心血管リモデリング

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of or pertaining to or involving the heart and blood vessels; "cardiovascular conditioning"

PrepTutorEJDIC

心臓と血管の(に影響する)

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1. 心血管MRIの臨床的有用性 clinical utility of cardiovascular magnetic resonance imaging
2. 心臓におけるアンギオテンシンⅡの作用 actions of angiotensin ii on the heart
3. 心臓リモデリング：臨床的評価および治療 cardiac remodeling clinical assessment and therapy
4. 急性心筋梗塞におけるアンギオテンシン変換酵素阻害剤：作用機序 angiotensin converting enzyme inhibitors in acute myocardial infarction mechanisms of action
5. 心臓再同期療法の利益の理論的根拠および機序 rationale for and mechanisms of benefit of cardiac resynchronization therapy

English Journal

Histone deacetylases in cardiac fibrosis: Current perspectives for therapy.

Tao H1, Shi KH2, Yang JJ3, Huang C4, Zhan HY1, Li J5.Author information 1Department of Cardiothoracic Surgery, The Second Hospital of Anhui Medical University, Hefei 230601, China; Cardiovascular Research Center, Anhui Medical University, Hefei 230601, China.2Department of Cardiothoracic Surgery, The Second Hospital of Anhui Medical University, Hefei 230601, China; Cardiovascular Research Center, Anhui Medical University, Hefei 230601, China. Electronic address: ayskh3@hotmail.com.3School of Pharmacy, Anhui Medical University, Hefei 230032, China; Department of Pharmacology, The Second Hospital of Anhui Medical University, Hefei 230601, China.4School of Pharmacy, Anhui Medical University, Hefei 230032, China.5School of Pharmacy, Anhui Medical University, Hefei 230032, China. Electronic address: yncs01@hotmail.com.AbstractCardiac fibrosis is an important pathological feature of cardiac remodeling in heart diseases. The molecular mechanisms of cardiac fibrosis are unknown. Histone deacetylases (HDACs) are enzymes that balance the acetylation activities of histone acetyltransferases on chromatin remodeling and play essential roles in regulating gene transcription. In recent years, the role of HDACs in cardiac fibrosis initiation and progression, as well as the therapeutic effects of HDAC inhibitors, has been well studied. Moreover, numerous studies indicated that HDAC activity is associated with the development and progression of cardiac fibrosis. In this review, the innovative aspects of HDACs are discussed, with respect to biogenesis, their role in cardiac fibrosis. Furthermore, the potential applications of HDAC inhibitors in the treatment of cardiac fibrosis associated with fibroblast activation and proliferation.
Cellular signalling.Cell Signal.2014 Mar;26(3):521-7. doi: 10.1016/j.cellsig.2013.11.037. Epub 2013 Dec 7.
Cardiac fibrosis is an important pathological feature of cardiac remodeling in heart diseases. The molecular mechanisms of cardiac fibrosis are unknown. Histone deacetylases (HDACs) are enzymes that balance the acetylation activities of histone acetyltransferases on chromatin remodeling and play ess
PMID 24321371

Reoxygenation-derived toxic reactive oxygen/nitrogen species modulate the contribution of bone marrow progenitor cells to remodeling after myocardial infarction.

Moldovan NI, Anghelina M, Varadharaj S, Butt OI, Wang T, Yang F, Moldovan L, Zweier JL.Author information Department of Internal Medicine/Division of Cardiovascular Medicine, The Ohio State University, Columbus, OH.AbstractBACKGROUND: The core region of a myocardial infarction is notoriously unsupportive of cardiomyocyte survival. However, there has been less investigation of the potentially beneficial spontaneous recruitment of endogenous bone marrow progenitor cells (BMPCs) within infarcted areas. In the current study we examined the role of tissue oxygenation and derived toxic species in the control of BMPC engraftment during postinfarction heart remodeling.
Journal of the American Heart Association.J Am Heart Assoc.2014 Feb 21;3(1):e000471. doi: 10.1161/JAHA.113.000471.
BACKGROUND: The core region of a myocardial infarction is notoriously unsupportive of cardiomyocyte survival. However, there has been less investigation of the potentially beneficial spontaneous recruitment of endogenous bone marrow progenitor cells (BMPCs) within infarcted areas. In the current stu
PMID 24419735

Galectin-3 testing: Validity of a novel automated assay in heart failure patients with reduced ejection fraction.

