Clinical trials of transcatheter aortic valve replacement

Al‐Azizi, Karim; Hamandi, Mohanad

doi:10.1136/heartjnl-2018-313511

Cited by 14 publications

(9 citation statements)

References 22 publications

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“…58 Taking these aspects into account, life-threatening or major bleeding rates have been reported to be between 2.4% and 41.7% at 30 days and between 3.2% and 46.1% at 1-year follow-up. [2][3][4][5][6][7][8]21 Notably, regardless of the aetiology, both acute and late bleeding are associated with poor clinical outcomes and increased mortality rate. 9,10,12 In addition, bleeds may be augmented by coexisting conditions, such as older age, frailty, fall risk, renal failure, liver disease, malignancy, anaemia and coagulation disorders, as well as by AF and antithrombotic therapy.…”

Section: Bleeding Eventsmentioning

confidence: 99%

“…Across TAVI landmark studies, the 30-day stroke incidence ranges between 0.6% and 6.7%, increasing to 1.2-10.6% at 1 year. [2][3][4][5][6][7][8]21 The mechanism underpinning CVEs following TAVI is multifactorial. It includes valve-related flow turbulence, vessel wall disruption, metallic frame exposure (which in turn induces platelet activation) and patientrelated prothrombotic factors, irrespective of the valve type (balloonor self-expandable) or procedural approach (transfemoral or transapical).…”

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confidence: 99%

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Anticoagulation after Transcatheter Aortic Valve Implantation: Current Status

Greco

Capodanno

2020

Interv Cardiol

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Transcatheter aortic valve implantation (TAVI) is the standard of care for symptomatic severe aortic stenosis. Antithrombotic therapy is required after TAVI to prevent thrombotic complications but it increases the risk of bleeding events. Current clinical guidelines are mostly driven by expert opinion and therefore yield low-grade recommendations. The optimal antithrombotic regimen following TAVI has yet to be determined and several randomised controlled trials assessing this issue are ongoing. The purpose of this article is to critically explore the impact of antithrombotic drugs, especially anticoagulants, on long-term clinical outcomes following successful TAVI.

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Section: Bleeding Eventsmentioning

confidence: 99%

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confidence: 99%

Anticoagulation after Transcatheter Aortic Valve Implantation: Current Status

Greco

Capodanno

2020

Interv Cardiol

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“… 2 A vast majority of clinical trials has failed to stop the progression of AVS, 3 and for that reason, the only available therapeutic treatment relies on aortic valve prosthesis implantation. 4 …”

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confidence: 99%

Omega-3 Polyunsaturated Fatty Acids Decrease Aortic Valve Disease Through the Resolvin E1 and ChemR23 Axis

et al. 2020

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Background: Aortic valve stenosis (AVS), which is the most common valvular heart disease, causes a progressive narrowing of the aortic valve as a consequence of thickening and calcification of the aortic valve leaflets. The beneficial effects of omega-3 polyunsaturated fatty acids (n-3 PUFAs) in cardiovascular prevention have recently been demonstrated in a large randomized, controlled trial. In addition, n-3 PUFAs serve as the substrate for the synthesis of specialized proresolving mediators, which are known by their potent beneficial anti-inflammatory, proresolving, and tissue-modifying properties in cardiovascular disease. However, the effects of n-3 PUFA and specialized proresolving mediators on AVS have not yet been determined. The aim of this study was to identify the role of n-3 PUFA–derived specialized proresolving mediators in relation to the development of AVS. Methods: Lipidomic and transcriptomic analyses were performed in human tricuspid aortic valves. Apoe −/− mice and wire injury in C57BL/6J mice were used as models for mechanistic studies. Results: We found that n-3 PUFA incorporation into human stenotic aortic valves was higher in noncalcified regions compared with calcified regions. Liquid chromatography tandem mass spectrometry–based lipid mediator lipidomics identified that the n-3 PUFA–derived specialized proresolving mediator resolvin E1 was dysregulated in calcified regions and acted as a calcification inhibitor. Apoe −/− mice expressing the Caenorhabditis elegans Fat-1 transgene (Fat-1 tg ×Apoe −/− ), which enables the endogenous synthesis of n-3 PUFA and increased valvular n-3 PUFA content, exhibited reduced valve calcification, lower aortic valve leaflet area, increased M2 macrophage polarization, and improved echocardiographic parameters. Finally, abrogation of the resolvin E1 receptor ChemR23 enhanced disease progression, and the beneficial effects of Fat-1 tg were abolished in the absence of ChemR23. Conclusions: n-3 PUFA-derived resolvin E1 and its receptor ChemR23 emerge as a key axis in the inhibition of AVS progression and may represent a novel potential therapeutic opportunity to be evaluated in patients with AVS.

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“…Randomized controlled trials have shown noninferiority of transcatheter AVR over surgical AVR in medium-and low-risk patients with severe aortic stenosis. 1 Thus, a number of patients with severe aortic stenosis will undergo transcatheter AVR. Nevertheless, surgical AVR still remains the gold standard treatment for aortic valve disease, as surgical bioprostheses have shown excellent hemodynamic performance with high freedom from structural valve degeneration and reoperation at very long-term follow-up.…”

mentioning

confidence: 99%