Hyperplastic Arteriosclerosis Versus Atherosclerosis

Abstract

This paper was stimulated by the serious need of a precise definition of the term "arteriosclerosis" as judged by the diversity of opinions expressed in recent years. Thus, a recent laborious review of many hundreds of articles on arteriosclerosis leaves one bewildered for the reason that under that eponym such different lesions as hyperplastic arteriosclerosis, atherosclerosis, infectious arteritis and M\l=o"\nckeberg's sclerosis are included, with little or no attempt at differentiation.In another instance, a review of "arteriosclerosis" represents an excellent presentation of atherosclerosis. The necessity for a precise definition of arteriosclerosis is not merely an academic matter. Aside from the obvious advantage of inducing precision of thought, it will help to clarify many current clinical problems associated with vascular disease. In order to arrive at a correct definition of the term, it is essential to survey the problem as a whole, not only from the point of view of morphology and morphogenesis but from the etiologic, the physiologic and especially the dynamic aspects. Regrettably, this has been done in only a desultory manner, and only too often a part of the total summation of processes that are represented within the rubric of arteriosclerosis have been emphasized to the exclusion of the whole.The main issue lies in the alleged identity of arterio¬ sclerosis with atherosclerosis, since these terms are so often used interchangeably. There is no doubt that the impetus created by Anitschkow'sx experiments is largely responsible for this misconception. He was one of the first to produce a lesion that simulated that observed in the human arterial tree. There is no question that both grossly and histologically these experiments reproduce some of the characters of human arteriosclerosis, especially in respect to distribution of the lipid deposits. However, there are many points of difference. 1. The ascending aorta is always and intensely involved, an unusual occurrence in the human aorta. 2. The deposits of lipid are not limited to the arteries of the greater circulation but involve the pul¬ monary artery, the veins, the reticuloendothelial system, the adrenal glands, the sciera, the cornea, the ciliary body of the eye, the tympanic membrane and even the tendons. As I have tried to show,2 the incidence of gross arteriosclerosis in the pulmonary artery is hide-pendent of that in the aorta, and phlebosclerosis never occurs unless a venous segment is subjected to increased intravascular pressure. 3. The renal arteries are sel¬ dom affected while in man arteriosclerotic lesions are practically omnipresent in senescence. 4. The lipid infiltration of the media occurs early in experimental arteriosclerosis but is a' late phenomenon in the human variety. 5. Ulcération of the atheromatous deposits rarely results. 6. Hyperplasia of the elástica and the deposition of collagen, when it occurs, are entirely dif¬ ferent in localization from that occurring in human arteriosclerosis. 7. The lesions are produced under un...

Lipid Metabolism and the Effect of a Combined Lipotropic Agent††

“…Enos (27), however, demonstrated marked atheromatous changes in the arteries of combatants killed in the Korean war (mean age 21 years) and noted that the incidence and degree of change were associated with alterations in the anatomy of the coronary tree. The descriptions of the coronary vessels by Yater and associates (28), French and Dock (29), Moschowitz (30), and Moon and Rinehart (31) are in agreement that a diseased unoccluded coronary vessel does not show cholesterol deposits but does show a fibroblastic proliferation of the intima.…”

Evidence of early degenerative changes in large arteries in human essential hypertension.

“…The regression equations for pulse wave velocity and diameter are as follows. Pulse wave velocity = (1.00 ± O.13)1O 3 [age x diastolic pressure] + (5.58 ± 0.37). Arterial diameter = (0.042 ± 0.006)10 3 |age x diastolic pressure] + (0.329 ± 0.020).…”

The pathogenesis of pulmonary hypertension — vessel wall ischemia as the driving force in disease initiation and progression

“…For sure, our assumption can be criticized judging upon a puristic standpoint of classical pathology that atherosclerosis starts from intima and spreads towards adventitia and should be strictly distinctive from arteriosclerosis, which, vice versa, takes origin from adventitia spreading inwards to intima [58].…”