis for gastrointestinal or genitourinary procedures is no longer recommended, unless in the presence of a known infection[31] : Urethral catheterization in the presence of a suspected urinary tract infection; vaginal delivery in the presence of infection

  • Incision and drainage of infected tissues

  • For dental, oral, or upper respiratory tract procedures, use oral (PO) amoxicillin 2 g 30-60 minutes before the procedure. If the patient is unable to take PO medication, use intramuscular (IM) or intravenous (IV) ampicillin 2 g OR cefazolin 1 g IM/IV, OR ceftriaxone 1 g IM/IV 30-60 minutes before the procedure. For penicillin-allergic patients, use clindamycin 600 mg PO/IM/IV OR azithromycin 500 mg PO OR clarithromycin 500 mg PO OR cephalexin 2 g PO 30-60 minutes before the procedure. (These are all single-dose regimens.) Do not use cephalexin in patients with a documented significant allergy to penicillin unless there is documentation that the patient can tolerate cephalosporins.

  • Further guidelines on the prevention, diagnosis, and treatment of infective endocarditis are available from the American Heart Association and the European Society of Cardiology.[30, 32, 33]

Long-Term Monitoring

Following heart valve replacement, every patient should undergo a history, physical examination, and appropriate testing at the first postoperative visit (2-4 wk after hospital discharge). An echocardiographic examination should be performed at this time. Thereafter, follow-up visits are recommended annually, or earlier (with echocardiography) if new symptoms develop that are attributable to a potential valvular dysfunction. In patients with a bioprosthetic valve, annual echocardiograms may be considered after the first 5 years in the absence of any changes in clinical status.[12]

Patients with postoperative left ventricular dysfunction should be treated with standard therapy for systolic heart failure, even if improved or asymptomatic.[12]

Although the risk of thromboembolic events is lower in patients with a bioprosthetic valve than in those with a mechanical prosthesis, low-dose aspirin (75-100 mg/d) is indicated in patients without thromboembolic risk factors (eg, atrial fibrillation, previous thromboembolism, hypercoagulable condition). Although the risk of early embolic events is relatively low in patients treated with aspirin only, the addition of warfarin at hospital discharge reduces the incidence of early embolic events, but that benefit is balanced by an increased risk of repeat hospitalization for bleeding.[34] For patients with risk factors, warfarin is indicated to achieve an international normalized ratio (INR) of 2.0 to 3.0, whether after aortic valve replacement or mitral valve replacement. Alternatively, aspirin in a dose of 75-325 mg per day is indicated in patients who are unable to take warfarin.

All patients with prosthetic valves should receive antibiotic prophylaxis against infective endocarditis prior to dental procedures.

 

Guidelines

Valvular Heart Disease Clinical Practice Guidelines (ACC/AHA, 2021)

The American College of Cardiology (ACC) and American Heart Association (AHA) released their updated recommendations on managing valvular heart disease in December 2020.[12, 35]  Ten key messages are outlined below.

Top 10 Take-Home Messages

Valvular heart disease (VHD) stages (stages A-D) in patients should be classified based on symptoms, valve anatomy, severity of valve dysfunction, and response of the ventricle and pulmonary circulation.

When evaluating patients with VHD, findings from the history and physical examination (PE) should be correlated with those from noninvasive testing (ie, electrocardiography [ECG], chest x-ray, transthoracic echocardiography [TTE]). If conflict exists between results on the PE and that of initial noninvasive studies, consider obtaining further noninvasive (computed tomography [CT], cardiac magnetic resonance imaging [CMRI], stress testing) or invasive (transesophageal echocardiography [TEE], cardiac catherization) studies to decide the optimal treatment strategy.

In the setting of VHD and atrial fibrillation (AF) (except for patients with rheumatic mitral stenosis [MS] or a mechanical prosthesis), the decision to use oral anticoagulation with either a vitamin K antagonist (VKA) or a non-VKA anticoagulant to prevent thromboembolic events should be a shared decision-making process based on the CHA2DS2-VASc score (congestive heart failure [CHF], hypertension, age ≥75 years, diabetes mellitus, previous stroke/transient ischemic attack/thromboembolic event, vascular disease, age 65-74 years, sex). Oral anticoagulation with a VKA should be given to those with rheumatic MS or a mechanical prosthesis and AF.

All those with severe VHD under consideration for valve intervention should be evaluated by a multidisciplinary team, either with a referral or in consultation with a primary or comprehensive valve center.

