2007 Fiscal Year Final Research Report Summary
New Strategy for Prevention of Thrombosis by Atrial Fibrillation : From a Viewpoint of Atrial Endocardium
Project/Area Number |
18590795
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Circulatory organs internal medicine
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Research Institution | The Cardiovascular Institute |
Principal Investigator |
TAKESHI Yamashita The Cardiovascular Institute, 循環器科, Researcher (20302721)
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Project Period (FY) |
2006 – 2007
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Keywords | atrial fibrillation / stroke / 循環器・脳梗塞 |
Research Abstract |
1. Basic Research To test a hypothesis that risk factors for stroke associated with atrial fibrillation (AF) could induce atrial endocardial dysfunction for themselves, we determined the expression level of tissue factor pathway inhibitor, thrombomodulin, eNOS, and PAI-1 in aged rats, SHR, and diabetic rats. Aging, hypertension, diabetes differentially down-regulated TFPI, TM, and eNOS in the atrial endocardium, suggesting that risk factors contribute to thrombus formation via atrial endocardial dysfunction. We also found out that the renin-angiotensin system plays a significant role in the atrial endocardial dysfunction by AF, using a specific AT1 blocker. 2. Clinical Research Using our hospital-based cohort of Shinken Database 2004-5, we determined the effects of RAS inhibitors and statins on the incidence of stroke in AF patients. Among the total 4255 patients enrolled into the database, 657 patients had AF at the initial visit. Stroke was observed in 1.1% of patients with RAS inhibitors and in 0.9% of those without, respectively. Also, there were no significant differences between patients with and without statins. Further studies will be required to determine the utility of endocardium-targeted strategy.
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