• 微博
  • 微信微信二维码

广东省人民政府首页  >  要闻动态  >  广东要闻

李宗瑞快播种子下载_

来源: 南方日报网络版     时间:2019-11-14 22:48:56

李宗瑞快播种子下载

Early Recent, Mar 09, 2019; DOI:10.1007/s10557-019-06871-3

Effects of Teneligliptin on the Progressive Left Ventricular Diastolic Dysfunction in Patients with Type 2 Diabetes Mellitus in Open-Label, Marker-Stratified Randomized, Parallel-Group Comparison, Standard Treatment-Controlled Multicenter Trial (TOPLEVEL Cardiovasc?Drugs?Ther ORIGINAL ARTICLEEarly Recent, Mar 09, 201910.1007/s10557-019-06871-3本文由“天纳”临床学术信息人工智能系统自动翻译点击文末“阅读原文”下载本文PDFBackground and AimsDiabetes mellitus (DM) can cause left ventricular (LV) diastolic dysfunction, leading to heart failure with preserved ejection fraction (HFpEF). Dipeptidyl peptidase IV (DPP-IV) inhibitors have failed to reduce hospitalization due to HF in type 2 DM (T2D) patients in a large-scale clinical trial, despite their cardiovascular protective effects. Therefore, it is important to investigate whether DPP-IV inhibitors can improve LV diastolic dysfunction in T2D patients. The aim of the study was to evaluate whether teneligliptin, the strongest of the DPP-IV inhibitors, improves LV dysfunction or prevents the worsening of LV diastolic function in T2D patients.糖尿病(dm)可导致左心室(lv)舒张功能障碍,导致射血分数(hfpef)维持的心力衰竭

尽管二肽基肽酶IV(DPP-IV)抑制剂具有心血管保护作用,但在一项大规模临床试验中,由于2型糖尿病(T2D)患者的心力衰竭,二肽基肽酶IV(DPP-IV)抑制剂未能减少住院率

因此,探讨DPP-IV抑制剂是否能改善T2D患者左室舒张功能障碍具有重要意义

本研究的目的是评价替格列汀(DPP-IV抑制剂中最强的)是否改善了T2D患者的左室功能障碍或预防左室舒张功能恶化

MethodsThe TOPLEVEL study is designed as an open-labeled, marker-stratified randomized, parallel-group comparison, standard treatment-controlled multicenter study. TOPLEVEL includes two marker-defined subgroups to give treatment recommendations for T2D patients with normal (E/e′?顶层研究设计为开放标记、标记分层随机、平行组比较、标准治疗对照多中心研究

TopLevel包括两个标记定义的亚组,为正常(e/e′Conclusion and PerspectivesTOPLEVEL is a clinical trial of teneligliptin targeting LV diastolic dysfunction in T2D patients. This study demonstrates the effectiveness of DPP-IV inhibitors on LV diastolic dysfunction, an important surrogate endpoint to predict the cardiovascular outcomes of HFpEF (UMIN000014589).TOPLEVEL是替格列汀治疗T2D患者左室舒张功能障碍的临床试验

本研究证实了DPP-IV抑制剂对左室舒张功能障碍的有效性,这是预测HFPEF心血管结局的重要替代终点(umin000014589)

