大動脈弁狭窄症 大動脈弁狭窄 AS
- abnormal narrowing of a bodily canal or passageway (同)stricture
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- The role of valvular endothelial cell paracrine signaling and matrix elasticity on valvular interstitial cell activation.
- Gould ST1, Matherly EE1, Smith JN1, Heistad DD2, Anseth KS3.Author information 1Department of Chemical and Biological Engineering, The BioFrontiers Institute, Boulder, CO 80303, USA.2Departments of Internal Medicine and Pharmacology, University of Iowa Health Care, Iowa City, IA 52242, USA.3Department of Chemical and Biological Engineering, The BioFrontiers Institute, Boulder, CO 80303, USA; Howard Hughes Medical Institute University of Colorado, Boulder, CO 80303, USA. Electronic address: Kristi.Anseth@Colorado.edu.AbstractThe effects of valvular endothelial cell (VlvEC) paracrine signaling on VIC phenotype and nodule formation were tested using a co-culture platform with physiologically relevant matrix elasticities and diffusion distance. 100 μm thin poly(ethylene glycol) (PEG) hydrogels of 3-27 kPa Young's moduli were fabricated in transwell inserts. VICs were cultured on the gels, as VIC phenotype is known to change significantly within this range, while VlvECs lined the underside of the membrane. Co-culture with VlvECs significantly reduced VIC activation to the myofibroblast phenotype on all gels with the largest percent decrease on the 3 kPa gels (∼70%), while stiffer gels resulted in approximately 20-30% decrease. Additionally, VlvECs significantly reduced αSMA protein expression (∼2 fold lower) on both 3 and 27 kPa gels, as well as the number (∼2 fold lower) of nodules formed on the 27 kPa gels. Effects of VlvECs were prevented when nitric oxide (NO) release was inhibited with l-NAME, suggesting that VlvEC produced NO inhibits VIC activation. Withdrawal of l-NAME after 3, 5, and 7 days with restoration of VlvEC NO production for 2 additional days led to a partial reversal of VIC activation (∼25% decrease). A potential mechanism by which VlvEC produced NO reduced VIC activation was studied by inhibiting initial and mid-stage cGMP pathway molecules. Inhibition of soluble guanylyl cyclase (sGC) with ODQ or protein kinase G (PKG) with RBrcGMP or stimulation of Rho kinase (ROCK) with LPA, abolished VlvEC effects on VIC activation. This work contributes substantially to the understanding of the valve endothelium's role in preventing VIC functions associated with aortic valve stenosis initiation and progression.
- Biomaterials.Biomaterials.2014 Apr;35(11):3596-606. doi: 10.1016/j.biomaterials.2014.01.005. Epub 2014 Jan 24.
- The effects of valvular endothelial cell (VlvEC) paracrine signaling on VIC phenotype and nodule formation were tested using a co-culture platform with physiologically relevant matrix elasticities and diffusion distance. 100 μm thin poly(ethylene glycol) (PEG) hydrogels of 3-27 kPa Young's moduli
- PMID 24462357
- microRNA-122 down-regulation may play a role in severe myocardial fibrosis in human aortic stenosis through TGF-β1 up-regulation.
- Beaumont J1, López B1, Hermida N1, Schroen B2, San José G1, Heymans S2, Valencia F3, Gómez-Doblas JJ3, De Teresa E3, Díez J, González A1.Author information 1*Division of Cardiovascular Sciences, Centre for Applied Medical Research, University of Navarra, 31008 Pamplona, Spain.2†Center for Heart Failure Research, Cardiovascular Research Institute Maastricht, Maastricht University, 6229 ER Maastricht, The Netherlands.3‡Division of Cardiology, Virgen de la Victoria University Hospital, 29010 Málaga, Spain.AbstractmiRNAs (microRNAs) have been shown to play a role in myocardial fibrosis. The present study was designed to analyse whether alterations in miRNA expression contribute to the progression of myocardial fibrosis in AS (aortic valve stenosis) patients through up-regulation of the pro-fibrotic factor TGF-β1 (transforming growth factor-β type 1). Endomyocardial biopsies were obtained from 28 patients with severe AS, and from the necropsies of 10 control subjects. AS patients presented increased myocardial CVF (collagen volume fraction) and TGF-β1 compared with the controls, these parameters being correlated in all patients. Patients were divided into two groups by cluster analysis according to their CVF: SF (severe fibrosis; CVF >15%; n=15) and non-SF (CVF ≤15%; n=13). TGF-β1 was increased in patients with SF compared with those with non-SF. To analyse the involvement of miRNAs in SF, the miRNA expression profile of 10 patients (four with non-SF and six with SF) was analysed showing that 99 miRNAs were down-regulated and 19 up-regulated in the SF patients compared with the non-SF patients. Those miRNAs potentially targeting TGF-β1 were validated by real-time RT (reverse transcription)-PCR in the whole test population, corroborating that miR-122 and miR-18b were down-regulated in patients with SF compared with those with non-SF and the control subjects. Additionally, miR-122 was inversely correlated with the CVF, TGF-β1 and the TGF-β1-regulated PCPE-1 (procollagen C-terminal proteinase enhancer-1) in all patients. Experiments in human fibroblasts demonstrated that miR-122 targets and inhibits TGF-β1. In conclusion, for the first time we show that myocardial down-regulation of miR-122 might be involved in myocardial fibrosis in AS patients, probably through TGF-β1 up-regulation.
