Bioprosthetic valve failure

Abstract

The overwhelming majority of patients who undergo valve replacement with either bioprosthetic or mechanical prosthetic valves have increased survival and enhanced functional status for extended intervals. Nevertheless, reoperation necessitated by or death caused by prosthesis-associated complications is common. Although thromboembolic complications are a frequent source of mortality and morbidity with mechanical prostheses, despite chronic anticoagulation, thromboembolic sequelae are infrequent in patients with bioprostheses, especially those in sinus rhythm. However, primary degenerative failure, predominantly due to cuspal mineralization, causing stenosis or regurgitation with or without cuspal tears, is a frequent cause of bioprosthetic valve dysfunction. Reoperation, largely owing to primary tissue failure, is required in approximately 20 to 30 percent of bioprosthetic valve recipients by 10 years postoperatively. Diagnosis of primary bioprosthetic valve dysfunction is enhanced substantially by 2-D Doppler echocardiography. Experimental models, using either circulatory implants in large animals or subcutaneous implants in rodents, have contributed substantially to our understanding of the pathophysiology of bioprosthetic valve mineralization and its determinants. A complex interplay of host factors (particularly those influencing calcium and phosphorus metabolism) and implant factors (particularly those concerned with tissue source and preservation) mediate bioprosthetic valve calcification. Mechanical stress accelerates but is not a prerequisite for mineralization. Immunologic and other inflammatory reactions appear to be noncontributory. Bovine pericardium calcifies equivalently to porcine aortic valve in experimental models, and recent clinical data suggest that rates of failure or pericardial valves will be less favorable than those of porcine valves. Current investigation is directed toward elucidation of the pathophysiology of mineralization, development of specific pharmocological modifications of host and implant in order to inhibit it, and design modification that could reduce degeneration and thus valve failure.