NotesAcknowledgmentsWe gratefully acknowledge Ms. M. Yoda, Ms. M. Takahashi, Ms. R. Umezawa, and Ms. M. Saida for their secretarial assistance.Authors’ ContributionsMI conceived the study. MI and SI wrote the manuscript. TH performed statistical analyses and provided the biostatistical study design. MK conceived and supervised the study and is the Principal Investigator on the grant. All authors read and approved the final manuscript.Sources of FundingThis study was conducted with funding provided by the Mitsubishi Tanabe Pharma Corporation.Compliance with Ethical StandardsConflict of InterestPersons from Mitsubishi Tanabe Pharma Corporation were not involved in conducting this study and analysis, and the intentions of Mitsubishi Tanabe Pharma Corporation are not reflected in the results or interpretations of this study.DisclosureDrs. Imadu, Ito, and Hamasaki have nothing to disclose. Dr. Nakano is now an employee of GlaxoSmithKline K.K. Dr. Kitakaze reports receiving grants from the Japanese government during the course of the study: grants from the Japanese government, grants from the Japan Heart Foundation, grants from the Japan Cardiovascular Research Foundation, grants and personal fees from Asteras, personal fees from Daiichi-sankyo, grants and personal fees from Pfizer, grants and personal fees from Ono, personal fees from Bayer, grants from Novartis, grants and personal fees from Mitubishi Tanabe Pharma, personal fees from Kowa, personal fees from MSD, grants from Nihon Kohden, personal fees from Shionogi, personal fees from AstraZeneca, grants and personal fees from AstraZeneca, personal fees from Taisho-Toyama, personal fees from Toyama-Kagaku, grants and personal fees from Kureha, and personal fees from Toaeiyo, outside of the currently proposed work.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.References1. Devereux RB, Roman MJ, Paranicas M, OGrady MJ, Lee ET, Welty TK, et al. Impact of diabetes on cardiac structure and function: the strong heart study. Circulation. 2000;101(19):2271–6.CrossRefGoogle Scholar 2. Eguchi K, Boden-Albala B, Jin Z, Rundek T, Sacco RL, Homma S, et al. Association between diabetes mellitus and left ventricular hypertrophy in a multiethnic population. Am J Cardiol. 2008;101(12):1787–91.CrossRefGoogle Scholar 3. From AM, Scott CG, Chen HH. The development of heart failure in patients with diabetes mellitus and pre-clinical diastolic dysfunction a population-based study. J Am Coll Cardiol. 2010;55(4):300–5.CrossRefGoogle Scholar 4. Vinereanu D, Nicolaides E, Tweddel AC, Madler CF, Holst B, Boden LE, et al. Subclinical left ventricular dysfunction in asymptomatic patients with type II diabetes mellitus, related to serum lipids and glycated haemoglobin. Clin Sci (London, England : 1979). 2003;105(5):591–9.CrossRefGoogle Scholar 5. Aneja A, Tang WH, Bansilal S, Garcia MJ, Farkouh ME. Diabetic cardiomyopathy: insights into pathogenesis, diagnostic challenges, and therapeutic options. Am J Med. 2008;121(9):748–57.CrossRefGoogle Scholar 6. Owan TE, Hodge DO, Herges RM, Jacobsen SJ, Roger VL, Redfield MM. Trends in prevalence and outcome of heart failure with preserved ejection fraction. N Engl J Med. 2006;355(3):251–9.CrossRefGoogle Scholar 7. Gomez N, Touihri K, Matheeussen V, Mendes Da Costa A, Mahmoudabady M, Mathieu M, et al. Dipeptidyl peptidase IV inhibition improves cardiorenal function in overpacing-induced heart failure. Eur J Heart Fail. 2012;14(1):14–21.CrossRefGoogle Scholar 8. Shigeta T, Aoyama M, Bando YK, Monji A, Mitsui T, Takatsu M, et al. Dipeptidyl peptidase-4 modulates left ventricular dysfunction in chronic heart failure via angiogenesis-dependent and -independent actions. Circulation. 