Relation Between Postprandial Lipogram and Coronary Artery Disease Severity

June 1, 2017 updated by: amgad youssef abdo deep, Assiut University

Coronary artery disease (CAD) is usually used to refer to the pathological problem affecting the coronary arteries (usually atherosclerosis) that leads to Coronary Heart disease (CHD) which includes the diagnoses of angina pectoris, MI and silent myocardial ischemia.

Despite the mortality for this condition has gradually declined over the last decades in western countries, it still causes about one-third of all deaths in people older than 35 years.

Dyslipidemia is very important risk factors of atherosclerosis that is one of the causes leading to cardiovascular disease Despite management of dyslipidemia by controling fasting total plasma cholesterol and LDL cholesterol as these are the best biomarkers for prediction of cardiovascular diseases (CVD) risk.

LDL elevation is absent in many patients with atherosclerosis and about 1/3 of cardiac events remains to be unpredicted using this method. Even more, in fasting normolipidemic subjects, increased CVD risk is associated with an exaggerated postprandial lipemic response.

Postprandial dyslipidemia is defined as a rise in triglyceride-rich lipoproteins (TRLs), including chylomicron remnants (CMRs) and remnant lipoproteins (RLPs), after eating, has drawn an increasing interest recently because of its association with cardiovascular events. Chylomicron remnants (CMRs) have been shown to penetrate the artery wall and to be retained within the intima.

Endothelial dysfunction is an initial process of atherogenesis and it contributes to the pathogenesis of CHD. Postprandial hyperlipidemia (postprandial hypertriglyceridemia) is involved in the production of proinflammatory cytokines, recruitment of neutrophils, and generation of oxidative stress, resulting in endothelial dysfunction

Study Overview

Status

Unknown

Conditions

Intervention / Treatment

Detailed Description

Coronary artery disease (CAD) is usually used to refer to the pathological problem affecting the coronary arteries (usually atherosclerosis) that leads to Coronary Heart disease (CHD) which includes the diagnoses of angina pectoris, MI and silent myocardial ischemia.

Despite the mortality for this condition has gradually declined over the last decades in western countries, it still causes about one-third of all deaths in people older than 35 years.

Dyslipidemia is very important risk factors of atherosclerosis that is one of the causes leading to cardiovascular disease.

Despite management of dyslipidemia by controling fasting total plasma cholesterol and LDL cholesterol as these are the best biomarkers for prediction of cardiovascular diseases (CVD) risk (5).LDL elevation is absent in many patients with atherosclerosis and about 1/3 of cardiac events remains to be unpredicted using this method. Even more, in fasting normolipidemic subjects, increased CVD risk is associated with an exaggerated postprandial lipemic response.

Atherosclerosis is initiated by vascular endothelium dysfunction followed by formation of macrophage foam cells, which is generated by scavenging of lipids from plasma lipoproteins. Accumulation of foam cells and then proliferation of vascular smooth muscle cells (VSMCs) causes the appearance of fatty streaks, the first visible lesions in the vessel wall.

Postprandial dyslipidemia is defined as a rise in triglyceride-rich lipoproteins (TRLs), including chylomicron remnants (CMRs) and remnant lipoproteins (RLPs), after eating, has drawn an increasing interest recently because of its association with cardiovascular events. Chylomicron remnants (CMRs) have been shown to penetrate the artery wall and to be retained within the intima

remnant-like lipoproteins (RLPs) have been found in human atherosclerotic plaque as well.(9,10) CMRs and TRLs have also been demonstrated to cause endothelial dysfunction, macrophage foam cell formation and the proliferation of VSMCs.

Endothelial dysfunction is an initial process of atherogenesis and it contributes to the pathogenesis of CHD. Postprandial hyperlipidemia (postprandial hypertriglyceridemia) is involved in the production of proinflammatory cytokines, recruitment of neutrophils, and generation of oxidative stress, resulting in endothelial dysfunction in healthy subjects, hypertriglyceridemic patients.

