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+