2012;126(15):1838–51.CrossRefGoogle Scholar 9. Son JW, Kim S. Dipeptidyl peptidase 4 inhibitors and the risk of cardiovascular disease in patients with type 2 diabetes: a tale of three studies. Diabetes Metab J. 2015;39(5):373–83.CrossRefGoogle Scholar 10. Fukuda-Tsuru S, Anabuki J, Abe Y, Yoshida K, Ishii S. A novel, potent, and long-lasting dipeptidyl peptidase-4 inhibitor, teneligliptin, improves postprandial hyperglycemia and dyslipidemia after single and repeated administrations. Eur J Pharmacol. 2012;696(1–3):194–202.CrossRefGoogle Scholar 11. Yoshihara F, Imazu M, Hamasaki T, Anzai T, Yasuda S, Ito S, et al. An exploratory study of Dapagliflozin for the attenuation of albuminuria in patients with heart failure and type 2 diabetes mellitus (DAPPER). Cardiovasc Drugs Ther. 2018;32(2):183–90.CrossRefGoogle Scholar 12. Gordon Lan K, DeMets DL. Discrete sequential boundaries for clinical trials. Biometrika. 1983;70(3):659–63.CrossRefGoogle Scholar 13. Cui L, Hung HM, Wang SJ. Modification of sample size in group sequential clinical trials. Biometrics. 1999;55(3):853–7.CrossRefGoogle Scholar 14. Matsushita K, Blecker S, Pazin-Filho A, Bertoni A, Chang PP, Coresh J, et al. The association of hemoglobin a1c with incident heart failure among people without diabetes: the atherosclerosis risk in communities study. Diabetes. 2010;59(8):2020–6.CrossRefGoogle Scholar 15. Gonzalez-Vilchez F, Ayuela J, Ares M, Pi J, Castillo L, Martin-Duran R. Oxidative stress and fibrosis in incipient myocardial dysfunction in type 2 diabetic patients. Int J Cardiol. 2005;101(1):53–8.CrossRefGoogle Scholar 16. Ihm SH, Youn HJ, Shin DI, Jang SW, Park CS, Kim PJ, et al. Serum carboxy-terminal propeptide of type I procollagen (PIP) is a marker of diastolic dysfunction in patients with early type 2 diabetes mellitus. Int J Cardiol. 2007;122(3):e36–8.CrossRefGoogle Scholar 17. Borlaug BA, Melenovsky V, Redfield MM, Kessler K, Chang HJ, Abraham TP, et al. Impact of arterial load and loading sequence on left ventricular tissue velocities in humans. J Am Coll Cardiol. 2007;50(16):1570–7.CrossRefGoogle Scholar 18. Saiki H, Moulay G, Guenzel AJ, Liu W, Decklever TD, Classic KL, et al. Experimental cardiac radiation exposure induces ventricular diastolic dysfunction with preserved ejection fraction. Am J Physiol Heart Circ Physiol. 2017;313(2):H392–h407.CrossRefGoogle Scholar 19. Kawaguchi M, Hay I, Fetics B, Kass DA. Combined ventricular systolic and arterial stiffening in patients with heart failure and preserved ejection fraction: implications for systolic and diastolic reserve limitations. Circulation. 2003;107(5):714–20.CrossRefGoogle Scholar 20. Elzinga G, Westerhof N. Pressure and flow generated by the left ventricle against different impedances. Circ Res. 1973;32(2):178–86.CrossRefGoogle Scholar 21. Hori M, Inoue M, Kitakaze M, Tsujioka K, Ishida Y, Fukunami M, et al. Ejection timing as a major determinant of left ventricular relaxation rate in isolated perfused canine heart. Circ Res. 1984;55(1):31–8.CrossRefGoogle Scholar 22. From AM, Scott CG, Chen HH. Changes in diastolic dysfunction in diabetes mellitus over time. Am J Cardiol. 2009;103(10):1463–6.CrossRefGoogle Scholar 23. van den Hurk K, Alssema M, Kamp O, Henry RM, Stehouwer CD, Smulders YM, et al. Independent associations of glucose status and arterial stiffness with left ventricular diastolic dysfunction: an 8-year follow-up of the Hoorn study. Diabetes Care. 2012;35(6):1258–64.CrossRefGoogle Scholar 24. Redfield MM, Jacobsen SJ, Burnett JC Jr, Mahoney DW, Bailey KR, Rodeheffer RJ. Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JAMA. 2003;289(2):194–202.CrossRefGoogle Scholar 25. Okura H, Kubo T, Asawa K, Toda I, Yoshiyama M, Yoshikawa J, et al. Elevated E/E predicts prognosis in congestive heart failure patients with preserved systolic function. Circ J. 2009;73(1):86–91.CrossRefGoogle Scholar 26. Akiyama E, Sugiyama S, Matsuzawa Y, Konishi M, Suzuki H, Nozaki T, et al. Incremental prognostic significance of peripheral endothelial dysfunction in patients with heart failure with normal left ventricular ejection fraction. J Am Coll Cardiol. 2012;60(18):1778–86.CrossRefGoogle Scholar 27. Ommen SR, Nishimura RA, Appleton CP, Miller FA, Oh JK, Redfield MM, et al. Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures: a comparative simultaneous Doppler-catheterization study. Circulation. 2000;102(15):1788–94.CrossRefGoogle Scholar 28. Mullens W, Borowski AG, Curtin RJ, Thomas JD, Tang WH. Tissue Doppler imaging in the estimation of intracardiac filling pressure in decompensated patients with advanced systolic heart failure. Circulation. 2009;119(1):62–70.CrossRefGoogle Scholar 29. Mitter SS, Shah SJ, Thomas JD. A test in context: E/A and E/e to Assess Diastolic Dysfunction and LV Filling Pressure. J Am Coll Cardiol. 2017;69(11):1451–64.CrossRefGoogle Scholar 30. Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland JG, Coats AJ, et al. 2016 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure: the task force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC)developed with the special contribution of the heart failure association (HFA) of the ESC. Eur Heart J. 2016;37(27):2129–200.CrossRefGoogle Scholar 31. Takahashi A, Ihara M, Yamazaki S, Asanuma H, Asakura M, Kitakaze M. Impact of either GLP-1 agonists or DPP-4 inhibitors on pathophysiology of heart failure. Int Heart J. 2015;56(4):372–6.CrossRefGoogle Scholar 32. Ihara M, Asanuma H, Yamazaki S, Kato H, Asano Y, Shinozaki Y, et al. An interaction between glucagon-like peptide-1 and adenosine contributes to cardioprotection of a dipeptidyl peptidase 4 inhibitor from myocardial ischemia-reperfusion injury. Am J Physiol Heart Circ Physiol. 2015;308(10):H1287–97.CrossRefGoogle Scholar 33. Aoyama M, Kawase H, Bando YK, Monji A, Murohara T. Dipeptidyl peptidase 4 inhibition alleviates shortage of circulating glucagon-like Peptide-1 in heart failure and mitigates myocardial remodeling and apoptosis via the exchange protein directly activated by cyclic AMP 1/Ras-related protein 1 Axis. Circ Heart Fail. 2016;9(1):e002081.CrossRefGoogle Scholar 34. Pyke C, Heller RS, Kirk RK, Orskov C, Reedtz-Runge S, Kaastrup P, et al. GLP-1 receptor localization in monkey and human tissue: novel distribution revealed with extensively validated monoclonal antibody. Endocrinology. 2014;155(4):1280–90.CrossRefGoogle Scholar 35. Takashima S, Fujita H, Fujishima H, Shimizu T, Sato T, Morii T, et al. Stromal cell-derived factor-1 is upregulated by dipeptidyl peptidase-4 inhibition and has protective roles in progressive diabetic nephropathy. Kidney Int. 2016;90(4):783–96.CrossRefGoogle Scholar 36. Kim M, Platt MJ, Shibasaki T, Quaggin SE, Backx PH, Seino S, et al. GLP-1 receptor activation and Epac2 link atrial natriuretic peptide secretion to control of blood pressure. Nat Med. 2013;19(5):567–75.CrossRefGoogle Scholar 37. Lee MY, Tsai KB, Hsu JH, Shin SJ, Wu JR, Yeh JL. Liraglutide prevents and reverses monocrotaline-induced pulmonary arterial hypertension by suppressing ET-1 and enhancing eNOS/sGC/PKG pathways. Sci Rep. 2016;6:31788.CrossRefGoogle Scholar ?Effects of Teneligliptin on the Progressive Left Ventricular Diastolic Dysfunction in Patients with Type 2 Diabetes Mellitus in Open-Label, Marker-Stratified Randomized, Parallel-Group Comparison, Standard Treatment-Controlled Multicenter Trial (TOPLEVEL Cardiovasc?Drugs?Ther ORIGINAL ARTICLEEarly Recent, Mar 09, 201910.1007/s10557-019-06871-3




相关文章

版权所有:57fak 粤ICP备05070829 网站标识码4400000131
主办:南方新闻网 协办:广东省经济和信息化委员会 承办:南方新闻网
建议使用1024×768分辨率 IE7.0以上版本浏览器