Sudden death and coronary intimal thickening

Abstract

We agree completely with Ottaviani's comments that intimal thickening has been observed in human coronary arteries in infants and children and that our study should have placed our findings in this broader context. The point of our study, in part, was to distinguish intimal thickening with extracellular lipid deposits from intimal thickening composed solely of smooth muscle cells and proteoglycan ground substance. The former has been termed “pathologic intimal thickening,” as initially coined byVirmani et al [1]. Pathologic intimal thickening was originally described as a substrate for plaque erosion, a major type of coronary thrombosis that does not necessarily occur after formation of a necrotic core. As we state in our study, plaque erosion has been associated with coronary events in young individuals and seemmore common in females [2]. Pathologic intimal thickening has subsequently been described to occur in late childhood and young adults [3] and may be considered a possible transition lesion between “adaptive” or “diffuse” intimal thickening, to which Ottaviani is referring, and fibroatheroma. The coronary wall changes, mainly intimalmodifications, described in the studies byMilei et al [4] andMatturri et al [5] are quite similar to the ones seen in the figures of our study. It remains to be studied if the in utero environment that yields the coronary abnormalities share similar pathogenesis in adult plaques without a necrotic core. Our study was the first, we believe, to emphasize that