The results of clinical trials with statins have shown that, after levels of low-density lipoprotein cholesterol (LDL-c) have been reduced, there is a substantial residual risk, even with figures of LDL-c < 100mg/dl or 70mg/dl. This residual risk is largely influenced by the presence of atherogenic dyslipidemia, which is frequently associated with metabolic syndrome or diabetes, as well as with renal insufficiency or established cardiovascular disease. This alteration is characterized by the association of elevated triglycerides (TG), low high-density lipoprotein cholesterol (LDL-c) levels and a high proportion of small, dense LDL particles. The pathogenesis of this alteration is strongly influenced by the role of hypertriglyceridemia, due to the increase in hepatic TG synthesis and the reduction in its peripheral catabolism. These two factors also explain other, associated lipoproteic alterations, such as the reduction in non-HDL-c and apolipoprotein B-100 and the increase in large VLDL particles, remnants of TG-rich particles and postprandial lipemia. Clinical evidence indicates that this alteration is highly atherogenic, independently of and in addition to LDL-c, as a result of the individual and synergic action of its three components. Low levels of HDL-c, or functional alteration of HDL, reduce its antiatherogenic functions. Among TG, those carried in remnant particles behave mainly as atherogens. Small, dense LDL particles penetrate more easily in the vascular wall, in addition to containing more cholesterol and being more susceptible to oxidation.