Thinking beyond low-density lipoprotein cholesterol: strategies to further reduce cardiovascular risk

Some trials have highlighted the significance of residual cardiovascular risk after treatment of LDL–C to target levels. This residual risk is partially due to low HDL–C and high triglycerides (TG) despite achievement of LDL goals with statin therapy. The NCEP ATP III guidelines reported that low HDL–C is a significant and an independent risk factor for coronary heart disease (CHD) and is inversely related to CHD. Epidemiologic studies have also shown a similar inverse relationship of HDL–C with CHD. High–density lipoprotein cholesterol (HDL–C) may directly participate in the anti–atherogenic process by promoting efflux of cholesterol of the foam cells of atherogenic lesions. Many studies have demonstrated multiple anti–atherogenic actions of HDL–C and its role in promoting efflux of cholesterol from the foam cells. The residual risk by increased TG with or without low HDL–C can be assessed by calculating non–HDL–C and a reduction in TG results in decreased CHD.