AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Implantation of prosthetic cardiac valves to treat hemodynamically significant valvular disease has become an increasingly common procedure. It is estimated that more than 60,000 patients per year are undergoing heart valve replacement in the United States. Replacement of diseased valves reduces the morbidity and mortality associated with native valvular disease but comes at the expense of risking complications unique to the implanted prosthetic device. These complications include primary valve failure, prosthetic valve endocarditis (PVE), prosthetic valve thrombosis (PVT), thromboembolism, anticoagulant-related hemorrhage, and mechanical hemolytic anemia.

Emergency physicians must be able to rapidly identify patients at risk and begin appropriate diagnostic testing, stabilization, and treatment. Even when promptly recognized and treated, acute prosthetic valve failure is associated with a high mortality rate.

More than 80 models of artificial valves have been introduced since 1950. In clinical emergency practice, however, it is necessary to be familiar with only a few. Prosthetic valves are either created from synthetic material (mechanical prosthesis) or fashioned from biological tissue (bioprosthesis).

Three main designs of mechanical valves exist: the caged ball valve, the tilting disc (single leaflet) valve, and the bileaflet valve. The only Food and Drug Administration (FDA)–approved caged ball valve is the Starr-Edwards valve. Tilting disc valve models include the Medtronic Hall valve, Omnicarbon (Medical CV) valves, Monostrut (Alliance Medical Technologies), and the discontinued Bjork-Shiley valves. Bileaflet valves include the St. Jude (St. Jude Medical), which is 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 (MCRI).

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). Pericardial valves include the Perimount series valves (Edwards LifeSciences). Ionescu-Shiley pericardial valves have been discontinued. More recently, stentless porcine valves have been used. They offer improved hemodynamics with a decreased transvalvular pressure gradient when compared with older stented models. These models include the Edwards Prima Plus, Medtronic Freestyle, and Toronto SPV valve (St. Jude Medical).

Homografts or preserved human aortic valves are used in a minority of patients.

Pathophysiology

Valve failure

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 more 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. 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.

Stenosis or incompetence of prosthetic valves occurs and may be due to a tear or perforation of the valve cusp, valvular thrombosis, pannus formation, valve calcification, or stiffening of the leaflets.

Primary failure of mechanical valves may be caused by suture line dehiscence, thrombus formation, or breakage or separation of the valve components. Acute valvular regurgitation or embolization of the valve fragments may result.

When the mitral valve acutely fails, rapid left atrial volume overload causes increased left atrial pressure. Pulmonary venous congestion and, ultimately, pulmonary edema occur. Cardiac output is decreased because a portion of the output is being regurgitated into the left atrium. 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 left ventricular outflow, thereby increasing the regurgitation.

Acute failure of a prosthetic aortic valve causes a rapidly progressive left ventricular volume overload. Increased left ventricular 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 is common, even in the absence of coronary artery disease.

Biological prosthetic valves often slowly degenerate over time, become calcified, or suffer from thrombus formation. These events result in the slowly progressive failure of the valve. The 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.

Prosthetic valve endocarditis

PVE occurring within 60 days of implantation (early PVE) usually is due to perioperative contamination or hematogenous spread. PVE occurring after 60 days (late PVE) usually is caused by hematogenous spread.

The pathologic hallmark of PVE in mechanical valves is ring abscesses. Ring abscess 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.

Frequency

United States

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, and bileaflet valves have the lowest. Valve thrombosis is increased with valves in the mitral position and in patients with subtherapeutic anticoagulation.

• 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.
• 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 in mitral valves. Mechanical and biological valves are equally susceptible.

Mortality/Morbidity

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.

• PVE has an overall mortality rate of 50%. In early PVE, the mortality rate is 74%. In late PVE, the mortality rate is 43%. The mortality rate with a fungal etiology is 93%. The mortality rate for staphylococcal infections is 86%.
• Fatal anticoagulant-induced hemorrhage occurs in 0.5% of patients per year.

Age

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

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

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

• 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 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 the sudden onset of dyspnea, syncope, or precordial pain.
• Patients with acute aortic valve failure often experience sudden death. Those surviving 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 embolization. Stroke syndromes are the most common presentation, although patients may present with myocardial infarction (MI), sudden death, or symptoms of visceral or peripheral embolization.
• Symptoms due to anticoagulant-related hemorrhage are related to the site of hemorrhage.
• A history of fever should alert the physician's suspicion to the possibility of PVE.

