Genes and dyslipoproteinaemias.

Abstract

The Prospective Cardiovascular Münster (PROCAM) Study clearly demonstrated that low levels of high density lipoprotein (HDL)-cholesterol are a powerful predictor of subsequent coronary heart disease (CHD) and that both exogenous factors (cigarette smoking, physical inactivity, obesity) and genetic factors (dyslipidaemia, diabetes mellitus) affect serum concentrations of HDL-cholesterol. In case-control studies, the apoprotein (apo) B/apo A-I ratio was found to be more meaningful than the lipoprotein lipid ratio in predicting risk of CHD in a group of young myocardial infarction (MI) survivors. Screening of young (less than or equal to 45 years) MI survivors did not show an increased prevalence of apo A-I variants compared with controls and newborns, thus apo A-I variants probably do not contribute substantially to low HDL-cholesterol levels and the risk of CHD in the general population. Genetic anomalies causing HDL-cholesterol depletion or apo A-I deficiency probably do not relate to structural anomalies of apo A-I but rather to regulatory anomalies in the production of HDL apolipoproteins or to catabolic or intracellular events that are important in the homeostasis of plasma HDL-cholesterol.