RESUMO
Elevated levels of low density lipoprotein (LDL) and smoking have long been recognized as risk factors for atherosclerosis and coronary heart disease (CHD). However, the mechanisms by which these factors contribute to the disease have not been fully elucidated. It has been postulated from in vitro studies using serum and LDL from smokers that smoking increases the oxidation of LDL, which in turn contributes to atherogenesis. We know of no direct evidence linking oxidized LDL (oxLDL) in human arteries to increased atherosclerosis in individuals who show elevated serum thiocyanate levels (HST) as an indicator of recent smoking. We have studied arterial samples from smokers micromorphometrically and found that 'smokers' have a greater area in which oxLDL can be identified in the early stages of the disease than do "nonsmokers', i.e., individuals with low serum thiocyanate levels (LST). This study demonstrates a positive correlation between the extent of oxLDL in the fatty streaks as well as the fatty plaques of standardized core sample areas of the thoracic and abdominal aortas of a sample group of young people, aged 15-34, who have evidence of recent smoking based on their postmortem serum thiocyanate levels.
