Postprandial Dyslipidemia Clinical Trial
Official title:
Relation Between Postprandial Lipogram and Coronary Artery Disease Severity
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
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.
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