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At least 19 recordsLinked to original sources
PubMed1977

Effect of increased serum urate levels on virgin rats with no arteriosclerosis versus breeder rats with preexistent arteriosclerosis.

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.

Animals↗
PubMed1978

Resistance to arteriosclerosis in pigs with von Willebrand's disease. Spontaneous and high cholesterol diet-induced arteriosclerosis.

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.

Animals↗
PubMed1976

[Clinical course of arteriosclerosis of coronary and lower limb arteries (author's transl)].

The clinical course of arteriosclerosis was evaluated in 9 patients with coronary sclerosis and in 25 with peripheral arterial occlusive disease by means of repeat angiographies following primary angiography after 22.5 and 36.6 months, respectively. During the period of observation arteriosclerosis had progressed in all cases except in two patients with peripheral arterial occlusive disease. Despite intensive therapeutic efforts including control of risk factors, dietary care, guided or unguided exercise and the attempt to change unsatisfactory living conditions, progression of arteriosclerosis could not be interrupted. If treatment delayed progression of arteriosclerosis cannot be decided. All vascular areas were affected indiscriminately by progression and no particular localisation was preferred. Intensive exercise does not seem to delay progression of arteriosclerosis.

Angiography↗
PubMed1977

[Arteriosclerosis and liver cirrhosis (author's transl)].

The degree of arteriosclerosis in 176 autopsies of liver cirrhosis (patients in the age range of 51 to 70 years) was compared with that of controls (without liver disease). It was found that the "protective influence" of liver cirrhosis of the process of arteriosclerosis is only true for normotonic. Associated with arterial hypertension severe arteriosclerosis is predominant in liver cirrhosis. There is even some evidence that arteriosclerosis in hypertonics with liver cirrhosis is more increased than in controls without liver diseases. The factors influencing arteriosclerosis in liver cirrhosis are discussed.

Aged↗
PubMed1977

Obliterative arteriosclerosis of extremities in patients with coronary heart disease.

In a group of 314 patients after past myocardial infarction or an episode of acute coronary insufficiency, angiological examination, repeated after a one-year interval, was performed. In the first examination, signs of obliterative arteriosclerosis in the lower extremities were found in 18.8% of the patients. It was noteworthy that 34% of patients with peripheral obliterative arteriosclerosis had no complaints connected with an impairment of circulation in the limbs. On the basis of the second examination, performed after a one-year interval, it was found that the annual incidence of obliterative arteriosclerosis in the lower extremities was 7.4%. In 66% of patients showing signs of obliterative arteriosclerosis at the first examination, objective impairment of peripheral circulation was observed after a one-year interval. In none of the patients did the investigators find signs of obliterative arteriosclerosis in the upper extremities.

Adult↗
PubMed1977

Relationship between arteriosclerosis and cerebral atrophy in Parkinson's disease.

Computed tomographic examinations of parkinsonian patients revealed a high incidence of cerebral atrophy, in most cases a combination of cortical atrophy and ventricular enlargement. The present study considered the relationship between cerebral atrophy and physical signs indicating or promoting arteriosclerosis such as overweight, electrocardiographic changes, hypertension, calcification of the internal carotid artery and aorta as well as elongation of the aorta. The study is based on 173 treated and untreated parkinsonian patients (89 men, 84 women) aged from 37--84 years (mean 64.6), on whom CT was performed about 5.4 years after the onset of the first symptoms of the illness. The results demonstrate an increase of pathological CT findings as well as of calcification in the carotid siphon with advanced age. No correlation was found between the other items and increasing age. Further analysis of the relationship between cerebral atrophy and signs of arteriosclerosis revealed only a statistically relevant correlation with calcification of the carotid siphon, especially with calcification of the media. Since pathological CT findings and calcification of the internal carotid artery are both related to advanced age, whereas all the other items which may be considered to be indications of arteriosclerosis do not have any clear relationship, it is concluded that the cerebral atrophy in Parkinson's disease is not caused by arteriosclerosis.

Adult↗
PubMed1975

Prognostic and therapeutic considerations in pure hypertension vs hypertension and superimposed arteriosclerosis.

In summary, a prognostic and therapeutic evaluation of 227 patients first seen from 1967 to the end of 1969 with a follow-up of 4-7 years was made. The results are indeed depressing. In spite of close follow-up and systematic treatment with modern antihypertensive agents, the mortality of patients having hypertension with superimposed arteriosclerosis was 27% (15 to 56) for males as contrasted to 3% (2 of 75) for females. Since the last casual blood pressure in both living and deceased patients of the mixed group were similar, the level of blood pressure following treatment could not be incriminated for the deceased patients. An exaggerated systolic and pulse pressure cold pressor response emerged as an important indicator of presence of arteriosclerosis alone. When hypertension and arteriosclerosis coexisted there was also exaggeration in diastolic cold pressor response. A further exaggeration in systolic and diastolic cold pressor response was seen in the decreased as compared to living male patients, a finding which appears to have grave prognostic significance for coronary heart disease and stroke. Thus a marked exaggeration in both systolic and diastolic cold pressor response in males might prove to be the single most important predictor of premature death from atherosclerotic vascular disease. A further analysis of the deceased male patients having hypertension and superimposed arteriosclerosis, indicates that treatment of hypertension may prevent oeath from stroke but not form coronary heart disease. Two-thirds of the deaths occur suddenly and only one-third of the deceased patients reached the hospital befor dying. In view of these distressing findings a plea for early detection and treatment of hypertension, prior to the development of superimposed arteriosclerotic changes, particularly in males, is made.

Arteriosclerosis↗
PubMed1979

[New aspects in the pathologic anatomy of arteriosclerosis obliterans].

