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Endothelial cells, explanted from human umbilical veins and cultured, maintained morphological characteristics of vascular endothelium. When exposed to human serum lipoproteins, the cells bound and took up low density lipoproteins in preference to high density lipoproteins. High density lipoproteins reduced markedly the uptake of low density lipoproteins and affected surface binding to a lesser extent. These data suggest that the different levels of high density lipoprotein encountered in normal plasma of males and females could modulate differently the transendothelial transport of low density lipoproteins and provide a possible explanation for the lesser severity of atheromatosis in the aortic intima of premenopausal females.

Some features of the aortic intima were examined with the scanning electron microscope (SEM) and found to contribute to the etiology of dissecting aneurysm. The endothelium over intimal plaques was not as pendulous as endothelium surrounding plaques. The pendulous appearance of aortic endothelial cells could be associated with the contractile nature of these cells. Some undescribable factor, which has been termed stress or atherosclerosis, seemed to reduce the contractile nature of endothelial cells on the plaque areas. Analyses with SEM revealed a probable cause of a dissecting aneurysm. The effect of pulsating blood pressure on an inelastic endothelium could create a separation between endothelial cells and the fluid pressure of blood could then separate the tissue until the vessel ruptured into the body cavity or back into the aorta. Because all abdominal aortic segments examined had atherosclerosis, it was not possible to show the amount of intimal alteration between normal and atherosclerotic aortas. Each blood pressure line showed a similar change which was 4.52 and 4.95% for the high and low blood pressure lines, respectively. There were no demonstrable correlations in this study between either high or low blood pressure lines of turkeys and atherosclerosis.

Acute non-thrombotic immobilization of the disc in the Bjork-Shiley aortic valve prosthesis occurred as a result of extrinsic factors in three patients. Unravelled suture or long suture ends were the cause in two cases. Tissue detached from the aortic intima migrated into the valve and locked the disc in closed position in one case. The mechanisms of extrinsic disc immobilization and its prevention and treatment are discussed.

This Workshop has examined the functional role of various components of the arterial wall in relation to atherogenesis. My task is now to summarise the new information which has been presented, to contrast this with existing knowledge and to consider points which are still the subject of controversy.

A combined transmission (TEM) and scanning (SEM) electron microscopic study was performed on aortae of deoxycorticosterone-salt (DOC-salt)-treated rats and spontaneously hypertensive rats (SHR) to compare the effects of hypertension as well as its reversal on the aortic intima. To best reproduce the in vivo state of the vasculature, rats were perfusion-fixed at pressures corrected for each individual animal (30 mm Hg below measured systolic pressure). The intimal alterations were focal and thus were best appreciated with the combined use of SEM and TEM. Qualitatively, both models of hypertension showed similar intimal changes, which consisted of subintimal thickening due to an accumulation of both extracellular material and cells. Subendothelial cells with a morphology indicating a blood-borne origin were present simultaneously with cells derived from the vessel wall. The increased subendothelial extracellular material included precipitated plasma proteins, reticulated basement membrane, collagen fibers, and fragments of elastin. Increase in the height of endothelial cells with distortion of nuclear shape was prominent. Withdrawal of DOC-salt combined with low-salt diet for 11 weeks did not result in a discernible regression of these intimal changes despite normalization of blood pressure. We conclude that vascular injury, once induced, may be difficult to reverse and suggest that areas of prior damage may serve as foci for later vascular complications.

This paper reports on the incidence, location, and fate of macrophages and macrophage foam cells in the coronary artery and aortic intima and in the atherosclerotic lesions of young human subjects. The work represents a preliminary report on one topic of a study now in progress and concerned with the evolution and progression of atherosclerosis in the coronary arteries and aortas of the population of New Orleans in the first 29 years of life.

These studies were undertaken to determine whether age-related changes in the aortic intima can be inhibited by prolonged blood pressure lowering. Normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were treated with a combination of chlorothiazide, reserpine, and hydralazine beginning at 20 weeks of age and continuing until 62 weeks. Aortic morphology was assessed at the termination of the study by light and electron microscopy. Average systolic blood pressures during the final 6 months of therapy were: for untreated WKY, 147 +/- 5 mm Hg (mean +/- SE); for treated WKY, 110 +/- 2; for untreated SHR, 206 +/- 3; and for treated SHR, 104 +/- 4. Intimal and medial abnormalities were maximal in untreated SHR, while untreated WKY showed moderate changes consistent with their age. In contrast, both treatment groups exhibited relatively minimal alterations despite their advanced age. The occurrence of intimal lesions in individual animals correlated with the average level of blood pressure during therapy. These data suggest that blood pressure reduction, even in normotensive animals, may reduce the effects of aging on the arterial wall.

