Role of Amino Acids and Genetic Disorder in Pathogenesis of Heart Failure
|The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Know the risks and potential benefits of clinical studies and talk to your health care provider before participating. Read our disclaimer for details.|
|ClinicalTrials.gov Identifier: NCT03590522|
Recruitment Status : Not yet recruiting
First Posted : July 18, 2018
Last Update Posted : January 9, 2019
Information provided by (Responsible Party):
Reham I El-mahdy, Assiut University
No Study Results Posted on ClinicalTrials.gov for this Study
|Recruitment Status :||Not yet recruiting|
|Estimated Primary Completion Date :||March 28, 2019|
|Estimated Study Completion Date :||March 30, 2019|
Czepluch FS, Wollnik B, Hasenfuß G. Genetic determinants of heart failure: facts and numbers. ESC Heart Fail. 2018 Jun;5(3):211-217. doi: 10.1002/ehf2.12267. Epub 2018 Feb 19.
Bond AR, Iacobazzi D, Abdul-Ghani S, Ghorbel M, Heesom K, Wilson M, Gillett C, George SJ, Caputo M, Suleiman S, Tulloh RMR. Changes in contractile protein expression are linked to ventricular stiffness in infants with pulmonary hypertension or right ventricular hypertrophy due to congenital heart disease. Open Heart. 2018 Jan 3;5(1):e000716. doi: 10.1136/openhrt-2017-000716. eCollection 2018.
Ather S, Respress JL, Li N, Wehrens XH. Alterations in ryanodine receptors and related proteins in heart failure. Biochim Biophys Acta. 2013 Dec;1832(12):2425-31. doi: 10.1016/j.bbadis.2013.06.008. Epub 2013 Jun 14. Review.
Alvarado FJ, Chen X, Valdivia HH. Ablation of the cardiac ryanodine receptor phospho-site Ser2808 does not alter the adrenergic response or the progression to heart failure in mice. Elimination of the genetic background as critical variable. J Mol Cell Cardiol. 2017 Feb;103:40-47. doi: 10.1016/j.yjmcc.2017.01.001. Epub 2017 Jan 6.