- Clinical science (London, England : 1979).Clin Sci (Lond).2014 Apr;126(7):497-506. doi: 10.1042/CS20130538.
- miRNAs (microRNAs) have been shown to play a role in myocardial fibrosis. The present study was designed to analyse whether alterations in miRNA expression contribute to the progression of myocardial fibrosis in AS (aortic valve stenosis) patients through up-regulation of the pro-fibrotic factor TGF
- PMID 24168656
- Transcatheter aortic valve implantation: status and challenges.
- Fishbein GA1, Schoen FJ2, Fishbein MC3.Author information 1Department of Pathology and Laboratory Medicine David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, CHS 13-145, Los Angeles, CA 90095-1732. Electronic address: email@example.comDepartment of Pathology Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115.3Department of Pathology and Laboratory Medicine David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, CHS 13-145, Los Angeles, CA 90095-1732.AbstractCalcific aortic valve disease of the elderly is the most prevalent hemodynamically-significant valvular disease, and the most common lesion requiring valve replacement in industrialized countries. Transcatheter aortic valve implantation is a less invasive alternative to classical aortic valve replacement that can provide a therapeutic option for high-risk or inoperable patients with aortic stenosis. These devices must be biocompatible, have excellent hemodynamic performance, be easy to insert, be securely anchored without sutures, and be durable, without increased risk of thrombosis or infection. To date, complications are related to the site of entry for insertion, the site of implantation (aorta, coronary ostia, base of left ventricle), and to the structure and design of the inserted device. However, as with any novel technology unanticipated complications will develop. Goals for future development will be to make the devices more effective, more durable, safer, and easier to implant, so as to further improve outcome for patients with severe aortic stenosis. The pathologist participating in research and development, and examination of excised devices will have a critical role in improving outcome for these patients.
- Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology.Cardiovasc Pathol.2014 Mar-Apr;23(2):65-70. doi: 10.1016/j.carpath.2013.10.001. Epub 2013 Oct 8.
- Calcific aortic valve disease of the elderly is the most prevalent hemodynamically-significant valvular disease, and the most common lesion requiring valve replacement in industrialized countries. Transcatheter aortic valve implantation is a less invasive alternative to classical aortic valve replac
- PMID 24183003
- Emergent balloon aortic valvuloplasty as a bridge to transcatheter aortic valve implantation with marked risk reduction of perioperative and postoperative mortality
- Cardiovascular intervention and therapeutics 31(2), 151-155, 2016-04
- NAID 40020789743
- Externalization of a stiff guide wire via the radial artery : a new technique to facilitate advancement of an Inoue balloon across the aortic valve in patients with aortic stenosis undergoing antegrade balloon aortic valvuloplasty
- Cardiovascular intervention and therapeutics 31(2), 140-146, 2016-04
- NAID 40020789718
- 日本保険医学会誌 = Japanese journal of insurance medicine 114(1), 28-44, 2016-03
- NAID 40020783660
- Overview Aortic valve stenosis — or aortic stenosis — occurs when the heart's aortic valve narrows. This narrowing prevents the valve from opening fully, which reduces or blocks blood flow from your heart into the main artery to your ...
- What is aortic valve stenosis (AS)? Aortic stenosis is one of the most common and most serious valve disease problems. Aortic stenosis is a narrowing of the aortic valve opening. Aortic stenosis restricts the blood flow ...
- Your aortic valve plays a key role in getting oxygen-rich blood to your body. Aortic valve stenosis is a common and serious heart problem when the valve doesn’t open fully. Learn about what causes it and how it can be ...
- aortic stenosis, AS, aortic valve stenosis
- 感染症 ：溶連菌感染によるリウマチ熱(現在では稀となっている)、感染性心内膜症
- 血管疾患：動脈硬化に続発 → 最も多い、らしい
- pocket medicine
||Max Jet Vel
- 奇異性分裂(A弁の狭窄により大動脈側の押し戻す圧力(back pressure)が上がるのに時間がかかり、A2音のdelayとなる)。収縮期雑音が両頚部で聴取される。
- 往復雑音 to-and-fro murmur：拡張期の逆流性雑音に加え、一回拍出量の増加による相対的大動脈弁狭窄による収縮期雑音を聴取。
- 表21 大動脈弁狭窄症の治療方針を判断する上での診断的手法の実施
- 1 心電図検査
- 2 胸部X線写真、心エコー・ドプラ法
- 1. 弁膜疾患の非薬物治療に関するガイドライン（2007年改訂版）
- 1. [charged] 成人における大動脈弁狭窄症の臨床像とその評価 - uptodate 
- 2. [charged] 成人における大動脈弁狭窄症の自然歴 - uptodate 
- aortic stenosis