[Biology of aging blood vessels]

The localisation of arteriosclerosis to foci of haemodynamic stress of sites of supporting collagen or elastic fibre deficiency illustrates the importance of mechanical factors in the fate of the smooth muscles. Excessive stress depletes stocks of ATP (adenosine triphosphate), resulting in osmotic lysis. Phosphate ions are released and precipitated in calcifications as apatite. The vascular lesion is followed by reparative and adaptive tissue inflammation. The haemodynamic stress is modified by a number of psychosocial factors, and is increased by traumatic and other injury to the ground substance. Some of the LDL (low-density lipoprotein) perfusing the intima is captured in the proteoglycan matrix, especially if the media is thickened. When cells and ground substance are lysed, fractions are incorporated in macrophages through metabolically uncontrolled receptors. Toxic oxidised LDL is then continuously ingested in the cells before they eventually die, leaving the amorphous lipid-rich mass of which an atheroma is formed. The macrophages produce free radicals which accelerate the damage and the inflammation. Thus, many factors working at different levels are involved in the aetiology of arteriosclerosis, with or without atheromatosis. The only theoretically feasible though insufficiently tested dietary recommendation for the general population would be to reduce the in vivo redox potential of food intake.