Ignite Creation Date:
2024-10-26 @ 3:35 PM
Last Modification Date:
2024-10-26 @ 3:35 PM
Study NCT ID:
NCT06510270
Status:
NOT_YET_RECRUITING
Last Update Posted:
None
First Post:
2024-07-15
Brief Title:
Dapagliflozin in Reducing Epicardial Adipose Tissue in Heart Failure with Preserved Ejection Fraction
Sponsor:
None
Organization:
None
Study Overview
Official Title:
Targeting Epicardial Adipose Tissue in Heart Failure with Preserved Ejection Fraction Exploring the Dapagliflozin Connection
Status:
NOT_YET_RECRUITING
Status Verified Date:
2024-07
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
No
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Heart failure with preserved ejection fraction HFpEF is becoming the most common cause of heart failure worldwide in part driven by a rising prevalence of obesity
Although generalized and visceral adiposity is important in the pathogenesis of obesity-related HFpEF there is increasing recognition of the potential role of epicardial adipose tissue EAT in disease pathogenesis EAT is metabolically active tissue located directly on the surface of the myocardium underneath the visceral pericardium By virtue of its anatomical interface with the heart and the lack of fascial separation between the underlying myocardium and epicardial fat locally secreted adipokines directly bathe the surface of the heart and result in underlying myocardial remodeling
Its position on the surface of the myocardium allows EAT to directly contribute to an increase in total heart size with stretch of the pericardium and results in relative pericardial restraint with constrictive physiology
EAT is most commonly measured by echocardiography in the parasternal long axis view perpendicular to the right ventricle RV to quantify epicardial fat thickness and this has been correlated with worse haemodynamic derangements and adverse outcomes in HFpEF
Alternatively cardiac MRI or CT can provide a more complete volumetric assessment of epicardial fat volume and has also demonstrated associations with adverse outcomes and functional metrics in most but not all HFpEF studies
Very little is understood about the impact of medical modulation of epicardial fat in HFpEF The first proven agents to improve heart failure hospitalization and quality of life in HFpEF are the sodium-glucose cotransporter-2 inhibitors SGLT2i Although the mechanisms of benefit of these drugs are uncertain they have demonstrated a reduction in epicardial fat despite only minimal weight loss suggesting a direct lipolytic effect on epicardial fat The use of SGLT2i has also been associated with reduced incident AF which may in part be due to the reduction in epicardial fat The diuretic effect of SGLT2i may facilitate a reduction in plasma volume and mechanistic studies have shown that they also promote ventricular mass regression which may cumulatively decrease pericardial restraint
By this work we aims To determine whether the addition of 10 mg of Dapagliflozin to a patient with HFPEF can lead to a decrease in epicardial adipose tissue volume which is a new approach to managing HFPEF or not
Although generalized and visceral adiposity is important in the pathogenesis of obesity-related HFpEF there is increasing recognition of the potential role of epicardial adipose tissue EAT in disease pathogenesis EAT is metabolically active tissue located directly on the surface of the myocardium underneath the visceral pericardium By virtue of its anatomical interface with the heart and the lack of fascial separation between the underlying myocardium and epicardial fat locally secreted adipokines directly bathe the surface of the heart and result in underlying myocardial remodeling
Its position on the surface of the myocardium allows EAT to directly contribute to an increase in total heart size with stretch of the pericardium and results in relative pericardial restraint with constrictive physiology
EAT is most commonly measured by echocardiography in the parasternal long axis view perpendicular to the right ventricle RV to quantify epicardial fat thickness and this has been correlated with worse haemodynamic derangements and adverse outcomes in HFpEF
Alternatively cardiac MRI or CT can provide a more complete volumetric assessment of epicardial fat volume and has also demonstrated associations with adverse outcomes and functional metrics in most but not all HFpEF studies
Very little is understood about the impact of medical modulation of epicardial fat in HFpEF The first proven agents to improve heart failure hospitalization and quality of life in HFpEF are the sodium-glucose cotransporter-2 inhibitors SGLT2i Although the mechanisms of benefit of these drugs are uncertain they have demonstrated a reduction in epicardial fat despite only minimal weight loss suggesting a direct lipolytic effect on epicardial fat The use of SGLT2i has also been associated with reduced incident AF which may in part be due to the reduction in epicardial fat The diuretic effect of SGLT2i may facilitate a reduction in plasma volume and mechanistic studies have shown that they also promote ventricular mass regression which may cumulatively decrease pericardial restraint
By this work we aims To determine whether the addition of 10 mg of Dapagliflozin to a patient with HFPEF can lead to a decrease in epicardial adipose tissue volume which is a new approach to managing HFPEF or not
Detailed Description:
None
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None