Bioprosthetic AVR Structural Valve Degeneration
- Rodriguez-Gabella T, Voisine P, Puri R, Pibarot P, Rodés-Cabau J.
- Aortic Bioprosthetic Valve Durability: Incidence, Mechanisms, Predictors, and Management of Surgical and Transcatheter Valve Degeneration. J Am Coll Cardiol 2017;70:1013-1028.
The biological tissue used in both surgical and transcatheter bioprostheses is prone to structural valve degeneration (SVD), a multifactorial process mediated by connective tissue calcification, and leading to valve dysfunction. This review summarizes available data on surgical and transcatheter aortic bioprosthesis durability; reviews the definitions, incidence, timing, and mechanisms of SVD; and discusses current treatment options for valve failure due to SVD. The following are points to remember:
- Bioprosthetic valves (background).
- Surgical bioprosthetic valves include homografts, pulmonary autografts, and porcine (stented and stentless) and pericardial bioprostheses.
- Sutureless and rapid-deployment valves (pericardial valves that anchor within the aortic annulus and involve no more than three sutures) recently have been introduced as an option to facilitate minimally invasive approaches and to reduce cardiopulmonary bypass time.
- Balloon-expandable and self-expanding transcatheter (bovine or porcine pericardial) valves are gaining increasing importance.
- Definition of SVD.
- SVD is a gradual process characterized by progressive calcification, fibrosis, and wear and tear of valve leaflets, ultimately leading to valve dysfunction secondary to stenosis (~40% of valves), regurgitation (~30% of valves), or combined stenosis and regurgitation (~30% or valves).
- To date, there is no unified definition of SVD.
- The authors propose the following definitions for SVD:
- Possible SVD: >10 mm Hg increase in mean transvalvular gradient with concomitant >0.3 cm2 decrease in effective orifice area (EOA) and/or decrease in Doppler velocity index >0.08, not leading to severe aortic stenosis according to current guidelines; and/or new onset of at least mild central (intra-prosthetic) regurgitation or increase by at least one grade of existing central regurgitation compared to baseline echocardiography performed 1–3 months post-intervention, resulting in a regurgitation grade = moderate.
- Clinically-relevant SVD: >20 mm Hg increase in mean transvalvular gradient with concomitant decrease in EOA by >0.6 cm2 and/or decrease in Doppler velocity index >0.15 during follow-up, leading to severe aortic stenosis; and/or new onset of or increase by at least 1 grade of intra-prosthetic regurgitation leading to moderate-to-severe or severe aortic regurgitation.
- Diagnosis of SVD.
- Transthoracic echocardiography (TTE) is the standard examination to evaluate prosthetic valve structure and function. Current American Heart Association/American College of Cardiology (AHA/ACC) and European Society of Cardiology guidelines recommend an initial postoperative TTE after prosthetic valve implantation. The authors recommend repeating TTE between 1- and 5-year follow-up, and yearly thereafter.
- Additional useful imaging modalities include transesophageal echocardiography, multi-detector computed tomography, and cardiovascular magnetic resonance imaging.
- Mechanisms of SVD.
- SVD is a multifactorial process with consequences of calcification and leaflet degradation, leading to valve stenosis or leaflet tear (and regurgitation). Bovine pericardial valves tend to have a greater propensity for SVD with stenosis, whereas porcine valves tend to have a greater tendency for SVD with leaflet tear and regurgitation. Stenosis may be more common with stented valves, and leaflet tear and regurgitation with stentless valves.
- Several studies suggest that, in addition to a passive degenerative process, active mechanisms that trigger inflammation followed by calcification may contribute to SVD. For example, gluteraldehyde fixation decreases but does not eliminate bioprosthesis tissue antigenicity, and an immune response may be triggered that results in accelerated tissue mineralization.
- Early post-implantation valve thrombosis may occur in up to 15% of patients; it is possible that valve thrombosis, even if subclinical or successfully treated with anticoagulants, might trigger inflammation and a subsequent fibrocalcific remodeling of valve leaflets.
- Incidence and timing of SVD.
- Surgical bioprostheses. Most studies reveal ≤15% incidence of SVD during the first decade after bioprosthetic aortic valve replacement. More limited and heterogeneous data exist on 20-year durability; one study of the Carpentier-Edwards Perimount pericardial bioprosthesis reported 67% freedom from reoperation at 20 years, but another study reported only 37% freedom from echocardiography-defined SVD.
- Transcatheter bioprostheses. Data on the durability of transcatheter bioprostheses are more limited, confined to a shorter experience in a generally older population with more comorbidities. However, data from the PARTNER-1 trial suggested no difference in SVD between surgical and transcatheter bioprostheses at 5 years.
- Factors associated with SVD.
- Surgical bioprostheses. Predictors of surgical aortic bioprosthesis SVD include patient-related factors (lower age, higher body mass index), cardiovascular and comorbid factors (smoking, diabetes, dyslipidemia, renal insufficiency), and valve-related factors (persistent LV hypertrophy, smaller prosthesis size, prosthesis-patient mismatch).
- Transcatheter bioprostheses. Although data are limited, concern has been raised of possible transcatheter aortic valve replacement (TAVR)-specific factors that might accelerate SVD, including potential leaflet damage during crimping, asymmetric expansion with suboptimal leaflet coaptation, and incomplete frame expansion leading to leaflet-frame interaction with increased mechanical stress.
- Management of bioprosthetic SVD.
- The treatment for bioprosthetic surgical valve dysfunction conventionally has been re-do surgery.
- Valve-in-valve TAVR within a degenerated surgical bioprosthesis is a feasible, less-invasive option for patients with bioprosthesis SVD; current AHA/ACC guidelines recommend this approach in high-risk patients with aortic bioprosthesis dysfunction.
Clinical Topics: Anticoagulation Management, Cardiac Surgery, Diabetes and Cardiometabolic Disease, Dyslipidemia, Invasive Cardiovascular Angiography and Intervention, Noninvasive Imaging, Prevention, Valvular Heart Disease, Aortic Surgery, Cardiac Surgery and VHD, Interventions and Imaging, Interventions and Structural Heart Disease, Echocardiography/Ultrasound, Magnetic Resonance Imaging, Smoking
Keywords: Anticoagulants, Aortic Valve Insufficiency, Aortic Valve Stenosis, Bioprosthesis, Cardiac Imaging Techniques, Cardiac Surgical Procedures, Cardiopulmonary Bypass, Constriction, Pathologic, Diabetes Mellitus, Dyslipidemias, Echocardiography, Transesophageal, Heart Valve Diseases, Heart Valve Prosthesis, Hypertrophy, Left Ventricular, Inflammation, Magnetic Resonance Imaging, Renal Insufficiency, Smoking, Tomography, Thrombosis, Transcatheter Aortic Valve Replacement
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