Clinical Trial Details
— Status: Recruiting
Administrative data
| NCT number |
NCT03429517 |
| Other study ID # |
TGHCACS |
| Secondary ID |
|
| Status |
Recruiting |
| Phase |
|
| First received |
|
| Last updated |
|
| Start date |
June 1, 2018 |
| Est. completion date |
June 1, 2020 |
Study information
| Verified date |
May 2019 |
| Source |
Assiut University |
| Contact |
Amr Youssef, MD |
| Phone |
01006554042 |
| Email |
amryoussef111[@]yahoo.com |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Observational
|
Clinical Trial 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.
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. That's 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 don't 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 thrombotic(increase 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 (i.e., 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)
