Antithrombotic pharmacotherapy after transcatheter aortic valve implantation: an update

ABSTRACT

Introduction: Transcatheter aortic valve implantation (TAVI) is the treatment of choice for a large proportion of patients with severe aortic stenosis. Despite numerous technological and clinical advances, TAVI remains associated with thrombotic complications requiring antithrombotic pharmacotherapy, which exposes to the risk of bleeding, especially in elderly individuals. The optimal antithrombotic regimen following TAVI is uncertain and several investigations are ongoing.

Areas covered: Clinical guidelines are mostly driven by observational trials and experts’ opinions, thus resulting into low-grade level of evidence. The aim of the current review is to critically explore the epidemiology, pathophysiology and prognostic value of thrombotic and bleeding events after TAVI, and to review the current literature on antithrombotic strategies following the procedure.

Expert opinion: Thrombotic and bleeding events remain major complications occurring in the frail population that is currently offered TAVI. Waiting for upcoming evidence from ongoing randomized clinical trials, tailoring antithrombotic therapies based on patients’ characteristics, values and circumstances is a preferable approach.

KEYWORDS:

• Anticoagulant therapy
• antiplatelet therapy
• antithrombotic therapy
• aortic stenosis
• bleeding
• cardiovascular events
• transcatheter aortic valve implantation

Article highlights

• Transcatheter aortic valve implantation (TAVI) patients display a clear tendency towards both thrombotic and bleeding complications, which are strongly associated with clinical outcomes and patient prognosis.

• The mechanism underpinning thrombotic events is likely to be multifactorial, including valve-related flow turbulence, vessel wall disruption, metallic frame exposure and patient-related prothrombotic tendency. While clinical thrombosis is rare, subclinical leaflet thrombosis is more prevalent.

• TAVI patients exhibit an intrinsic augmented bleeding risk due to age, frailty, fall risk, comorbidities, coagulation disorders, antithrombotic regimen. Both acute and late bleeding events have shown to be associated with poor clinical outcomes, reduced quality of life and increased morbidity and mortality.

• Antithrombotic drugs are required after TAVI to minimize thrombotic complications, even at the cost of an unavoidable increase in bleeding risk. A major challenge in this frail and comorbid-rich population is to balance thrombotic and bleeding risks, a delicate process in which a proper antithrombotic therapy is of paramount importance.

• Current societal heart valvular diseases guidelines yielded several recommendations on antithrombotic regimens after TAVI, largely based on small observational studies and experts’ opinions and thus resulting in an empirical low-level evidence.

• Apart from special high-risk subsets (recent acute coronary syndrome or percutaneous coronary intervention, extensive coronary stenting or large aortic arch atheroma), dual antiplatelet therapy following TAVI should not be considered the standard of care.

• If anticoagulant therapy is needed, adding an antiplatelet drug should not be a first option because of the higher risk of bleeding, unless an absolute antiplatelet indication coexists (e.g., recent acute coronary syndrome or percutaneous coronary intervention).

• The appraisal of efficacy and safety of direct oral anticoagulants represents another unsolved issue and many currently ongoing trials are evaluating whether these drugs could be more effective and safer than vitamin K-antagonists in patients who have undergone TAVI.

• The debate on the optimal antithrombotic strategy after TAVI is far from over and several ongoing randomized clinical trials are expected to shed light on this area in the next few years. In the meanwhile, the best approach seems to tailor antithrombotic regimens to the individual patient, in the attempt to meet the optimal therapeutic window.

Declaration of interest

D Capodanno receives speakers’ honoraria from Bayer, AstraZeneca and Daiichi Sankyo. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Reviewer Disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.