Perspective:

This review article summarizes discussions from the Platelet Colloquium scientific meeting. The definition, risks, mechanisms, and timing of bleeding and stroke events related to transcatheter aortic valve implantation (TAVI) are discussed, and a critical review of antiplatelet and antithrombotic treatment during and following the TAVI procedure are provided. The key points of this manuscript are as follows:

1. The 30-day risk of major stroke (~3.5%) and major bleeding or vascular complications (~10%) following TAVI is very high, with a rate that is over 10 times that associated with percutaneous coronary interventions (PCIs).

2. Antithrombotic and antiplatelet therapy has most commonly consisted of heparin during the perioperative period; during the postoperative period, indefinite aspirin use and 1-6 months of a second antiplatelet agent such as clopidogrel are typically used. The duration of clopidogrel, the role for a loading dose, and the need for antiplatelet medications when warfarin is also indicated have varied in studies and clinical practice.

3. Strokes are common during positioning and deployment of the valve prosthesis, suggesting a mechanical role for early stroke as the valve is positioned and implanted, and the native valve is displaced. Proposed risk factors for stroke include the severity of valve calcification, smaller valve orifice area, early delivery catheters, balloon post-dilation, valve embolization, and repeat deployment attempts. Later strokes may represent embolization of atheromatous material, ongoing thrombogenicity of the prosthesis, or post-procedural atrial fibrillation.

4. Bleeding events may be mechanical, and large delivery catheters, a greater sheath to femoral artery ratio, and increased arterial calcification have been associated with risk of major bleeding complications. Further, many patients require blood transfusions following TAVI without any clear source of bleeding or with a source not related to the procedure.

5. There is a need for studies comparing alternative anticoagulants during the procedure to the current standard of heparin.

6. The risk of thromboembolic events is greatest in the first few days following TAVI. Whether dual antiplatelet therapy is beneficial following TAVI has not been robustly examined, and is based on experience with PCI. It is possible that the prosthetic material may trigger thrombus formation, and one hypothesis is that antithrombotic therapy after TAVI may reduce embolic events. Future studies are needed to determine whether dual antiplatelet therapy, antithrombotic therapy, or a combination of these would result in the best outcomes.

7. Rigorous prospective studies are needed to determine the best approach for per-procedural and post-procedural antiplatelet and antithrombotic agents, and their effect on major stroke and bleeding.