In our case the participation of lipid deposits in the structural abnormalities of calcific aortic stenosis cannot be questioned. Nests of lipophages or foam cells and deposits of cholesterol crystals are apparent on the sur¬ face of the valve, in its substance, at its base, and in the endocardium proximal to it. These characteristic stigmas of atherosclerosis or xanthomatosis are surrounded by partially calcified fibrous tissue. The lesions in the valve resemble closely the classical atherosclerotic changes in the aorta and its main branches. This demonstration of xanthomatous lesions in the valve does not preclude the possibility that they were accompanied or preceded by inflammatory or proliferative damage from rheumatic fever. In studying this case considerable effort was ex¬ pended in evaluating this possibility. The criteria out¬ lined by Gross and his associates9 were followed in the examination of the heart. Many sections were taken from the valves, pericardium, endocardium, and various stra¬ tegic parts of the cardiac muscle. None of these examina¬ tions revealed any stigma of rheumatic fever. The only lesion that might be interpreted as indicative of rheu¬ matic disease was the network of small blood vessels noted grossly adjacent to one of the largest of the athero¬ matous patches on the mitral valve. Such vascular changes may accompany rheumatic fever but are also seen adja¬ cent to fresh xanthomatous lesions.The absence of any recognizable active lesions of rheu¬ matic fever is more remarkable when one considers the age of the patient. Rothschild, Kugel, and Gross 10 and Console 3I have found that Aschoff bodies can be shown in the hearts of 75 to 95% of patients who die of rheu¬ matic heart disease in the first two decades of life. It might be added that these authors have emphasized also the rarity of the more advanced degrees of deformity in younger persons with aortic stenosis. From our examina¬ tions it is not possible to classify the heart as rheumatic though even the most careful inspection cannot exclude completely the possibility of previous rheumatic damage.The lesions shown in the aortic valve of this young man must be regarded as extremely rare, and it may be that the circumstances of the case have little relevance to the cause of the usual calcific stenotic aortic valve.Considerable significance attaches, however, to the oc¬ currence of even one instance in which atherosclerotic or xanthomatous lesions are obtrusively displayed and no stigma of rheumatic fever can be found. Such a demonstration should lead to some caution in accepting too literally the belief that rheumatic fever is the only pathogenic factor of importance in the development of calcific aortic stenosis. It suggests an obligation to ex¬ amine diseased aortic valves, particularly in older sub¬ jects, for the presence of lipophages, cholesterol crystals, and other characteristic changes of atherosclerosis, and to use in this scrutiny the same meticulous care and dili¬ gence exercised by Karsner and Koletzky in their search ...
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