Levels of Triglycerides and HDL-C in ACS Patients

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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-de...

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)

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