In addition, glutaraldehyde fixation used to reduce allograft immunogenicity and promote collagen linkage for a solid tissue structure is a contributor and potentiates calcification. A mitral position also confers a higher risk, possibly related to higher mechanical stress on the closed leaflets during ventricular systole as opposed to the lower diastolic pressure acting on a BPV in the aortic position. SVD of BPVs results from two not necessarily independent processes, leaflet calcification and non-calcific tissue degeneration.Ĭlinical factors associated with accelerated calcification include young age, end-stage renal disease, and disorders of the calcium metabolism, thus mirroring some of the risk factors for native aortic valve calcification. SVD is an acquired intrinsic valve abnormality defined as progressive deterioration of the leaflets or supporting structures, resulting in thickening, calcification, tearing, or disruption of the prosthetic valve (PV) with eventual haemodynamic dysfunction, manifesting as stenosis, regurgitation or a combination of both. While contemporary mechanical heart valves (MHV) are durable, structural valve deterioration (SVD) is a clinically important long-term complication of bioprosthetic valves (BPVs), whether surgical or transcatheter, resulting in a limited life span. Structural failure (bioprosthetic valves)Įvery valve prosthesis introduces a new disease process, and prosthesis-related complications undermine their attractiveness.Part 4 – Prosthetic valves: complications and dysfunction, pregnancy Prosthesis-related complicationsĪ range of early or late complications can occur with prosthetic valves depending on the valve type and patient-related factors, including the following: Part 2 – Prosthetic valves: antithrombotic therapy This mini-series is divided into 4 parts: Prosthetic heart valves are designed to replicate the function of native valves by maintaining unidirectional blood flow and can be separated into two broad categories, mechanical and bioprosthetic (also called tissue) valves, each with different advantages and disadvantages. In patients with severe valvular heart disease, guideline-based surgical valve replacement or transcatheter implantation of a prosthetic heart valve is associated with improved survival and relief of symptoms. In addition, the increased haemodynamic burden during pregnancy can lead to heart failure symptoms in case of pre-existing prosthetic dysfunction or prosthesis-patient mismatch. The known changes in haemostasis, potential teratogenicity of vitamin K antagonists and need for interruption of anticoagulation at the time of delivery represent a particular challenge. In mechanical valves, the need for anticoagulation is a predictor of maternal and foetal mortality. Women contemplating pregnancy often decide on a bioprosthetic valve. Patients with paravalvular complications are rarely cured by antibiotic therapy alone. Prosthetic valve endocarditis carries a higher mortality risk and risk of post-treatment complications compared to native valve endocarditis, regardless of the adopted treatment strategy. The differential diagnosis of abnormally high transprosthetic gradients is crucial for a targeted management including medical, surgical and interventional therapeutic strategies. Periprosthetic regurgitation can lead to heart failure or haemolysis. Valve thrombosis, thromboembolic complications and pannus formation occur more frequently with mechanical valves. Structural valve deterioration is a clinically important long-term complication of bioprosthetic valves, causing stenosis, regurgitation or a combination of both, ultimately necessitating reintervention. Valve replacement is not a curative procedure but introduces a new disease process with prosthetic valve-related complications.
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