Prosthetic Heart Valves 

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, and mechanical hemolytic anemia. In addition, anticoagulant-related hemorrhage may occur.

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 a few basic types. 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, shown in the image below.

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

Bileaflet valves include the St. Jude (St. Jude Medical), shown in the image below, 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); both valves are shown in the images below.

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).^[1]

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

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 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 left ventricular 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 may occur, 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.^[2]

• 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.