Postprandial Triglyceride Impact on Coronary Atherosclerosis in Non-Diabetic Patient in Sohag University Hospital

NCT ID: NCT06501287

Last Updated: 2024-07-15

Basic Information

• Recruitment Status: RECRUITING
• Total Enrollment: 160 participants
• Study Classification: OBSERVATIONAL
• Study Start Date: 2024-05-01
• Study Completion Date: 2024-12-25

Brief Summary

INTRODUCTION Cardiovascular diseases, including coronary artery disease (CAD), are the leading cause of mortality worldwide. Despite remarkable advancements in diagnostic and therapeutic approaches, CAD continues to pose formidable challenges. Atherosclerosis, characterized by the deposition of lipids, inflammatory cells, and fibrous tissue within the arterial walls, is the fundamental pathology underpinning CAD. Atherosclerosis development and progression are closely intertwined with lipid metabolism, particularly elevated levels of low-density lipoprotein cholesterol (LDL-C) and reduced levels of high-density lipoprotein cholesterol (HDL-C) *1+. However, emerging evidence suggests that postprandial triglyceride levels, the transient increase in triglycerides following a meal, may play a pivotal role in atherosclerotic processes *2+. Postprandial hypertriglyceridemia has been linked to various cardiovascular risk factors, including inflammation, endothelial dysfunction, oxidative stress, and altered hemostasis *3+. cardiovascular disease (CVD) causes death for 4 million subjects in Europe every year. It causes death for women *2.2 million (55%)+ than men *1.8 million (45%)+, and cardiovascular (CV) deaths under 65 years more prevalent in men (490 000 versus 193 000) *4+. Endothelial dysfunction was the main cause of vascular atherosclerosis. The damage of Endothelium cause lipids and macrophages accumulation (mostly lowdensity lipoprotein) in vessel injury site *5+. Lipids considered the major cause of atherosclerosis *6+. The increase of blood cholesterol (especially LDL) considered the main cause of the disease. High levels of triglycerides could be independent risk factor for coronary artery disease (CAD), particularly in women. Although, it was suggested that high level of density lipoproteins (HDLs) can prohibit these risk factors. Extensive examinations showed that lipid decrease the prevention of CAD in primary and secondary cases *7+. The level > 90% of total glyceride and/or LDL and level > 10% of HDL confirm dyslipidemia *8+

Conditions

Coronary Atheroscleroses

Study Design

• Observational Model Type: CASE_CONTROL
• Study Time Perspective: PROSPECTIVE

Study Groups

Group I (control group):

patients with normal coronary angiography and normal postprandial triglycerides

Postprandial triglyceride

Intervention Type: DIAGNOSTIC_TEST

impact of postprandial triglyceride level on coronary atherosclerosis

Group II

: patients with abnormal coronary angiography and high level of postprandial triglycerides more than 200mg/dl. They will be divided into subgroups according to severity of coronary artery disease (mild, moderate and severe) according to (Syntax score)

Postprandial triglyceride

Intervention Type: DIAGNOSTIC_TEST

impact of postprandial triglyceride level on coronary atherosclerosis

Group III

: patients with abnormal coronary angiography and normal postprandial triglycerides.

Postprandial triglyceride

Intervention Type: DIAGNOSTIC_TEST

impact of postprandial triglyceride level on coronary atherosclerosis

Interventions

Postprandial triglyceride

impact of postprandial triglyceride level on coronary atherosclerosis

Intervention Type: DIAGNOSTIC_TEST

Eligibility Criteria

Exclusion Criteria

Patients with other co-morbidities diseases, such as liver and kidney disorders and thyroid diseases. Diabetic patients.

• Eligible Sex: ALL
• Accepts Healthy Volunteers: No

Sponsors

Fatma Madhy Eissa

OTHER

Sponsor Role: lead

Responsible Party

Fatma Madhy Eissa

resident internal medecine

Responsibility Role: SPONSOR_INVESTIGATOR

Locations

Sohag university Hospital

Sohag, , Egypt

Site Status: RECRUITING

Countries

Egypt

Central Contacts

Fatma M Eissa, resident

Role: CONTACT

fatma_mdhy_post@med.sohag.edu.eg

01150754924

Ali M kassem, professor

Role: CONTACT

01003459738

Facility Contacts

Magdy M Amin, professor

Role: primary

References

Grundy SM, Stone NJ, Bailey AL, Beam C, Birtcher KK, Blumenthal RS, Braun LT, de Ferranti S, Faiella-Tommasino J, Forman DE, Goldberg R, Heidenreich PA, Hlatky MA, Jones DW, Lloyd-Jones D, Lopez-Pajares N, Ndumele CE, Orringer CE, Peralta CA, Saseen JJ, Smith SC Jr, Sperling L, Virani SS, Yeboah J. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019 Jun 18;139(25):e1082-e1143. doi: 10.1161/CIR.0000000000000625. Epub 2018 Nov 10.

Reference Type: BACKGROUND

PMID: 30586774 (View on PubMed)

Nordestgaard BG, Benn M, Schnohr P, Tybjaerg-Hansen A. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA. 2007 Jul 18;298(3):299-308. doi: 10.1001/jama.298.3.299.

Reference Type: BACKGROUND

PMID: 17635890 (View on PubMed)

Tushuizen ME, Nieuwland R, Scheffer PG, Sturk A, Heine RJ, Diamant M. Two consecutive high-fat meals affect endothelial-dependent vasodilation, oxidative stress and cellular microparticles in healthy men. J Thromb Haemost. 2006 May;4(5):1003-10. doi: 10.1111/j.1538-7836.2006.01914.x.

Reference Type: BACKGROUND

PMID: 16689751 (View on PubMed)

Catapano AL, Graham I, De Backer G, Wiklund O, Chapman MJ, Drexel H, Hoes AW, Jennings CS, Landmesser U, Pedersen TR, Reiner Z, Riccardi G, Taskinen MR, Tokgozoglu L, Verschuren WMM, Vlachopoulos C, Wood DA, Zamorano JL, Cooney MT; ESC Scientific Document Group. 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias. Eur Heart J. 2016 Oct 14;37(39):2999-3058. doi: 10.1093/eurheartj/ehw272. Epub 2016 Aug 27. No abstract available.

Reference Type: BACKGROUND

PMID: 27567407 (View on PubMed)

Other Identifiers

Soh-Med-24-04-02Ms

Identifier Type: -

Identifier Source: org_study_id