Proteoglycans (PGs) of the arterial intima form complexes with apo B-100 containing lipoproteins. Several lines of evidences indicate that this process IS a key pathogenic event for the development of atherosclerosis (for review, see ref. 1). First, retained apo B in early as well as advanced lesions is closely associated with arterial PGs (2, 3). Second, purified arterial PGs, partrcularly those from lesion-prone sites, bmd low-density lipoprotein (LDL) in vitro (4). Third, LDL from patrents with coronary-artery disease has a higher affinity for arterial PGs than LDL from apparently healthy subjects (5).