Despite their relevant physiological and structural role, phospholipids (PL) have not gained favour in clinical assessment of human atherosclerosis. Already in 1951, Gertler et al. recorded higher values of serum lipid phosphorus in coronary patients than in controls. Furthermore, it was shown that the serum cholesterol/lipid phosphorus is increased in the presence of coronary heart disease (CHD). The same authors suggested a “chemotype” which included the analysis of serum cholesterol, phospholipids and uric acid. A recommandation was also given to increase the values of plasma PL, thus reestablishing a normal C/PL ratio. The meaning of the recorded variations of PL plasma values has not been discussed. An increased C/PL ratio has also been recorded in type II hyperlipoproteinaemia (Peeters 1976). Increased values of ratio sphyngomye-lin/phosphatidylcholine (SM/PC) was observed in types II and IIB, being normal in type IV (Peeters 1976). The lecithin/sphyngomyelin ratio is abnormally low in homozygotes with familial xanthomatosis hypercholesterolaemia (FXH) (Mills et al. 1976). In the low density lipoproteins (LDL) of FXH, an increased C/PL ratio was recorded with a decreased lecithin/sphyngomyelin ratio (Jadhav and Thompson 1979). Since this abnormal composition of LD1 normalizes following plasma exchange it has been suggested that the abnormal composition of LDL in FHX is due to hypocatabolism and then to the aging of LDL (Jashav and Thompson 1979). The chemical percentage composition of the major lipoprotein classes has been studied in survivors of myocardial infarction (Avogaro et al. 1979).