Heart FailureNCT06503601
The Impact of Genetic Polymorphism on the Echocardiographic Parameters and Cardiac Fibrosis Markers in Response to Empagliflozin Treatment Among Patients With Heart Failure
An observational study of Heart Failure, run by Ain Shams University at 1 site in Egypt.
Trial summary
It is important to assess the implications of genetic variants of the TGF-β1 gene in patients with HFrEF and the association of this polymorphism with treatment response to SGLT2I. Read more about this study
- Who is it for?
- Ages 18 to 80 years
- Conditions the study is for
- Heart Failure
- How many people
- 92 participants
- Where
- 1 siteEgypt
- Study dates
- 30 Jul 2023to 1 Oct 2025
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 80 years
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Heart failure patients treated with empagliflozin
Who may be able to join
- Heart failure patients NYHA class II to IV.
- Treatment with beta blockers, MRAs, ACEIs in addition to empagliflozin.
- Age of 18 years to 80 years.
- Written informed consent of the subject to participate in the study.
Who cannot join
- Contraindication to empagliflozin: pregnancy, hypersensitivity, and severe renal impairment.
- CABG or valve surgery within 3 months.
- Mild-to-severe valvular stenosis or severe (grade III/IV) valvular regurgitation
- Pregnant or nursing women.
Trial locations and contacts
1 site in 1 country.
About this study
It is important to assess the implications of genetic variants of the TGF-β1 gene in patients with HFrEF and the association of this polymorphism with treatment response to SGLT2I. Therefore, by correlating the pharmacogenetics hand in hand with the mechanistic markers involved in the pathogenesis of HF, this can aid in the development of individualized, therapeutic strategies and improve the patient's drug response.
Read the detailed description
Cardiovascular diseases are the leading cause of morbidity and mortality worldwide. According to the American heart association (AHA) over 19.1 million deaths worldwide in 2020 were attributed to CVD. Heart failure (HF) is considered one of the most frequent causes of hospitalization and the final stage of many heart disorders. It is associated with high rates of morbidity and mortality. Heart failure (HF) affects more than 5.8 million people in the USA and over 23 million people worldwide, making it a serious public health issue. According to the 2022 guidelines of American heart association (AHA) a variety of non-pharmacologic and pharmacologic are available to treat heart failure (HF) to prevent or reverse its symptoms. Nonpharmacologic treatments may involve dietary sodium and fluid restriction, proper physical activity, and attention to weight gain depending on the illness\'s severity. Pharmacologic treatments include the use of diuretics, vasodilators, inotropic agents, anticoagulants, beta blockers, angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), calcium channel blockers (CCBs), digoxin, nitrates, B-type natriuretic peptides (BNPs), I(f) inhibitors, angiotensin receptor-neprilysin inhibitors (ARNIs), soluble guanylate cyclase stimulators, sodium-glucose cotransporter-2 inhibitors (SGLT2Is), and mineralocorticoid receptor antagonists (MRAs). Recent study has shown that SGLT2I not only lowers blood sugar levels but also protects the kidney and heart, which can dramatically lower cardiovascular events, stall the advancement of renal failure, significantly raise patient quality of life, and lower medical costs for families and society. A study showed that Empagliflozin has cardio-renal protective effects as it reduced inflammatory and fibrotic markers, such as NF-κB, TGF-β1, and improved fibrosis. However, it was found that the variation in treatment response with SGLT2I may be due to the genetic polymorphism of TGF-β1 since this polymorphism may influence its expression. Therefore, it is important to assess the implications of genetic variants of the TGF-β1 gene in patients with HFrEF and the association of this polymorphism with treatment response to SGLT2I. Therefore, by correlating the pharmacogenetics hand in hand with the mechanistic markers involved in the pathogenesis of HF, this can aid in the development of individualized, therapeutic strategies and improve the patient's drug response.
- Conditions
- Heart Failure
- Keywords
- Heart Failure, genetic polymorphism, cardiac fibrosis markers, empagliflozin, echocardiographic parameters
- Medical subject headings
- Heart Failure
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
| Study group | Role | What they receive |
|---|---|---|
| Responders to empagliflozin | Heart failure patients who showed response to empagliflozin | |
| Non responders to empagliflozin | Heart failure patients who showed no response to empagliflozin |
What is being measured
The primary outcome is the main question the study is designed to answer.
Genetic polymorphism and echocardiographic parameters
To detect association between a TGFβ1 gene polymorphism variants and echocardiographic outcome of patients with HFrEF in response to empagliflozin.
Measured: 3-6 months
Secondary outcomes (1)
Cardiac fibrosis biochemical markers
- To detect association between serum TGFβ1, MMP-2 and TNF-α levels (cardiac fibrosis biochemical marker) and echocardiographic parameters of patients with HFrEF in response to empagliflozin
Measured: 3-6 months
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted16 Jul 2024
- Study start30 Jul 2023
- Primary completion30 Jul 2025 (estimated)
- Study completion1 Oct 2025 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for Heart FailureStudies of the same condition, open and under way.
