Purpose of review: To review recent advances in the field of remnant cholesterol as a contributor to the development of ischemic heart disease (IHD).
Recent findings: Epidemiologic, mechanistic, and genetic studies all support a role for elevated remnant cholesterol (=cholesterol in triglyceride-rich lipoproteins) as a contributor to the development of atherosclerosis and IHD. Observational studies show association between elevated remnant cholesterol and IHD, and mechanistic studies show remnant cholesterol accumulation in the arterial wall like LDL-cholesterol (LDL-C) accumulation. Furthermore, large genetic studies show evidence of remnant cholesterol as a causal risk factor for IHD independent of HDL-cholesterol levels. Genetic studies also show that elevated remnant cholesterol is associated with low-grade inflammation, whereas elevated LDL-C is not. There are several pharmacologic ways of lowering remnant cholesterol levels; however, it remains to be seen in large randomized clinical intervention trials if lowering of remnant cholesterol, in individuals with elevated levels, will reduce the risk of IHD.
Summary: Evidence is emerging for elevated remnant cholesterol being a causal risk factor for IHD. Elevated remnant cholesterol levels likely are part of the explanation of the residual risk of IHD observed after LDL-C has been lowered to recommended levels.