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Levels of Triglycerides and HDL-C in ACS Patients

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ClinicalTrials.gov Identifier: NCT03429517
Recruitment Status : Not yet recruiting
First Posted : February 12, 2018
Last Update Posted : May 11, 2018
Sponsor:
Information provided by (Responsible Party):
Michael Abdo, Assiut University

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.

Condition or disease Intervention/treatment
Dyslipidemia Associated With Acute Coronary Syndrome Diagnostic Test: Lipogram

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. 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)


Study Type : Observational
Estimated Enrollment : 110 participants
Observational Model: Case-Control
Time Perspective: Prospective
Official Title: Evaluation of Triglycerides and HDL-C Levels in Patients With Acute Coronary Syndrome and Normal LDL-C Level
Estimated Study Start Date : June 1, 2018
Estimated Primary Completion Date : June 1, 2019
Estimated Study Completion Date : June 1, 2020

Group/Cohort Intervention/treatment
Patients
ACS Lipogram
Diagnostic Test: Lipogram
liporgram samples

Controls
Normal LDL-C level Lipogram
Diagnostic Test: Lipogram
liporgram samples




Primary Outcome Measures :
  1. Decrease ACS events [ Time Frame: 1 year ]
    ACS and Dyslipidemia



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Ages Eligible for Study:   Child, Adult, Older Adult
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Sampling Method:   Non-Probability Sample
Study Population

Patients with a first or subsequent ACS will be enrolled in our study, who are admitted to CCU of Assiut university hospital and Sohag cardiac & digestive system center, more over patients should have LDL-C level below 130mg/dl and lipid samples should be obtained within 4 days of admission. They also should receive treatment according to ACS guidelines.

Patients and control group data will be collected during a year .

Patients will be subjected to:

-Full History taking including : History of chest pain or dysnpea History of renal or liver diseases History of drug abuse History of diabetes and hypertension Family history of cardiovascular diseases and dyslipidemia Assessment of risk factors: smoking, alcohol intake, physical inactivity and poor quality diet.

Patient Examination :

Full general and cardiac examination including :

Xanthelasma Body mass index Waist circumference

Criteria

Inclusion Criteria:

  • ACS
  • Normal LDL-C
  • Not on statin therapy

Exclusion Criteria:

  • Liver disease
  • Drug abuse
  • End stage renal disease
  • Nephrotic syndrome
  • Drug abuse

Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT03429517


Contacts
Contact: Amr Youssef, MD 01006554042 amryoussef111@yahoo.com
Contact: Mahmoud Abdallah, MD 01001202779 m_abd_elsabour@yahoo.com

Sponsors and Collaborators
Assiut University

Publications of Results:
Responsible Party: Michael Abdo, Principal investigator, Assiut University
ClinicalTrials.gov Identifier: NCT03429517     History of Changes
Other Study ID Numbers: TGHCACS
First Posted: February 12, 2018    Key Record Dates
Last Update Posted: May 11, 2018
Last Verified: May 2018
Individual Participant Data (IPD) Sharing Statement:
Plan to Share IPD: Undecided

Studies a U.S. FDA-regulated Drug Product: No
Studies a U.S. FDA-regulated Device Product: No

Keywords provided by Michael Abdo, Assiut University:
HDL-C
Triglycerides
Non HDL-C and Acute coronary syndrome

Additional relevant MeSH terms:
Acute Coronary Syndrome
Disease
Heart Diseases
Cardiovascular Diseases
Vascular Diseases
Lipid Metabolism Disorders
Metabolic Diseases
Syndrome
Dyslipidemias
Pathologic Processes
Myocardial Ischemia