NCT03590522

Brief Summary

Heart failure (HF) is a continuously growing public health problem. The study aim to provide novel insights into the role of amino acids in pathogenesis of heart failure, to obtain a better understanding of cardiac ryanodine Receptor 2 role as an essential player in excitation-contraction coupling in pathogenesis of heart failure and clarify the potential value of these markers as targets for heart failure therapy

Trial Health

35
At Risk

Trial Health Score

Automated assessment based on enrollment pace, timeline, and geographic reach

Trial has exceeded expected completion date
Enrollment
50

participants targeted

Target at P25-P50 for all trials

Timeline
Completed

Started Jan 2019

Shorter than P25 for all trials

Status
unknown

Health score is calculated from publicly available data and should be used for screening purposes only.

Trial Relationships

Click on a node to explore related trials.

Study Timeline

Key milestones and dates

First Submitted

Initial submission to the registry

July 7, 2018

Completed
11 days until next milestone

First Posted

Study publicly available on registry

July 18, 2018

Completed
6 months until next milestone

Study Start

First participant enrolled

January 17, 2019

Completed
2 months until next milestone

Primary Completion

Last participant's last visit for primary outcome

March 28, 2019

Completed
2 days until next milestone

Study Completion

Last participant's last visit for all outcomes

March 30, 2019

Completed
Last Updated

January 9, 2019

Status Verified

January 1, 2019

Enrollment Period

2 months

First QC Date

July 7, 2018

Last Update Submit

January 8, 2019

Conditions

Heart Failure

Keywords

pathogenesis of heart failurecardiac ryanodine Receptor 2Amino acids

Outcome Measures

Primary Outcomes (1)

  • Decrease cardiac ryanodine Receptor 2 gene expression and change of amino acids levels in patients with heart failure.

    better understanding of cardiac ryanodine Receptor 2 role as an essential player in excitation-contraction coupling in pathogenesis of heart failure and the role of amino acids in pathogenesis of heart failure

    Baseline

Study Arms (2)

Group I:

Thirty heart failure patients

Genetic: Ryanodine Receptor 2 gene expression

Group II:

Twenty healthy controls

Genetic: Ryanodine Receptor 2 gene expression

Interventions

Ryanodine Receptor 2 gene expressionGENETIC

Ryanodine Receptor 2 gene expression will be measured by real time PCR. In addition, amino acids analysis will be measured in plasma by amino acid analyzer.

Group I:Group II:

Eligibility Criteria

Age18 Years - 75 Years
Sexall
Age GroupsAdult (18-64), Older Adult (65+)
Sampling MethodNon-Probability Sample
Study Population

Heart failure patients

You may qualify if:

  • According to American Heart Association, patients with manifestation of heart failure (dyspnea, edema in the feet, ankles, legs or abdomen, heart palpitations) as diagnosed by clinical examination, laboratory investigations and imaging techniques.

You may not qualify if:

  • Diabetic patients
  • Neurological disorders
  • Cancers.
  • Obese patient
  • Smokers
  • Patient with chest infection

Contact the study team to confirm eligibility.

Sponsors & Collaborators

Related Publications (5)

  • 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.

    PMID: 29457878BACKGROUND

  • 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.

    PMID: 29344379BACKGROUND

  • 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.

    PMID: 23770282BACKGROUND

  • 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.

    PMID: 28065668BACKGROUND

  • Aquilani R, La Rovere MT, Corbellini D, Pasini E, Verri M, Barbieri A, Condino AM, Boschi F. Plasma Amino Acid Abnormalities in Chronic Heart Failure. Mechanisms, Potential Risks and Targets in Human Myocardium Metabolism. Nutrients. 2017 Nov 15;9(11):1251. doi: 10.3390/nu9111251.

    PMID: 29140312BACKGROUND

MeSH Terms

Conditions

Heart Failure

Condition Hierarchy (Ancestors)

Heart DiseasesCardiovascular Diseases

Central Study Contacts

reham elmahdy

CONTACT

+201002714637rehamibrahimelmahdy@gmail.com

Study Design

Study Type
observational
Observational Model
CASE CONTROL
Time Perspective
CROSS SECTIONAL
Sponsor Type
OTHER
Responsible Party
PRINCIPAL INVESTIGATOR
PI Title
Principal Investigator

Study Record Dates

First Submitted

July 7, 2018

First Posted

July 18, 2018

Study Start

January 17, 2019

Primary Completion

March 28, 2019

Study Completion

March 30, 2019

Last Updated

January 9, 2019

Record last verified: 2019-01