Physical

• 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 also may 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 are similar to those of native valves. A low-frequency early opening sound may present in the mitral position.
  • 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 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 since 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.
• Patients with acute valvular failure present with cardiogenic shock and severe hypotension.
• • 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 presence of an abnormal regurgitant murmur is an important clue to the presence of prosthetic valvular failure.
• Patients with subacute valvular failure often present with signs of gradually worsening left-sided congestive heart failure.
• • Rales and jugular venous distention may 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.
• The clinical manifestations of PVE are often obscure.
• • 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, often are absent in PVE.
  • Splenomegaly supports the diagnosis but 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 MI, sudden death, or visceral or peripheral embolization. Systemic embolization should alert the physician to suspect valve thrombosis or PVE.
• Anticoagulant-related hemorrhage: Signs due to anticoagulant-related hemorrhage depend on the site of hemorrhage.

Causes

• PVE has been divided into 2 subcategories. These reflect differences in clinical features, microbial patterns, and mortality. Early PVE occurs within 60 days of valve insertion, whereas late PVE occurs after 60 days.
• • 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, GI manipulation, or intravenous drug abuse. The causative organisms are similar to those causing native valve endocarditis. These include 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%).
• Multiple negative blood culture results are unusual with common pathogens but often 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.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Hemolytic anemia
Thromboembolic disease

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Complete blood 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.
  • A hematocrit lower than 34% is present in 74% of patients with PVE and is the most common hematologic finding.
  • A WBC count lower than 12,000 is present in as many as 54% of patients with PVE.
• Urinalysis: Hematuria is present in 57% of patients with PVE.
• Blood cultures
• • Culture results are positive in multiple samples in 97% of patients with PVE.
  • Blood cultures should be held for 3 weeks.
  • Multiple blood cultures should be taken.
• Prothrombin time (PT)/international normalized ratio (INR): Recommendations vary as to the target INR. The following is offered as a general guideline, but remember that therapy must be individualized.
• • Bioprosthetic valves: INR 2-3 for 3 months following implantation; anticoagulation may then be discontinued unless the patient has another indication, such as atrial fibrillation or development of prosthetic valve thrombosis.
  • Mechanical valves: INR 2.5-3.5; patients with atrial fibrillation and those with valves in the mitral position should be kept at the higher end of this range. Patients with bileaflet valves may be kept at the lower end of this range.
  • Nontherapeutic values should raise the suspicion of valve thrombosis or systemic embolization.

Imaging Studies

• An overpenetrated anteroposterior chest radiograph helps to delineate the valvular morphology and whether or not the valve and occluder are intact. In more stable patients, a lateral chest film helps identify the valve position and type.
• The following are descriptions of the radiographic appearance of the more commonly seen valves. For a more comprehensive algorithmic approach to radiographic identification, see the article by Mehlman (1988).
• • Starr-Edwards caged ball valve
    • Radiopaque base ring
    • Radiopaque cage
    • Three struts for the aortic valve; 4 struts for the mitral or tricuspid valve
    • Silastic ball impregnated with barium that is mildly radiopaque (but not in all models)
  • Bjork-Shiley tilting disc valve (discontinued, but many patients still have these valves implanted)
    • Base ring and struts are radiopaque.
    • Two U-shaped struts project into base ring.
    • Edge of occluder disc is also radiopaque.
  • Medtronic-Hall tilting disc valve
    • Radiopaque base ring
    • Radiopaque struts that project into base ring: 3 small ones and 1 large hook-shaped one
    • Occluder disc that is mildly opaque but often cannot be seen
  • Alliance Monostrut valve
    • Occluder has a radiopaque rim.
    • The base ring and two struts are radiopaque.
  • St. Jude medical bileaflet valve
    • Mildly radiopaque leaflets are best seen when viewed on end. Seen as radiopaque lines when the leaflets are fully open.
    • Base ring is not visualized on most models.
    • The valve may not be visualized on some radiographs.
  • CarboMedics bileaflet valves: 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: Base ring and wide fenestrated stents are one piece.
• Echocardiography
• • 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.
  • Two-dimensional and Doppler echocardiography, while not as reliable, may demonstrate perivalvular leaks, vegetations, and inadequate valve/occluder movement.
  • Two-dimensional echocardiography and Doppler echocardiography can detect the presence of acute valvular regurgitation and grade the severity.
  • Transesophageal echocardiography has emerged as the imaging study of choice in patients with a suspected prosthetic valve complication. This applies especially to prosthetic mitral valves, where transthoracic Doppler is often insensitive. Adequately excluding prosthetic valve regurgitation with a transthoracic echocardiogram is difficult.
  • In cases where any significant suspicion of valvular stenosis or regurgitation exists, an unremarkable transthoracic echocardiogram is unlikely to be sufficient to adequately rule out a pathologic process.

