Author + information
- Received May 29, 2018
- Revision received August 9, 2018
- Accepted August 13, 2018
- Published online August 27, 2018.
- Thomas G. Nührenberg, MD# (, )
- Julia Hromek, MD,
- Alexander Kille, MD,
- Willibald Hochholzer, MD,
- Manuel Hein, MD,
- Dietmar Trenk, PhD,
- Franz-Josef Neumann, MD,
- Christian Stratz, MD∗ and
- Philipp Ruile, MD∗
- University Heart Center Freiburg • Bad Krozingen, Department of Cardiology and Angiology II, Bad Krozingen, Germany
- ↵#Address for Correspondence: Thomas G. Nührenberg, MD University Heart Center Freiburg • Bad Krozingen Department of Cardiology and Angiology II D-79189 Bad Krozingen, Germany Phone +49 7633 4808 Fax: +49 761 402 2489,
Background It is unclear whether the apparent ineffectiveness of clopidogrel in preventing hypo-attenuated leaflet thickening (HALT) after transcatheter aortic valve implantation (TAVI) questions the concept of P2Y12 inhibition after TAVI or is a consequence of an inadequate response to clopidogrel in elderly patients with severe aortic stenosis.
Objectives To assess the impact of on-clopidogrel platelet reactivity (PR) on HALT, we prospectively tested if patients with below-median on-clopidogrel PR have a lower incidence of HALT compared to patients with above-median on-clopidogrel PR.
Methods Patients were either on chronic dual antiplatelet therapy with clopidogrel and ASA or were given bolus doses of both drugs the day before TAVI. ADP-induced multi-electrode impedance aggregometry was performed before TAVI. After TAVI, clopidogrel was continued in all patients. Computed tomography angiography (CTA) was performed to detect HALT.
Results Of 331 patients enrolled, CTA was performed in 200 patients at 5[4-6, interquartile range] days. In patients with below-median ADP-induced PR (< 180 AU*min), 16 were diagnosed with HALT whereas 20 patients with above-median PR were diagnosed with HALT (p=0.58). Among patients with high on-clopidogrel PR (>468 AU*min, n=29), 7 (24%) patients displayed HALT compared to 19 (17%) patients with ADP-induced PR ≤468 AU*min (p=0.43). Consistently, ADP-induced PR as continuous variable was not significantly associated with HALT (p=0.75). Oral anticoagulation was associated with reduced rates of HALT (OR 0.41 [0.18– 0.96], p=0.04).
Conclusions On-clopidogrel ADP-induced PR is not significantly associated with the occurrence of HALT. In contrast, oral anticoagulation was associated with reduced rates of HALT.
↵∗ These authors contributed equally to this work
This trial was supported by the University Heart Center Freiburg • Bad Krozingen.
Dr. Hochholzer reports receiving consulting and lecture fees from AstraZeneca, Boehringer Ingelheim, Daiichi Sankyo, and The Medicines Company.
Dr. Stratz reports receiving lecture fees or travel expense from Eli Lilly, Daiichi Sankyo and Bayer.
Dr. Trenk reports receiving consulting and lecture fees from Amgen, AstraZeneca, Bayer, Berlin Chemie, Bristol-Myers Squibb/Pfizer, Boehringer Ingelheim, Daiichi Sankyo, and Sanofi.
All other authors report no conflict of interests.
- Received May 29, 2018.
- Revision received August 9, 2018.
- Accepted August 13, 2018.
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