Predictors of haemodynamic structural valve deterioration following transcatheter aortic valve implantation with latest-generation balloon-expandable valves

Abstract

Aims: Elevated gradients have been proposed to be associated with haemodynamic structural valve deterioration (SVD) after transcatheter aortic valve implantation (TAVI); however, data regarding their characterisation remain scarce. This study sought to investigate the prevalence and predictors of moderate or greater SVD and the prevalence of valve thrombosis during follow-up after TAVI with balloon-expandable valves.Methods and results: A total of 691 patients undergoing transfemoral TAVI were enrolled. The primary endpoint was moderate or severe haemodynamic SVD during 12-month follow-up after TAVI, defined as (I) mean transvalvular gradient ≥20 mmHg or (II) mean transvalvular gradient increase ≥10 mmHg. The primary endpoint was observed in 10.3% after TAVI. Use of a 20 mm valve, valve-in-valve procedure and absence of oral anticoagulation (OAC) were independently associated with haemodynamic SVD, whereas valve-in-valve procedure and absence of OAC were the only significant variables after accounting for death as a competing event. Absence of OAC was significantly associated with haemodynamic SVD (RR 8.65; p=0.004) and death (RR 3.57; p=0.06), whereas valve-in-valve procedure was only associated with haemodynamic SVD (RR 52.76; p<0.001). Valve thrombosis was present in 0.87% (6/691) of the patients. Conclusions:The prevalence of moderate or greater haemodynamic SVD during the first 12 months after TAVI is 10.3%. Procedural factors and pharmacotherapy seem to play a key role during manifestation. Future studies should focus on the underlying mechanisms.

New advances in the prevention of transcatheter aortic valve implantation failure: current and future perspectives

“…The absence of anticoagulant therapy indeed has been proven to be an independent risk factor for SVD. [53][54][55] Regarding patients with mandatory indication for OAC (eg, atrial fibrillation), most recent evidence 56 showed that antiplatelet therapy on top of OAC increased the incidence of bleeding without any additional benefit in term of further reduction of thrombotic events, suggesting at least in this population the superiority of OAC monotherapy. While OAC could be considered the optimal medical strategy when chronic oral anticoagulation is mandatory, the same conclusions cannot be extended to patients without a real need for anticoagulation therapy.…”

Open transcatheter double valve-in-valve replacement for degenerated bioprostheses on the arrested heart

“… 2 Predictors for SVD include the size of the used valve prosthesis, patient-prosthesis mismatch (PPM), diabetes, smoking, dyslipidaemia, renal function, the oral anticoagulation regime, and the patient’s age at implantation. 3 Structural valve deterioration is defined according to the European Association of Cardiovascular Imaging Guidelines as (i) an increase in mean gradient ≥ 5 mmHg for mitral prosthetic valves and >20 mmHg for aortic prosthetic valves (possible SVD) or ≥10 mmHg for mitral prosthetic valves and ≥35 mmHg for aortic prosthetic valves (significant SVD) during follow-up, with a concomitant decrease in valve orifice area and abnormal morphology of the prosthetic leaflets and (ii) presence of new transprosthetic regurgitation. 4 , 5 …”

Next-generation transcatheter aortic valve implantation

“…endothelial hyperplasia, fibrosis, tissue remodeling, and calcification. [3][4][5][6] Immune reaction to the galactose-a-1,3 galactose b-1,4-N-acetylglucosamine (a-Gal) of cardiac xenografts leads to calcification. 7,8 Conventional glutaraldehyde (GA) crosslinking and anticalcification protocols of cardiac xenografts don't avoid bioprosthetic valve failure caused by immune rejection 9,10 and deleterious effects of tissue phospholipids, conformational changes in collagen, and free aldehyde groups.…”

“… 2 , 3 Conventional management strategies are less efficient due to time-dependent and frequent structural valve degeneration of transcatheter heart valves consisting of thrombus formation, endothelial hyperplasia, fibrosis, tissue remodeling, and calcification. 3 , 4 , 5 , 6 …”