- More trials run by Ain Shams UniversityThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 92 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Ain Shams University
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Ruwan Mokhtar, Ain Shams University
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06503601
- Sponsor's protocol ID
- rec#264
- Status last verified
- Jul 2024
- First submitted
- 10 Jul 2024
- Last updated
- 16 Jul 2024
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- Undecided
Study at a glance
From the registry record, last updated by the sponsor on 16 Jul 2024. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- The Impact of Genetic Polymorphism on the Echocardiographic Parameters and Cardiac Fibrosis Markers in Response to Empagliflozin Treatment Among Patients With Heart Failure
- ClinicalTrials.gov ID
- NCT06503601
- Acronym / sponsor ID
- rec#264
- Conditions
- Heart Failure
- Keywords
- Heart Failure, genetic polymorphism, cardiac fibrosis markers, empagliflozin, echocardiographic parameters
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 92 participants (estimated)
- Lead sponsor
- Ain Shams UniversityUniversity, hospital or other
- Study start
- 30 Jul 2023 (actual)
- Primary completion
- 30 Jul 2025 (estimated)
- Study completion
- 1 Oct 2025 (estimated)
- First posted
- 16 Jul 2024 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
It is important to assess the implications of genetic variants of the TGF-β1 gene in patients with HFrEF and the association of this polymorphism with treatment response to SGLT2I. Therefore, by correlating the pharmacogenetics hand in hand with the mechanistic markers involved in the pathogenesis of HF, this can aid in the development of individualized, therapeutic strategies and improve the patient's drug response.
Detailed description
Cardiovascular diseases are the leading cause of morbidity and mortality worldwide. According to the American heart association (AHA) over 19.1 million deaths worldwide in 2020 were attributed to CVD. Heart failure (HF) is considered one of the most frequent causes of hospitalization and the final stage of many heart disorders. It is associated with high rates of morbidity and mortality. Heart failure (HF) affects more than 5.8 million people in the USA and over 23 million people worldwide, making it a serious public health issue. According to the 2022 guidelines of American heart association (AHA) a variety of non-pharmacologic and pharmacologic are available to treat heart failure (HF) to prevent or reverse its symptoms. Nonpharmacologic treatments may involve dietary sodium and fluid restriction, proper physical activity, and attention to weight gain depending on the illness\'s severity. Pharmacologic treatments include the use of diuretics, vasodilators, inotropic agents, anticoagulants, beta blockers, angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), calcium channel blockers (CCBs), digoxin, nitrates, B-type natriuretic peptides (BNPs), I(f) inhibitors, angiotensin receptor-neprilysin inhibitors (ARNIs), soluble guanylate cyclase stimulators, sodium-glucose cotransporter-2 inhibitors (SGLT2Is), and mineralocorticoid receptor antagonists (MRAs). Recent study has shown that SGLT2I not only lowers blood sugar levels but also protects the kidney and heart, which can dramatically lower cardiovascular events, stall the advancement of renal failure, significantly raise patient quality of life, and lower medical costs for families and society. A study showed that Empagliflozin has cardio-renal protective effects as it reduced inflammatory and fibrotic markers, such as NF-κB, TGF-β1, and improved fibrosis. However, it was found that the variation in treatment response with SGLT2I may be due to the genetic polymorphism of TGF-β1 since this polymorphism may influence its expression. Therefore, it is important to assess the implications of genetic variants of the TGF-β1 gene in patients with HFrEF and the association of this polymorphism with treatment response to SGLT2I. Therefore, by correlating the pharmacogenetics hand in hand with the mechanistic markers involved in the pathogenesis of HF, this can aid in the development of individualized, therapeutic strategies and improve the patient's drug response.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Responders to empagliflozin | – | –Heart failure patients who showed response to empagliflozin |
| Non responders to empagliflozin | – | –Heart failure patients who showed no response to empagliflozin |
Who may qualify
- Ages
- 18 to 80 years
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Heart failure patients treated with empagliflozin
Key inclusion criteria (4 listed)
- Heart failure patients NYHA class II to IV.
- Treatment with beta blockers, MRAs, ACEIs in addition to empagliflozin.
- Age of 18 years to 80 years.
- Written informed consent of the subject to participate in the study.
Key exclusion criteria (4 listed)
- Contraindication to empagliflozin: pregnancy, hypersensitivity, and severe renal impairment.
- CABG or valve surgery within 3 months.
- Mild-to-severe valvular stenosis or severe (grade III/IV) valvular regurgitation
- Pregnant or nursing women.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
Genetic polymorphism and echocardiographic parameters
Time frame: 3-6 months
To detect association between a TGFβ1 gene polymorphism variants and echocardiographic outcome of patients with HFrEF in response to empagliflozin.
1 secondary outcome
Cardiac fibrosis biochemical markers
Time frame: 3-6 months
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 16 Jul 2024.
- Individual participant dataSharing planned: Undecided
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
The record lists no contact. Use the official record to reach the sponsor.
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Heart Failure, run by Ain Shams University at 1 site in Egypt.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 4 inclusion and 4 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 16 Jul 2024. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Egypt. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Genetic polymorphism and echocardiographic parameters (time frame: 3-6 months). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 16 Jul 2024.