Ignite Creation Date:
2024-05-06 @ 11:03 AM
Last Modification Date:
2024-10-26 @ 12:40 PM
Study NCT ID:
NCT03429517
Status:
UNKNOWN
Last Update Posted:
2019-05-10
First Post:
2018-02-06
Brief Title:
Levels of Triglycerides and HDL-C in ACS Patients
Sponsor:
Assiut University
Organization:
Assiut University
Study Overview
Official Title:
Evaluation of Triglycerides and HDL-C Levels in Patients With Acute Coronary Syndrome and Normal LDL-C Level
Status:
UNKNOWN
Status Verified Date:
2019-05
Last Known Status:
RECRUITING
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
Background Changes in high-density lipoprotein cholesterol and triglyceride levels have been linked to residual cardiovascular risk whereas non-high density lipoprotein levels have been shown to be more predictive of cardiovascular risk than are low-density lipoprotein cholesterol levels We aimed to investigate the impact of high density lipoproteins triglyceride and non-high density lipoproteins levels on acute coronary syndrome risk with on-target low density lipoproteins levels
Detailed Description:
Dyslipidemia A disorder of lipoprotein metabolism including lipoprotein overproduction or deficiency Dyslipidemias may be manifested by elevation of the total cholesterol the bad low-density lipoprotein LDL cholesterol and the triglyceride concentrations and a decrease in the good high-density lipoprotein HDL cholesterol concentration in the blood LDL cholesterol is considered the bad type of cholesterol Thats because it can build up and form clumps or plaques in the walls of your arteries Too much plaque in the arteries of your heart can cause a heart attack HDL is the good cholesterol because it helps remove LDL from blood
HDLs exert multiple anti-atherogenic inhibition of monocyte adhesion inhibition of LDL-cholesterol oxidation and MCP-1 expression and anti-thrombotic effects decrease platelet aggregability that together are consistent with a marked reduction in the risk of a morbid cardiovascular event
Triglycerides come from the calories you eat but dont burn right away they stored in fat cells and released as energy when you need them Elevated triglycerides have inflammatory increase the expression of proinflammatory genes eg interleukin-6 intercellular adhesion molecule-1 vascular cell adhesion molecule-1 and monocyte chemotactic protein-1 atherogenic promote proatherogenic responses in macrophages and endothelial cells possess unique constituents that may contribute to atherogenicity and their by-product ie RLPs may lead to foam cell formation and thromboticincrease the expression of coagulation factors or leukocyte adhesion molecules they also may interfere with the ability of HDL to suppress inflammatory responses in cultured endothelial cells and the capacity of apo AI or HDL to promote sterol efflux from monocytes or macrophages
The relationship between atherogenic dyslipidemia and cardiovascular risk has been known for decades however to date therapeutic approaches have primarily focused on the lowering of the apoB-containing low-density lipoprotein LDL particles Statin therapy was proven to be effective in the reduction of cardiovascular risk and progression of atherosclerosis Treatment guidelines are targeted at reaching very low LDL-C levels in high-risk patient groups however some studies indicated a residual risk for further cardiovascular events in patients achieving target LDL-C levels with statin therapy
One potential impediment limiting further reduction in CHD events despite low on-treatment LDL-C is residual elevation in serum triglyceride TG levels Historically elevated TG has predicted CHD events in univariate analysis only to weaken after adjustment for other covariates including plasma glucose and high-density lipoprotein cholesterol HDL-C to which it is strongly and inversely correlated Yet even after adjustment for HDL-C detailed evaluation of population-based prospective studies has disclosed an independent effect of TG on CHD events Coupled with the knowledge that combined hyperlipidemia ie elevated LDL-C and TG promotes CHD to a significantly greater extent than either high LDL-C or TG alone
Prospective cohort studies as well as randomized controlled trials of antidyslipidemic therapies support a powerful inverse correlation between circulating HDL-C levels and coronary risk among patients with elevated normal or low low-density lipoprotein cholesterol LDL-C
HDLs exert multiple anti-atherogenic inhibition of monocyte adhesion inhibition of LDL-cholesterol oxidation and MCP-1 expression and anti-thrombotic effects decrease platelet aggregability that together are consistent with a marked reduction in the risk of a morbid cardiovascular event
Triglycerides come from the calories you eat but dont burn right away they stored in fat cells and released as energy when you need them Elevated triglycerides have inflammatory increase the expression of proinflammatory genes eg interleukin-6 intercellular adhesion molecule-1 vascular cell adhesion molecule-1 and monocyte chemotactic protein-1 atherogenic promote proatherogenic responses in macrophages and endothelial cells possess unique constituents that may contribute to atherogenicity and their by-product ie RLPs may lead to foam cell formation and thromboticincrease the expression of coagulation factors or leukocyte adhesion molecules they also may interfere with the ability of HDL to suppress inflammatory responses in cultured endothelial cells and the capacity of apo AI or HDL to promote sterol efflux from monocytes or macrophages
The relationship between atherogenic dyslipidemia and cardiovascular risk has been known for decades however to date therapeutic approaches have primarily focused on the lowering of the apoB-containing low-density lipoprotein LDL particles Statin therapy was proven to be effective in the reduction of cardiovascular risk and progression of atherosclerosis Treatment guidelines are targeted at reaching very low LDL-C levels in high-risk patient groups however some studies indicated a residual risk for further cardiovascular events in patients achieving target LDL-C levels with statin therapy
One potential impediment limiting further reduction in CHD events despite low on-treatment LDL-C is residual elevation in serum triglyceride TG levels Historically elevated TG has predicted CHD events in univariate analysis only to weaken after adjustment for other covariates including plasma glucose and high-density lipoprotein cholesterol HDL-C to which it is strongly and inversely correlated Yet even after adjustment for HDL-C detailed evaluation of population-based prospective studies has disclosed an independent effect of TG on CHD events Coupled with the knowledge that combined hyperlipidemia ie elevated LDL-C and TG promotes CHD to a significantly greater extent than either high LDL-C or TG alone
Prospective cohort studies as well as randomized controlled trials of antidyslipidemic therapies support a powerful inverse correlation between circulating HDL-C levels and coronary risk among patients with elevated normal or low low-density lipoprotein cholesterol LDL-C
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None