Study Type

Observational

Enrollment (Anticipated)

100

Contacts and Locations

This section provides the contact details for those conducting the study, and information on where this study is being conducted.

Study Locations

  • Egypt
      • Assiut, Egypt
        • Recruiting
        • Assiut University hospital
        • Contact:
        • Contact:
        • Principal Investigator:
          • Hosam Elaraby, Md

Participation Criteria

Researchers look for people who fit a certain description, called eligibility criteria. Some examples of these criteria are a person's general health condition or prior treatments.

Eligibility Criteria

Ages Eligible for Study

  • Child
  • Adult
  • Older Adult

Accepts Healthy Volunteers

No

Genders Eligible for Study

All

Sampling Method

Probability Sample

Study Population

documented stable coronary artery disease patients submitted to coronary angiography at assiut university catheterization lab

Description

Inclusion Criteria:

  • Patients with documented coronary artery disease and stable for 3 months with no secondary dyslipidemia as hypothyroidism and renal impairment

Exclusion Criteria:

  • patients with acute coronary syndrome or any cause of Secondary dyslipidemia

Study Plan

This section provides details of the study plan, including how the study is designed and what the study is measuring.

How is the study designed?

Design Details

  • Observational Models: Case-Only
  • Time Perspectives: Cross-Sectional

Cohorts and Interventions

Group / Cohort
Intervention / Treatment
postprandial dyslipidemia
Device: coronary angiography
per cutaneous coronary intervention to identify severity of coronary artery disease by syntx score

What is the study measuring?

Primary Outcome Measures

Outcome Measure
Measure Description
Time Frame
Relationship of postprandial lipid profile .HDL and coronary artery disease severity
Time Frame: 1 year

candidates will be subjected to ;

Full History taking including:

  • history of DM and its management
  • history of hypertension and its management
  • history of drug abuse
  • family history

Patient Examination as:

  • BMI

  • waist circumference

    -investigations as:

  • ECG
  • Echocardiography
  • lipid profile

We will check fasting (14 hours fasting) and 2 hours postprandial lipogram after fat loading with 17 g/body surface (m2),then we will assess CAD severity by coronary angiography using syntax score
1 year

Collaborators and Investigators

This is where you will find people and organizations involved with this study.

Sponsor

Assiut University

Investigators

  • Study Chair: Hosam Elaraby, MD, Assiut University

Publications and helpful links

The person responsible for entering information about the study voluntarily provides these publications. These may be about anything related to the study.

General Publications

Study record dates

These dates track the progress of study record and summary results submissions to ClinicalTrials.gov. Study records and reported results are reviewed by the National Library of Medicine (NLM) to make sure they meet specific quality control standards before being posted on the public website.

Study Major Dates

Study Start (Anticipated)

July 1, 2017

Primary Completion (Anticipated)

April 1, 2018

Study Completion (Anticipated)

April 1, 2018

Study Registration Dates

First Submitted

May 31, 2017

First Submitted That Met QC Criteria

June 1, 2017

First Posted (Actual)

June 5, 2017

Study Record Updates

Last Update Posted (Actual)

June 5, 2017

Last Update Submitted That Met QC Criteria

June 1, 2017

Last Verified

June 1, 2017

More Information

Terms related to this study

Additional Relevant MeSH Terms

Other Study ID Numbers

  • assiutU01

Plan for Individual participant data (IPD)

Plan to Share Individual Participant Data (IPD)?

No

Drug and device information, study documents

Studies a U.S. FDA-regulated drug product

No

Studies a U.S. FDA-regulated device product

No

This information was retrieved directly from the website clinicaltrials.gov without any changes. If you have any requests to change, remove or update your study details, please contact register@clinicaltrials.gov. As soon as a change is implemented on clinicaltrials.gov, this will be updated automatically on our website as well.

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