This relationship was preserved even after adjustment for LDL ‐C, HDL ‐C and triglycerides. HDL ‐P was a strong, independent predictor of a new CHD event both at baseline and on ‐trial. HDL ‐C was not a significant predictor of CHD risk either at baseline or on–trial. On gemfibrozil treatment, HDL ‐C increased by 6% while total HDL ‐P increased by 10%. James Otvos and his colleagues report data from a prospective, nested case ‐control study of 364 men with a new CHD event to determine if low ‐density lipoprotein particle number ( LDL ‐P) and HDL ‐P provide additional information relative to CHD risk reduction at baseline and after 7 months of treatment with gemfibrozil or placebo. These data suggest that the association of HDL particle size is confounded by metabolic dysregulation, but that HDL ‐P is an independent predictor of CHD even after correction for metabolic parameters. Upon correction for metabolic syndrome markers, the HDL size was no longer associated with risk of future CHD events while the relationship of HDL particle number (HDL ‐P) to CHD risk was not affected by adjustment for these same parameters. They observed that both HDL size and number were independently associated with other CHD risk factors and CHD risk. Karim El Harchaoui and his colleagues performed a nested case ‐control study of 822 apparently healthy men and women within the EPIC ‐Norfolk cohort to determine the relationship of HDL particle size and number to risk of future CHD events. Therefore, the overall risk of CHD is greatly dependent upon the balance of these atherogenic and anti ‐atherogenic processes. HDL particles antagonize the atherosclerotic process by facilitating reverse cholesterol transport back to the liver, by inhibiting oxidation of LDL and blocking the deposition of lipids into the arterial wall, stimulating vasodilatation, inhibiting platelet aggregation and inhibiting endothelial cell apoptosis. These macrophages become cholesterol ‐rich foam cells that then deposit their lipid contents into the vessel wall and initiate development of atherosclerotic plaque. Low ‐density lipoprotein particles promote atherosclerosis by penetrating the artery wall and subsequently becoming oxidized and ingested by macrophages. 1,2įor this reason, HDL ‐C levels may not be a good indicator of the number of circulating HDL particles present and the amount of cardioprotection they confer.ĬHD risk is impacted by the interaction of lipoproteins within the arterial wall. What is not as well appreciated is that, similar to the discordant relationship between the level of LDL ‐C and number of low density lipoprotein particles in patients with residual CHD risk, the amount of cholesterol carried within high density lipoprotein particles may also vary significantly between individuals who have the same level of HDL ‐C. The idea that HDL cholesterol is cardioprotective is well accepted.
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