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After presenting an overview on classification and history of arteriosclerosis theories, the physiological factors involved in the transmural permeability of the arteries are discussed in detail. The development and characteristic features of the altered transmural permeability were studied in various experimental models such as in rat's hypercholesterolemia, local aortic hypoxia, lymphedema of the vascular wall and in hypertension. Results appear to show that alterations in permeability invariably developed in all of the pathological conditions examined, they were transient in nature and preceded the onset of intimal proliferation(s). The disturbance of transmural permeability might be the common pathologic clue which initiates uniform vascular responses to injuries produced by a variety of noxious stimuli. The possible role of the altered transmural permeability in the induction of smooth muscle cell proliferation is also discussed and evidence is provided that after withdrawal of stimulus for vascular injury intimal proliferation will not develop despite the manifest disorders in permeability.
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Noninvasive screening of subclinical atherosclerosis is possible with ultrasonic biopsy (UB) performed with high resolution ultrasound scanning. Five UB classes have been identified, each class corresponding to a different incidence of cardiovascular events (CVE) in 4 years and silent coronary ischemia (SCI). In a study including 2230 asymptomatic subjects 3 risk groups were defined. In the low risk group (class I and II; 82.01% of the population sample) the incidence of CVE and SCI was zero. These subjects may be seen again after 3 years. In the moderate risk group (class II and IV; 13.3%) monitoring and early intervention may be needed. In the high risk group (class V; 4.6%) prophylaxis or treatment may be necessary. The screening is effective, simple and may be organised at very low cost--i.e. 30.000 asymptomatic subjects may be scanned at the cost of 100.000 ECU. Each scan, including carotid and femoral bifurcations, may be performed in 15 minutes. In our communities this cost is equivalent to the average cost of a single major stroke or major coronary ischemic event in a working adult aging between 45 and 60. Organization problems and the fragmentation of competences has prevented the evolution of atherosclerosis screening. The problem can be solved organising a network including epidemiologists, angiologists and cardiovascular surgical centres where all phases of atherosclerosis may be studied and detected, progression prevented and complications treated with a global vision of the disease.
Spontaneous occlusive arteriosclerosis is rarely present in rats or other laboratory rodents. Instead, the common vascular lesion in these animals is a mineralization resembling Mönkeberg's medial calcinosis, or non-atheromatous and non-obstructive arteriosclerosis. For reasons yet unknown, the lingual arteries of Fischer rats behave differently; they develop extensive sclerotic lesions with progressive narrowing of the lumen, leading to complete occlusion and sometimes recanalization, comparable to lesions seen in human coronaries, carotids, tibials, etc. The spontaneous plaque-forming, thrombotic, occlusive arteriosclerosis of the lingual artery in Fischer rats can serve as an experimental model for the same lesion of medium- and small-sized arteries in man. As such, it can considerably facilitate the testing of nutritional, hormonal, immunological and other chemical or physical factors for a possible role in promoting or inhibiting the thrombotic-occlusive arteriopathy in man.
Healthy virgin and breeder rats (Sprague-Dawley) with naturally occurring hypertension and arteriosclerosis were fed 5% oxonic acid and 1% uric acid added to their regular diet for 30 days. Although rats are able to convert uric acid into excretable allantoin, abnormal urinary and serum urate levels appeared. Males and females, virgins and breeders, differed in the severity of their increased urate levels. Animals with elevated urate levels developed hypertension, hyperglycemia, and hypertriglyceridemia, with only slight changes in cholesterol and free fatty acids. The kidneys were greatly enlarged and manifested medullary streaking indicative of urate deposits but were free of significant damage; BUN levels in these animals were abnormally high. Adrenal glands were reduced in size and depleted of lipid, circulating corticosterone levels were subnormal, and thymi were involuted. Serum enzymes CPK and LDH were greatly increased, whereas SGOT and SGPT levels were not elevated. The abnormal urate levels did not induce de novo arterial disease in the formerly healthy virgin rats and did not cause exacerbation of the pre-existing, naturally occurring arteriosclerosis characteristic of repeatedly bred rats. It is suggested that Sprague-Dawley rats are endowed with an especially efficient hepatic and renal capacity to metabolize uric acid. Increased urate levels in rats may have some direct metabolic relationship to the production of hypertension, hyperglycemia, and hypertriglyceridemia.
In a pilot study the therapeutic effect of 2 x 500 mg etofibrate (Lipo Merz retard) on lipids and lipoproteins, fibrinolytic activity and clinical parameters was studied for four weeks in hyperlipidemic patients suffering from arteriosclerosis obliterans (Fontaine stage II/III). The study parameters were evaluated prior to and after the four weeks of treatment. Administration of etofibrate resulted in a significant decrease in serum cholesterol and triglyceride levels, the decrease in LDL-/HDL-cholesterol-ratio due mainly to an elevation of the HDL-cholesterol fraction, an increase in plasma fibrinolytic activity, an increased peripheral blood flow in the ischemic leg, and an increase in the pain-free walking distance. Thus, etofibrate applied twice daily might be recommended for the treatment of hyperlipidemic patients with signs of arteriosclerosis obliterans, Fontaine stage II/III.
The aortas of 11 pigs (aged 1-3 yr) with homozygous von Willebrand's disease (vWd) were compared with those of 11 normal pigs of the same ages. Six of the controls exhibited multiple arteriosclerotic plaques with intimal thickening of 63-130 mum. In contrast, none of the pigs with vWd had multiple plaques, and only one had a lesion >2 mm in diameter. In a subsequent study, 3-mo-old pigs (11 controls and 7 with homozygous vWd) were placed on a 2% cholesterol diet for up to 6 mo. All of the controls developed arteriosclerotic plaques in the aorta, and in nine of the controls, at least 13% of the entire surface was involved. Intimal thickness ranged up to 390 mum. In contrast, four of the pigs with vWd did not develop such lesions, two developed arteriosclerotic lesions affecting 6 and 7% of the aortic surface, and the seventh had 13% of the aortic surface involved. Most of the pigs with vWd, however, developed flat fatty lesions in contrast to the normal pigs whether on the normal or the high cholesterol diet. There was blue staining of the flat fatty lesions when two pigs with vWd were injected with Evans blue dye antemortem. By electron microscopy, severe endothelial damage was apparent, but there was no intimal proliferation. The coincidence of the impaired platelet-arterial wall interaction and lack of arteriosclerosis in this bleeding disease is discussed.
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