In response to my previous article,1 Serjeant questions my contention that elevated levels of serum low-density lipoprotein (LDL) play a central role in the pathogenesis of coronary heart disease (CHD) and that the primary mechanism whereby statin drugs reduce risk for CHD is by decreasing levels of LDL.
That elevated serum concentrations of total cholesterol and LDL cholesterol are necessary for atherogenesis and the development of CHD is based on evidence from epidemiological studies, genetic forms of hypercholesterolemia, animal models, laboratory investigations, and clinical trials.2 Populations that have very low levels of LDL do not have substantial rates of CHD even when other risk factors, such as hypertension, cigarette smoking, and diabetes, are common. Serjeant's claim that most patients with CHD have normal serum levels of LDL is no longer tenable. What used to be considered normal is now considered too high and can be atherogenic.
Grundy SM. The Key to Atherogenicity. Arch Intern Med. 1998;158(10):1157–1158. doi:
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