| Autor: |
Hemetsberger R; Department of Cardiology, 2nd Department of Internal Medicine, Medical University of Vienna, 1090 Vienna, Austria., Farhan S; Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA., Lukovic D; Department of Cardiology, 2nd Department of Internal Medicine, Medical University of Vienna, 1090 Vienna, Austria., Zlabinger K; Department of Cardiology, 2nd Department of Internal Medicine, Medical University of Vienna, 1090 Vienna, Austria., Hajagos-Toth J; Department of Pharmacology and Pharmacotherapy, Albert Szent-Györgyi Medical School, University of Szeged, 6720 Szeged, Hungary., Bota J; Department of Pharmacology and Pharmacotherapy, Albert Szent-Györgyi Medical School, University of Szeged, 6720 Szeged, Hungary., Garcia-Garcia HM; Medstar Hospital Center, Department of Cardiology, Washington, DC 20010, USA., Ay C; Clinical Division of Haematology and Haemostaseology, Department of Medicine I, Medical University of Vienna, 1090 Vienna, Austria., Samaha E; Department of Cardiology, 2nd Department of Internal Medicine, Medical University of Vienna, 1090 Vienna, Austria., Gaspar R; Department of Pharmacology and Pharmacotherapy, Albert Szent-Györgyi Medical School, University of Szeged, 6720 Szeged, Hungary., Garamvölgyi R; Institute of Diagnostics and Radiation Oncology, University of Kaposvar, 7400 Kaposvar, Hungary., Huber K; 3rd Medical Department with Cardiology, Wilhelminen Hospital, 1160 Vienna, Austria., Spannbauer A; Department of Cardiology, 2nd Department of Internal Medicine, Medical University of Vienna, 1090 Vienna, Austria., Gyöngyösi M; Department of Cardiology, 2nd Department of Internal Medicine, Medical University of Vienna, 1090 Vienna, Austria. |
| Abstrakt: |
(1) Background: Coronary artery stenting leads to local inflammation, disturbs vasomotion, and slows endothelialization, increasing vascular thrombus risk. We used a pig stenting coronary artery model to assess how peri-interventional triple therapy with dabigatran ameliorates these effects. (2) Methods: In a total of 28 pigs bare-metal stents were implanted. Four days before the percutaneous coronary intervention (PCI), we started 16 of the animals on dabigatran, maintained through 4 days after the procedure. As controls, the remaining 12 pigs received no therapy. In both groups, dual antiplatelet therapy (DAPT) (clopidogrel, 75 mg plus aspirin, 100 mg) was administered until animals were euthanized. Just after the PCI and on day 3 after the procedure, we performed optical coherence tomography (OCT) in eight animals in the dabigatran group and four controls and euthanized them. We followed the eight remaining animals in each group with OCT and angiography for one month before euthanizing them and performed in vitro myometry and histology on harvested coronary arteries from all animals. (3) Results: The dabigatran group showed a significantly increased vasoconstriction at 3 days after PCI (10.97 ± 3.85 mN vs. 7.32 ± 5.41 mN, p = 0.03), but we found no differences between endothelium-dependent and -independent vasodilatation. We also found no group differences in OCT, quantitative angiography, or histomorphometry findings. (4) Conclusions: Starting a short course of dabigatran just before PCI and continuing for a 3-day window along with usual post-PCI DAPT is associated with enhanced vasoconstriction after bare-metal stent implantation without reducing neointimal formation at one month. |