Treatment of severe aortic stenosis (AS) with either a transcatheter or surgical valve prosthesis should be based primarily on symptoms or reduced ventricular systolic function. Consider earlier intervention if indicated by the results of exercise testing, biomarkers, rapid progression, or the presence of very severe stenosis.

Expanded indications for transcatheter aortic valve implantation (TAVI) are a result of findings from multiple randomized trials of TAVI versus surgical aortic valve replacement (SAVR). The selection of intervention type for patients with severe AS should be a shared decision-making process that considers the lifetime risks and benefits associated with the valve type (mechanical vs bioprosthetic) and approach type (transcatheter vs surgical).

Indications for intervention for valvular regurgitation are symptomatic relief and prevention of the irreversible long-term consequences of left ventricular volume overload. Lowered thresholds for intervention than they were previously are owing to more durable treatment options and lower procedural risks.

A mitral transcatheter edge-to-edge repair benefits patients with severely symptomatic primary mitral regurgitation (MR) who are at high or prohibitive surgical risk, as well as benefits a select subset of patients with secondary MR who remain severely symptomatic despite guideline-directed management and heart failure therapy.

Patients who present with severe symptomatic isolated tricuspid regurgitation, commonly associated with device leads and AF, may benefit from surgical intervention to reduce symptoms and recurrent hospitalizations if performed before the onset of severe right ventricular dysfunction or hepatic and renal end-organ damage.

Bioprosthetic valve dysfunction may occur because of either degeneration of the valve leaflets or valve thrombosis. Catheter-based treatment for prosthetic valve dysfunction is reasonable in selected patients for bioprosthetic leaflet degeneration or paravalvular leak in the absence of active infection.

For more information, please go to Aortic Stenosis, Aortic Regurgitation, Mitral Stenosis, Mitral Regurgitation, and Tricuspid Regurgitation.

 

Medication

Medication Summary

Antibiotics, vasodilators, inotropic agents, and anticoagulants are the therapeutic agents most commonly used in heart-valve complications.

Vasodilators

Class Summary

A significant portion of cardiac output is regurgitated through an incompetent valve in acute mitral or aortic valve failure. By increasing peripheral vascular resistance, catecholamines worsen this effect. Vasodilators reduce SVR, which may allow forward flow, improving cardiac output.

Nitroprusside (Nitropress)

Produces vasodilation and increases inotropic activity of the heart. Causes peripheral vasodilation by direct action on venous and arteriolar smooth muscle, reducing peripheral resistance. At higher dosages, may exacerbate myocardial ischemia by increasing heart rate.

Inotropic agents

Class Summary

These agents increase cardiac output. Agents used in the setting of acute valvular failure should not induce vasoconstriction, as this increases valve regurgitation.

Dobutamine (Dobutrex)

Produces vasodilation and increases inotropic state. At higher dosages, may cause increased heart rate, exacerbating myocardial ischemia. Synthetic direct-acting catecholamine and beta-receptor agonist. Compared with other sympathomimetic drugs, does not significantly increase myocardial oxygen demands, which is its major advantage compared with other direct-acting catecholamines.

Inamrinone (Inocor)

Formerly amrinone. Phosphodiesterase inhibitor with positive inotropic and vasodilator activity. Produces vasodilation and increases inotropic state. More likely to cause tachycardia than dobutamine and may exacerbate myocardial ischemia.

Anticoagulants

Class Summary

Patients receiving bioprosthetic valves should receive anticoagulants for 3 months. Lifelong anticoagulation is needed in patients with mechanical valves and in patients with atrial fibrillation. Any patients presenting with thromboembolic complications must be promptly anticoagulated if they do not have a therapeutic INR of 2.5-3.5.

Heparin

Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis.

Antibiotics

Class Summary

These agents are given to patients with prosthetic heart valves prior to performing procedures that may cause bacteremia (see Deterrence/Prevention).

Amoxicillin (Amoxil, Polymox, Trimox)

Derivative of ampicillin and has similar antibacterial spectrum, namely certain gram-positive and gram-negative organisms. Superior bioavailability and stability to gastric acid and has broader spectrum of activity than penicillin. Somewhat less active than that of penicillin against Streptococcus pneumococcus. Penicillin-resistant strains also resistant to amoxicillin, but higher doses may be effective. More effective against gram-negative organisms (eg, N meningitidis, H influenzae) than penicillin. Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria. DOC for prophylaxis in nonallergic patients undergoing dental, oral, or respiratory tract procedures. Patients must be able to take oral medications.

