An observational study in Heart Failure, sponsored by Ain Shams University. Active, not recruiting at 1 site in Egypt. Open to participants aged 18 Years to 80 Years. Per ClinicalTrials.gov, last updated 2024-07-16.
Sponsored by Ain Shams University · Observational
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.
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.
5,701 studies on the registry are indexed under Heart Failure; 1,220 are open to participants now.
This study's planned enrollment of 92 is below the median of 200 across 1,679 observational studies indexed under Heart Failure.
Browse Heart Failure studies →Ain Shams University is the lead sponsor of 1,876 studies on the registry; 423 are open to participants now.
Of its 32 completed or terminated interventional studies of FDA-regulated products, 0 (0%) have results posted.
Counted across the registry records on this site, refreshed daily.
Heart failure patients treated with empagliflozin
Exclusion Criteria:
Heart failure patients who showed response to empagliflozin
Heart failure patients who showed no response to empagliflozin
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.
Time frame: 3-6 months
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
Time frame: 3-6 months
Plan to share: Undecided
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This study is active, not recruiting, as verified in Jul 2024. You cannot join it, but the record below documents what was studied.
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Ain Shams University