ABSTRACT
On the basis of light microscopy of sections only one micron in thickness and electron microscopy, the intimal changes that represent minimal atherosclerosis have been subdivided into two successive developmental stages, namely lesion types I and II. The very first changes consist of an increase in intimal macrophages and collections of a few macrophages loaded with and enlarged by lipid droplets (macrophage foam cells; type I lesion). Later, layers of these foam cells may be present, as well as lipid droplets within some intimal smooth muscle cells (type II lesion). With the unaided eye, many of these collections of lipid-laden cells are visible as yellow dots or streaks (fatty streaks) in constant locations on the inner surfaces of longitudinally opened arteries. Additional (but not all) foam cell accumulations are revealed to the unaided eye when the arteries are immersed in a Sudan stain solution. Accumulation of extracellular lipid, changes in the composition of the intercellular matrix and disruption of the intimal architecture are absent in types I and II. Accumulation of extracellular lipid (defined on page 23) must not be confused with the excess lipoprotein in the intima. The latter (in contrast to the former) does not displace and disrupt normal intima structures. Indeed, without immunostaining for low-density lipoprotein, neither light nor electron microscopy is able to reveal the excess of lipoprotein in the intimal intercellular space. Its presence can only be deduced from the accumulation of lipid droplets (much larger in size than lipoproteins) in the cytoplasm of macrophages and, usually subsequently, in a variable number of intimal smooth muscle cells. Neither the media adjacent to the lesions nor the adventitia is affected by the disease in these stages.
