@article{01f0c37473cb446db37e653d062f3448,
title = "Effects of vitamin K antagonist on aortic valve degeneration in non-valvular atrial fibrillation patients: Prospective 4-year observational study",
abstract = "Background The prevalence of atrial fibrillation (AF) is high in elder subjects. Our previous observational study suggested that vitamin K antagonist (VKA) promotes aortic valve degeneration, a principal cause of aortic stenosis in the elderly, and that angiotensin receptor blocker (ARB) attenuates its progression. This study aimed to prospectively investigate these observations in non-valvular AF patients. Methods Of enrolled 430 patients with calcification on no or one aortic valve leaflet, all of the planned 4-year follow-up data were obtained in 122 non-valvular AF patients treated with warfarin (warfarin group) and 101 patients with cardiovascular diseases and without AF and prescription of warfarin (non-warfarin group). Results Despite higher atherosclerotic risks in the non-warfarin group, 2 or 3 newly calcified leaflets emerged during 4 years in 18.0\% of patients in the warfarin group and in 6.9\% in the non-warfarin group (p = 0.014). Aortic valve area (AVA) did not significantly change in the non-warfarin group during the follow-up, but tended to decrease in the warfarin group (p = 0.057). Non-vitamin K antagonist oral anticoagulant got available in Japan after this study started, and warfarin was discontinued in 15 patients of the warfarin group. The reduction of AVA was significant in the remaining 107 patients on the continuous warfarin treatment (p = 0.002). The effects of ARB on AVA were obscure. Conclusion Major bleeding associated with VKA is well recognized. This study suggests that the development of aortic valve degeneration is another risk of long-term use of VKA in non-valvular AF patients with no or mild aortic valve degeneration.",
keywords = "Anticoagulation, Aortic stenosis, Atrial fibrillation, Vitamin K antagonist",
author = "\{On behalf of the\} and \{Japanese Aortic Stenosis Study-2 (JASS-2) Investigators\} and Kazuhiro Yamamoto and Yukihiro Koretsune and Takashi Akasaka and Akira Kisanuki and Nobuyuki Ohte and Takashi Takenaka and Masaaki Takeuchi and Kiyoshi Yoshida and Kazunori Iwade and Yuji Okuyama and Yutaka Hirano and Yasuharu Takeda and Yasumasa Tsukamoto and Yoshiharu Kinugasa and Satoshi Nakatani and Takashi Sakamoto and Katsuomi Iwakura and Takashi Sozu and Tohru Masuyama",
note = "Funding Information: This study was supported by grants from the Ministry of Health, Labour and Welfare (Tokyo, Japan), and the Japan Heart Foundation (Tokyo, Japan). Funding Information: Dr. M Takeuchi reported receiving lecturer's fees from Philips Medical Systems, GE Healthcare, and research grants from Roche Diagnostics Co. Ltd., Philips Medical Systems, GE Healthcare and Epsilon Imaging. Funding Information: Dr. K Yamamoto reported receiving lecturer's fees from Ono Pharmaceutical Co. Ltd., Otsuka Pharmaceutical Co. Ltd. Bristol-Myers Squibb Co. Ltd. Abbott Vascular Japan Co. Ltd., and research grants from St. Jude Medical Japan Co. Ltd.、Otsuka Pharmaceutical Co. Ltd., Daiichi-Sankyo Co. Ltd., Boston Scientific Co. Ltd. Johnson \& Johnson, Biotronik Japan Inc., Japan Lifeline Co. Ltd., Astellas, Teijin Pharma Ltd., Mitsubishi Tanabe Pharma Co. Ltd., Fukuda Denshi, Takeda Pharmaceutical Co. Ltd., Ono Pharmaceutical Co. Ltd., Public Health Research Foundation, Nihon Kohden Co. Ltd. and Novartis. Funding Information: Dr. S Nakatani reported receiving lecturer's fees from Edwards Lifesciences Co. Ltd. and a research grant from Toshiba Medical Systems, Co. Ltd. Publisher Copyright: {\textcopyright} 2017 Elsevier Ltd",
year = "2017",
month = dec,
doi = "10.1016/j.thromres.2017.10.027",
language = "English",
volume = "160",
pages = "69--75",
journal = "Thrombosis Research",
issn = "0049-3848",
publisher = "Elsevier Limited",
}