Gruson D1, Mancini M2, Ahn SA3, Rousseau MF3.Author information 1Pôle de Recherche en Endocrinologie, Diabète et Nutrition, Institut de Recherche Expérimentale et Clinique, Cliniques Universitaires St.-Luc and Université Catholique de Louvain, Brussels, Belgium; Department of Laboratory Medicine, Cliniques Universitaires St.-Luc and Université Catholique de Louvain, Brussels, Belgium. Electronic address: damien.gruson@uclouvain.be.2Department of Laboratory Medicine, Cliniques Universitaires St.-Luc and Université Catholique de Louvain, Brussels, Belgium.3Division of Cardiology, Cliniques Universitaires St.-Luc and Pôle de Recherche Cardiovasculaire, Institut de Recherche Expérimentale et Clinique, Université Catholique de Louvain, Brussels, Belgium.AbstractCirculating levels of galectin-3 (Gal-3), a marker of cardiac fibrosis and remodeling, contribute to the risk stratification of patients with heart failure (HF). The aim of our study was to determine the analytical validity and clinical validity of a novel automated Gal-3 assay in HF patients with reduced ejection fraction. We showed an excellent agreement between the VIDAS® Gal-3 automated assay and the ELISA reference method (r=0.90, p<0.001) and a mean difference of -1.3ng/mL was observed on the Bland and Altman plot. Gal-3 levels measured with the VIDAS® assay were significantly related to NYHA functional classes (p<0.001) and mean Gal-3 levels were 13.8ng/mL in NYHA II patients, 17.7ng/mL in NYHA III and 19.6ng/mL in NYHA IV. Furthermore, our results showed that Gal-3 levels measured with the VIDAS® assay were not only predictive of long-term cardiovascular death in patients with systolic HF but have also provided added value to natriuretic peptide testing in multimarker strategies. Therefore, our data are also supporting the clinical validity of the Gal-3 automated assay.
Clinica chimica acta; international journal of clinical chemistry.Clin Chim Acta.2014 Feb 15;429:189-93. doi: 10.1016/j.cca.2013.12.017. Epub 2013 Dec 21.
Circulating levels of galectin-3 (Gal-3), a marker of cardiac fibrosis and remodeling, contribute to the risk stratification of patients with heart failure (HF). The aim of our study was to determine the analytical validity and clinical validity of a novel automated Gal-3 assay in HF patients with r
PMID 24365381

Japanese Journal

Reverse Remodeling Achieved by Combination Therapy With High-Dose Beta Blocker and Cardiac Resynchronization

Muraoka Hironori,Imamura Teruhiko,Kinugawa Koichiro
International Heart Journal 56(4), 462-465, 2015
… Although both beta-blocker treatment and cardiac resynchronization therapy (CRT) have been established as the standard therapeutic strategy to achieve left ventricular reverse remodeling (LVRR) and improve prognosis in heart failure (HF) patients with systolic LV dysfunction, some patients do not respond to such treatments. …
NAID 130005087563

Advantage of Pulsatility in Left Ventricular Reverse Remodeling and Aortic Insufficiency Prevention During Left Ventricular Assist Device Treatment

Imamura Teruhiko,Kinugawa Koichiro,Nitta Daisuke,Hatano Masaru,Kinoshita Osamu,Nawata Kan,Ono Minoru
Circulation Journal advpub(0), 2015
… The PF LVAD was explanted in 5 patients (25%), and a CF LVAD was explanted in 1 patient (5%).Conclusions:Compared with CF LVADs, PF LVADs seem to have an advantage in improving LV reverse remodeling and preventing AI. …
NAID 130005083973

Reverse Remodeling Achieved by Combination Therapy With High-Dose Beta Blocker and Cardiac Resynchronization

Muraoka Hironori,Imamura Teruhiko,Kinugawa Koichiro
International Heart Journal advpub(0), 2015
… Although both beta-blocker treatment and cardiac resynchronization therapy (CRT) have been established as the standard therapeutic strategy to achieve left ventricular reverse remodeling (LVRR) and improve prognosis in heart failure (HF) patients with systolic LV dysfunction, some patients do not respond to such treatments. …
NAID 130005078535