Other Tests

• Electrocardiography
• • An atrioventricular (AV) block may indicate the presence of a myocardial abscess. A fever and new AV block is considered PVE until proven otherwise.
  • Atrial fibrillation is common in mitral valve replacement and may cause hemodynamic compromise.

Procedures

• Certain procedures may cause bacteremia and thereby increase the chance of PVE. The emergency physician must be up to date with the latest prophylaxis guidelines. See Deterrence/Prevention.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Emergency Department Care

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

• Primary valve failure: Patients with valvular failure due to breakage or abrupt tearing of the components usually present with acute hemodynamic deterioration. They need emergent valve replacement. Adjunctive therapy may be initiated while these 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).
• • Begin afterload reduction and inotropic support in order to reduce the impedance to forward flow and improve peripheral perfusion. If the mean arterial pressure is higher than 70 mm Hg, sodium nitroprusside may be used. If the mean arterial pressure is lower than 70 mm Hg, dobutamine alone or in combination with inamrinone may be used.
  • Avoid inotropic agents with vasoconstricting properties.
  • Intra-aortic balloon counterpulsation may be useful in cases of acute mitral regurgitation where the patient is in extremis and surgical facilities are not immediately available. Intra-aortic balloon counterpulsation is relatively contraindicated in the presence of an incompetent aortic valve.
• Prosthetic valve endocarditis
• • Administer intravenous antibiotics as soon as 2 sets of blood cultures are drawn. Vancomycin and gentamicin may be used empirically pending blood cultures and determination of methicillin resistance.
  • Consider anticoagulation in PVE, since 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 nontherapeutic INR.
  • Assessment of valve function is needed.
• Prosthetic valve thrombosis
  • Surgery had historically been the mainstay of treatment but is associated with a high mortality.
  • Thrombolytic therapy may be used to treat select patients with thrombosed prosthetic valves.
  • Patients with right-sided prosthetic valve thrombosis (PVT) and those with left-sided PVT and New York Heart Association (NYHA) class III and IV, pulmonary edema, or hypotension may benefit from thrombolysis due to the higher operative mortality.
  • Thrombolytic therapy should be done in conjunction with cardiovascular surgical consultation.
  • The chance of a successful thrombolysis is inversely related to the size of the thrombus and the amount of time that has elapsed since the onset of symptoms.
  • Outcomes are superior in patients who are relatively stable, although thrombolysis is often performed in patients who are poor surgical candidates.
• Anticoagulant-related hemorrhage
  • 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.

Consultations

• In patients presenting with any degree of prosthetic valvular failure, early consultation with a cardiologist is recommended in order to perform and interpret an echocardiogram.
• Consult a cardiothoracic surgeon early in cases of severe hemodynamic compromise.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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

Drug Category: Vasodilators

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.

Drug Category: Inotropic agents

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

Drug Category: Anticoagulants

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.

Drug Category: Antibiotics

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

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Transfer

• 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.
• The mortality rate in patients with acute prosthetic valvular failure is related directly to the delay of surgical correction.

Deterrence/Prevention

• Provide antibiotic prophylaxis to patients undergoing procedures that may result in bacteremia. This list, although not exhaustive, includes most inpatient and outpatient procedures performed in the ED that may result in bacteremia and, therefore, may lead to PVE.
• • Dental and oral procedures
  • Intestinal surgery
  • Procedures on the respiratory mucosa
  • Bronchoscopy (rigid)
  • Sclerotherapy of bleeding esophageal varices
  • Gallbladder surgery
  • Urethral catheterization in the presence of a suspected urinary tract infection
  • Incision and drainage of infected tissues
  • Vaginal delivery in the presence of infection
• For dental, oral, or upper respiratory tract procedures, use amoxicillin 2 g PO 1 hour before the procedure.
• • If unable to take PO medication, use ampicillin 2 g IV 30 minutes before procedure.
  • For penicillin-allergic patients, use clindamycin 600 mg PO/IV 1 hour before the procedure, followed by 150 mg PO/IV 6 hours after initial dose.
• For genitourinary or GI procedures, use ampicillin 2 g IV and gentamicin 80 mg IV 30 minutes before the procedure. Repeat this regimen or give amoxicillin 1.5 PO 6 hours after the first dose. In penicillin-allergic patients, use vancomycin 1 g IV and gentamicin 80 mg IV 1 hour before the procedure.

Complications

• Glomerulonephritis, mycotic aneurysms, and metastatic abscesses may complicate PVE.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• 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 PVE in any patient with a prosthetic valve and a fever.

