There are few pathologic descriptions of fatal coronary artery disease in the young. The morphologic characteristics of sudden coronary deaths in 47 hearts from patients younger than 40 years were studied. Numbers of plaques with necrotic cores were quantitated in each heart. Compared to 194 sudden coronary deaths >40 years, heart weight was lower, acute plaque erosions more frequent, and extent of disease less in the 40 years group. Plaque burden was less in hearts with erosions, and healed infarcts more common in hearts with stable plaque. The numbers of fibroatheromas increased with age until the 6th decade ( ) as well as the proportion of total plaques that were atheromatous. Plaques in younger patients have fewer lipid-rich cores. Most thrombi show areas of organization, with layering frequent in erosions, suggesting a possible method of plaque enlargement in the absence of necrotic core formation. 1. Introduction The morphologic characteristics of acute, fatal coronary thrombi in patients aged 40 years or less are not well characterized. Patients younger than 40 undergoing coronary artery bypass graft surgery have a high incidence of coronary risk factors, especially smoking; by angiography, a high proportion of these cases have left main (13.8%) and triple vessel disease (60%) [1]. A more recent autopsy study has shown that in 11 sudden coronary deaths under age 35, there were few lipid-rich plaques, and most thrombi were erosions with ongoing organization of thrombus [2]. The purpose of this study is to determine the types of thrombi, frequency of organization, and degree of inflammation in a series of premature sudden coronary deaths with underlying thrombosis. These findings should confirm previous observations in a larger number of cases and document the progression of relatively nonlipid rich plaques to lethal occlusive thrombi. 2. Materials and Methods Hearts were prospectively studied in cases of sudden coronary death, with semiserial sectioning of epicardial coronary arteries. Cases were seen in consultation from a statewide medical examiner’s office over a 6-year period. Noncardiac causes of death were established by postmortem toxicology. Risk factors were determined by scene investigation. Epicardial arteries were sectioned at 5？mm intervals and all areas with grossly identified plaque submitted for histologic analysis. Hearts were weighed with 2？cm of aorta attached, and cavitary blood removed. Myocardial scarring was classified as subendocardial ( 1.3 mural thickness) and transmural. Acute plaque rupture was defined as identification
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