It has been known since the last century that the atherosclerotic fatty dots and streaks occur in the arterial intima, particularly in the aorta, of very young children. It was uncertain, however, at that time whether in fact these represented precursors of atherosclerotic plaques. The early publications on this subject and the problems relevant to this question were discussed in detail by Jores [13]. Fat was observed by Klotz and Manning [14] in the superficial yellow streaks in children in the first decade of life who died of scarlet fever. Schmidtmann, who studied with Antischkow, reported subsequently the results of her important morphological observations made at post mortem of 44 patients, ranging in age from 14 days to 16 years [23]. On that occasion she reviewed thoroughly the literature pertaining to fatty dots and streaks in young children. Similar studies were undertaken and reported by Zinserling [28] and Zeek [27] around the same time, and later by Holman and associates [11, 12] and Schwartz et al. [24]. Holman et al. found [11, 12] that many children under the age of 3 years had fatty streaks in the aorta and that some degree of fatty streaking was present in every person older than that age. Other data indicate that by the age of 1 year, all children exhibit some degree of fatty streaking at one or more areas of the aortic intima [1, 6, 7, 9, 10, 15, 16, 25]. A study involving 19 different geographical and racial groups of populations from different areas of the world [15, 16] showed that the initial appearance of the fatty streaks were similar with respect to the extent of intimal involvement. This feature did not differ in various geographic areas or races, and was not related to socio-economic strata, nutrition and dietary habits [16]. The percentage of the surface involvement with the fatty streaks reportedly increased with age, amounting to approximately 5% in the first decade. In the second decade the reported average percentage varied from 20% to almost 100% [1].

Frozen sections of the aorta of a patient with pulmonary aspergillosis were studied for fibrinolytic activity by the histochemical fibrin slide technique. High fibrinolytic activity, caused by a plasminogen activator, was observed along the aortic intima. This unusual observation suggests the existence of a potential for development of fibrinolytic activity in the normal, inactive aortic endothelium of man.

Quantitative analysis of platelet lipids showed that the amount of cholesterol present is too low to make a significant contribution to the cholesterol in atherosclerotic lesions. Platelet mural thrombi which were in contact with intact aortic intima showed no increase in lipid compared to fresh platelets. There is thus no evidence that they trap or accumulate plasma lipid.

One hundred forty-seven aortas obtained from medicolegal autopsies were studied. According to the extent of involvement of the intimal surface and the types of lesions, aortic atherosclerosis was classified as mild, moderate, and severe. The globulin content of the intima and its lipid-binding, and cholesterol-binding capacity were determined in each specimen. No relation could be established between the globulin content of aortic intima and the degree of atherosclerosis. A direct correlation was observed, however, between the lipid-binding capacity and the cholesterol-binding capacity of the globulins and the severity of atherosclerosis, suggesting the possibility of a qualitative change in the globulins of the ground substance in atherosclerosis.

The effect of trauma to the aortic intima of the rabbit and the combination of trauma and hyperlipemia were studied with the electron microscope. It was found that the cells engaged in the repair processes and eventually forming intimal plaques were apparently derived from smooth muscle. Hyperlipemia led to the accumulation of foam cells in these plaques. During the experimental period such foam cells were confined almost entirely to the luminal surfaces of the plaques. Reasons are advanced for considering that many of these foam cells are derived from blood borne cells.

No problem in pathology has caused so much interest, discussion and controversy in the last few decades as the syphilitic affections of the aorta. The pathologic anatomists were foremost among those who endeavored to throw more light on this question. Ignorance concerning the etiologic agent of syphilis, and the difficulty of morphologic diagnosis postmortem have prevented and delayed the ultimate solution of this problem. First I shall attempt to present a brief historical survey in order to show with what zeal and with what perseverance the solution was pursued. The oldest experiences concerned observations and descriptions of the aortic aneurysms. The first fact which the old observers thereby determined was the occurrence of aneurysms of the aorta in comparatively young persons at a time when the changes of aortic intima due to increasing age cannot bring about any serious damages to the aortic tube. Therefore the atheromatous changes of the