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During the past 10 years, much clinical information has been obtained on cardiovascular (C-V) risk factors in pediatric populations. Impetus to study C-V risk in children for adult heart diseases evolved naturally from adult population studies, i.e., Framingham, Tecumseh, Evans County and others. The major medical advance was made in documenting clinical parameters that predict morbid C-V events. It became apparent that similar clinical parameters could be observed in children. Equally important to the clinical observations has been recognition that atherosclerotic lesions are already present in early life. ZEEK (1), HOLMAN et al. (2) noted atherosclerotic lesions developed early, even in infancy. Findings of coronary artery lesions in soldiers necropsied in the Korean War (3), and later in Vietnam (4), were impressive. The nature of coronary artery lesions, occurring early and gradually increasing during a subclinical phase, is now well recognized. As an outgrowth to this history, it became important as part of an epidemiology program, to study the early natural history of coronary artery disease in children (5) and to correlate anatomic changes along with clinical C-V risk factors.

The role of connective tissue of the arterial wall is often overlooked in the consideration of the development of atherosclerosis. In part, this may be due to overemphasis in one area, cholesterol and lipid deposition, yet it is not clear whether the role of lipids is primary or secondary. Virchow, as early as 1856, suggested that atherosclerosis was caused primarily by nonspecific injury and that lipid deposition was a secondary phenomena. It is interesting that current observations are suggesting a mechanism(s), for these phenomena (Wagner and Clarkson, 1973; Ross and Glomset, 1976).

There is considerable controversy on what actually constitutes the ‘early lesion’, on whether all lesions begin in the same way and whether all develop into fibro-fatty plaques. This introduction outlines the morphology and histochemistry of lesions regarded as ‘early’ in terms of chronology and the general pathology of atherosclerosis (Movat et al., 1959; Haust, 1971a; Geer and Haust, 1972).