Ampicillin (Omnipen, Marcillin)

Broad-spectrum penicillin. Interferes with bacterial cell wall synthesis during active replication, causing bactericidal activity against susceptible organisms. Alternative to amoxicillin when unable to take medication orally.

For prophylaxis in patients undergoing dental, oral, or respiratory tract procedures. Coadministered with gentamicin for prophylaxis in GI or genitourinary procedures.

Azithromycin (Zithromax)

Acts by binding to 50S ribosomal subunit of susceptible microorganisms and blocks dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Nucleic acid synthesis is not affected. Concentrates in phagocytes and fibroblasts as demonstrated by in vitro incubation techniques. In vivo studies suggest that concentration in phagocytes may contribute to drug distribution to inflamed tissues. Treats mild-to-moderate microbial infections.

Plasma concentrations are very low, but tissue concentrations are much higher, giving it value in treating intracellular organisms. Has a long tissue half-life.

Used in penicillin-allergic patients undergoing dental, esophageal, and upper respiratory procedures.

Cefazolin (Ancef)

First-generation semisynthetic cephalosporin that by binding to 1 or more penicillin-binding proteins arrests bacterial cell wall synthesis and inhibits bacterial replication. Poor capacity to cross blood-brain barrier. Primarily active against skin flora, including S aureus. Typically used alone for skin and skin-structure coverage. Regimens for IV and IM dosing are similar. Primarily active against skin flora, including staphylococcal species.

Ceftriaxone (Rocephin)

Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Bactericidal activity results from inhibiting cell wall synthesis by binding to one or more penicillin-binding proteins. Exerts antimicrobial effect by interfering with synthesis of peptidoglycan, a major structural component of bacterial cell wall. Bacteria eventually lyse due to the ongoing activity of cell wall autolytic enzymes while cell wall assembly is arrested.

Highly stable in presence of beta-lactamases, both penicillinase and cephalosporinase, of gram-negative and gram-positive bacteria. Approximately 33-67% of dose excreted unchanged in urine, and remainder secreted in bile and ultimately in feces as microbiologically inactive compounds. Reversibly binds to human plasma proteins, and binding has been reported to decrease from 95% bound at plasma concentrations < 25 mcg/mL to 85% bound at 300 mcg/mL.

Cephalexin (Keflex)

First-generation cephalosporin that inhibits bacterial replication by inhibiting bacterial cell wall synthesis. Bactericidal and effective against rapidly growing organisms forming cell walls.

Resistance occurs by alteration of penicillin-binding proteins. Effective for treatment of infections caused by streptococcal or staphylococci, including penicillinase-producing staphylococci. May use to initiate therapy when streptococcal or staphylococcal infection is suspected.

Used orally when outpatient management is indicated.

Clarithromycin (Biaxin)

Semisynthetic macrolide antibiotic that reversibly binds to P site of 50S ribosomal subunit of susceptible organisms and may inhibit RNA-dependent protein synthesis by stimulating dissociation of peptidyl tRNA from ribosomes, causing bacterial growth inhibition.

Used in penicillin-allergic patients undergoing dental, esophageal, and upper respiratory procedures.

Clindamycin (Cleocin)

Inhibits bacterial growth. Widely distributes in the body without penetration of CNS. Protein bound and excreted by the liver and kidneys.

Used in penicillin-allergic patients undergoing dental, oral, or respiratory tract procedures. Useful for treatment against streptococcal and most staphylococcal infections.

Semisynthetic antibiotic produced by 7(S)-chloro-substitution of 7(R)-hydroxyl group of parent compound lincomycin. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Widely distributes in the body without penetration of CNS. Protein bound and excreted by the liver and kidneys.

Useful in penicillin-allergic patients who require antibiotic prophylaxis prior to dental, oral, gastrointestinal, or respiratory tract procedures.

Gentamicin

Aminoglycoside antibiotic for gram-negative coverage bacteria including Pseudomonas species. Synergistic with beta-lactamase against enterococci. Interferes with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits.

Dosing regimens are numerous and are adjusted based on CrCl and changes in volume of distribution, as well as body space into which agent needs to distribute. Dose of gentamicin may be given IV/IM. Each regimen must be followed by at least trough level drawn on third or fourth dose, 0.5 h before dosing; may draw peak level 0.5 h after 30-min infusion.

Vancomycin (Vancocin)

Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in the treatment of septicemia and skin structure infections. Indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or who have infections with resistant staphylococci. Use creatinine clearance to adjust dose in patients with renal impairment.