Special Concerns

• Pregnancy
• • Some debate exists concerning the most advantageous method of providing adequate anticoagulation in pregnant patients with mechanical prostheses.
  • Warfarin increases the chance of spontaneous abortion and stillbirths and is associated with teratogenicity from 6-12 weeks' gestation.
  • Current recommendations are to use heparin from 6-12 weeks and from 38-40 weeks' gestation. Warfarin may be used for the remainder of pregnancy.
  • The American College of Obstetrics and Gynecology have recommended that low molecular weight heparin not be used in pregnancy.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Medtronic Hall mitral valve. Reproduced with permission from Medtronic, Inc.
	View Full Size Image
Media type:  Photo

Media file 2:  The Hancock M.O. II aortic bioprosthesis (porcine). Reproduced with permission from Medtronic, Inc.
	View Full Size Image
Media type:  Photo

Media file 3:  Starr-Edwards Silastic ball valve mitral Model 6120. Reproduced with permission from Baxter International, Inc.
	View Full Size Image
Media type:  Photo

Media file 4:  Carpentier-Edwards Duralex mitral bioprosthesis (porcine). Reproduced with permission from Baxter International, Inc.
	View Full Size Image
Media type:  Photo

Media file 5:  Carpentier-Edwards Perimount pericardial aortic bioprosthesis.Reproduced with permission from Baxter International, Inc.
	View Full Size Image
Media type:

Media file 6:  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.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

• American College of Obstetricians and Gynecologists. ACOG Committee Opinion: safety of Lovenox in pregnancy. Obstet Gynecol. Oct 2002;100(4):845-6. [Medline].
• Baddour LM, Wilson WR, Bayer AS. Infective endocarditis: diagnosis, antimicrobial therapy, and management of complications. Circulation. Jun 14 2005;111(23):e394-434. [Medline].
• Bussey HI. An overview of anticoagulants, antiplatelet agents, and the combination in patients with mechanical heart valves. J Heart Valve Dis. May 2004;13(3):319-24. [Medline].
• Butany J, Ahluwalia MS, Munroe C, et al. Mechanical heart valve prostheses: identification and evaluation (erratum). Cardiovasc Pathol. Nov-Dec 2003;12(6):322-44. [Medline].
• Butany J, Fayet C, Ahluwalia MS, et al. Biological replacement heart valves. Identification and evaluation. Cardiovasc Pathol. May-Jun 2003;12(3):119-39. [Medline].
• Cannegieter SC, Rosendaal FR, Briet E. Thromboembolic and bleeding complications in patients with mechanical heart valve prostheses. Circulation. Feb 1994;89(2):635-41. [Medline].
• Dajani AS, Taubert KA, Wilson W, et al. Prevention of bacterial endocarditis. Recommendations by the American Heart Association. Circulation. Jul 1 1997;96(1):358-66. [Medline].
• Goldman ME. Echocardiographic doppler evaluation of prosthetic valve function and dysfunction. Adv Cardiol. 2004;41:179-84. [Medline].
• Kahn S. Long-term outcomes with mechanical and tissue valves. J Heart Valve Dis. 2002;11, Suppl 1:S8-S14.
• Lengyel M, Fuster V, Keltai M, et al. Guidelines for management of left-sided prosthetic valve thrombosis: a role for thrombolytic therapy. Consensus Conference on Prosthetic Valve Thrombosis. J Am Coll Cardiol. Nov 15 1997;30(6):1521-6. [Medline].
• MacKenzie GS, Heinle SK. Echocardiography and Doppler assessment of prosthetic heart valves with transesophageal echocardiography. Crit Care Clin. Apr 1996;12(2):383-409. [Medline].
• Mehlman DJ. A pictorial and radiographic guide for identification of prosthetic heart valve devices. Prog Cardiovasc Dis. May-Jun 1988;30(6):441-64. [Medline].
• Piper C, Kprfer R, Horstkotte D. Prosthetic valve endocarditis. Heart. May 2001;85(5):590-3. [Medline].
• Roudaut R, Lafitte S, Roudaut MF, et al. Fibrinolysis of mechanical prosthetic valve thrombosis: a single-center study of 127 cases. J Am Coll Cardiol. Feb 19 2003;41(4):653-8. [Medline].
• Stein PD, Alpert JS, Bussey HI, et al. Antithrombotic therapy in patients with mechanical and biological prosthetic heart valves. Chest. Jan 2001;119(1 Suppl):220S-227S. [Medline].
• Vongpatanasin W, Hillis LD, Lange RA. Prosthetic heart valves. N Engl J Med. Aug 8 1996;335(6):407-16. [Medline].

Article Last Updated: Feb 26, 2007