Pathophysiology

Prosthetic valves tend to be slightly stenotic, and a very small amount of regurgitation is common because of incomplete closure. Patients with mechanical valves require continuous anticoagulation. Some bioprostheses do not require anticoagulation. Several complications can lead to dysfunction of artificial valves. Thrombi can form on a prosthetic valve and become large enough to obstruct flow or prevent closure. The dysfunction due to thrombi can be acute or slowly progressive. Bioprostheses may gradually degenerate, undergoing gradual thinning, stiffening, and possibly tearing, which result in valvular incompetence. The sutures that secure the prosthetic valve may become disrupted, leading to paravalvular regurgitation as a fistula forms at the periphery of the valve. Mechanical models may suddenly fracture or fail. These failures usually bring sudden symptoms and often are fatal before corrective surgery can be accomplished.

Bleeding and systemic embolism originating from a thrombus on the prosthetic valve are the most important complications of mechanical heart valves, occurring at a rate of 1.4 percent and 1 percent per year, respectively, for patients on warfarin. Life-long anticoagulation is required to reduce the risk of thromboembolism and valve thrombosis. The optimal anticoagulation regimen is controversial, with disagreement concerning the intensity of warfarin therapy as well as the need for an antiplatelet agent. Embolism is more common after mitral valve replacement. Embolism occurs less frequently with bioprostheses, and bleeding complications depend on the therapy given.

Patients with artificial valves develop endocarditis at a rate of 0.5 percent per year. Infections occur more frequently during the first 2 months after operation. The most common organisms during this period are Staphylococcus epidermidis and S. aureus. Gram-negative organisms and fungi are also frequent causes of endocarditis during this early period. Late cases of endocarditis are similar to those affecting native valves. The most frequent organism is Streptococcus viridans, but Serratia and Pseudomonas also occur. Patients with prosthetic valves and endocarditis may develop a ring abscess around the valve, which requires valve replacement. Patients with mechanical prostheses have an increased rate of intravascular destruction of red blood cells. Usually the red blood cell loss is easily corrected by the bone marrow, but hemolytic anemia may be severe and indicate a paravalvular leak. Finally, patients with prosthetic valves may be particularly susceptible to hemodynamic compromise from a new dysrhythmia, such as atrial fibrillation.

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