The pathogenetic notion of arteriosclerosis and the clinical syndrome of the arterial obstructive diseases are not identical, but interfere in different points which are discussed in detail. Arteriosclerotic changes must be delimitated from pure age-conditioned changes of the arteries, since the two are sufficiently defined and deviate from each other in important characteristics. Only the so-called fibrous thickening of the intima is still doubtful concerning its classification. For the understanding of the severe obliterating arteriosclerosis the knowledge of the early stages is necessary. The disease begins with focal proliferations of smooth muscle cells and a disturbance of permeability of the arterial endothelium. The two cell forms are discussed more in detail and estimated in its significance for the vascular disease. Particularly the lesion of the endothelium nowadays plays an increasing role as causative factor for the development of an arteriosclerosis, since already simple increases of permeability via and edema of the intima may lead to an accumulation of lipoproteins in the vascular wall, also when the lipid level in blood is not increased. At present in clinical practice often the question of the delimitation of an obliterating arteriosclerosis from other arteriopathies leading to a vascular obstruction arises. Since a part of these diseases is to be diagnosed by biopsies of the arteries, the histological differential diagnosis of the most important inflammatory arterial diseases is discussed.

Aging↗
PubMed1978

[Possibilities of prevention and therapy of arteriosclerosis by influencing hemostatic functions].

Thrombotic processes play a role not only as a sequel of arteriosclerosis, but also for its pathogenesis. Under this aspect a pharmacological regulation of the course of the reaction of thrombpcytes, the blood coagulation and the fibrinolysis gets significance. The prevention of the formation of fibrin by well-known anticoagulants, such as coumarines and heparin, seems little suited for a prophylaxis of arteriosclerosis. By a pharmacological regulation of the reaction of the blood platelets which are decisive for the initial phase of the formation of thrombi new possibilities for an intervention into the pathomechanisms of arteriosclerosis are the result. Her also realizations concerning the prostaglandin metabolism of the blood platelets and of the wall of vessels can be evaluated. The activation of fibrinolysis by means of the hitherto introduced fibrinolytics, such as streptokinase and urokinase, is used above all for the treatment of acute thrombi. In the sense of a prevention of arteriosclerosis the activation of the endogenic fibrinolysis with the help of indirect fibrinolytics, which effect a liberation of the activators of fibrinolysis localised in the wall of the vessels, is a hopful way.

Anticoagulants↗
PubMed1977

Do risk factor interventions prevent or reverse arteriosclerosis?

We have attempted to summarize the current controversies regarding risk factors and preventive measures for control of arteriosclerosis and coronary heart disease. Recognizing that the genesis and development of the disease process are extremely complex and the basic knowledge is limited, it is not likely that conclusive answers to questions will be forthcoming soon which will provide more effective preventive or therapeutic measures. It might be desirable to institute educational and control program aimed at curtailing, at a young age, known AS risk factors such as heavy smoking, particularly if the family history indicates severe risk. Few will question the normal approaches to the treatment of complications of coronary heart disease by control of hypertension, elevated cholesterol, and smoking. However, great caution must be exercised when trying to institute large scale modifications in prevailing life patterns, particularly when based on indefinite risk factor studies and in the face of potentially profound and frequently unknown consequences. The unknowns of atherosclerotic heart disease risk factors, coupled with uncertainties and even doubts about protracted and expensive population studies, lead us to propose an emphasis on alternate selective approaches. We strongly believe that fundamental to progress in the field of arteriosclerosis is an amplification of preventive research efforts with stronger attention focused upon influencing the atherosclerotic processes within the arterial wall. But, more immediately, we urge systematic gathering and careful evaluation of patient data in particular population subsets which exhibit and accelerated mode of arteriosclerosis. Comparative studies of patients, particularly twins, families, and ethnic populations with redilection to early or accelerated arteriosclerosis may be extremely rewarding. Our repeated review of the enormous literature suggests that worldwide collaboration is needed to perfect more meaningful protocols as well as to correlate and critically evaluate existing data provided by population studies of this insidious disease process which represents an evermounting burden to society.

Adult↗
PubMed1975

[Arteriosclerosis: morbid anatomy (author's transl)].

Pathology is a variant of physiology with obstacles. No arterial wall is absolutely impermeable. The basic form of arteriosclerosis results from a disturbance of the lifelong flow of humors ab intima in adventitiam et ex centro in peripheriam (author's "Perfusion theory"). Special forms develop from this basic form. Analysis of postmortem material with special reference to the so-called risk factors allowed us to establish connections between some of these factors and arteriosclerosis, while some other connections, e.g. with smoking, were called in question. It is pointed out that prospective treatment of arteriosclerosis will begin only when the cluster of risk factors can be broken down.

Arteriosclerosis↗
PubMed1978

The natural course of arteriosclerosis in animals and man.

A thorough search for the natural history of arteriosclerosis involving the cerebrum, aorta, and peripheral vessels has been made. The disease's rate of progress has been studied anatomically, clinically, radiologically, and plethysmographically. We conclude that arteriosclerosis is usually associated with other diseases such as diabetes, high blood cholesterol, and hypertension. Heart disease in particular is often the cause of the patient's death, rather than the peripheral arteriosclerotic disease itself. The usually slow development and course of arteriosclerosis indicate that its treatment is largely a medical problem. It seems important to control the various risk factors and to utilize surgical therapy to attack specific lesions which threaten the tissues. A thorough cardiovascular profile of the patient should be compiled and should include a glucose tolerance test and lipoprotein phenotyping.

Aged↗
PubMed1975

[Contribution to the morphometry of coronary arteriosclerosis (author's transl)].

In 94 cases with and without coronary arteriosclerosis or various cardiac diseases the coronary arteries were pressure fixed, filled with a mixture of barium sulfate and gelatine for coronary angiography and dissected in 1 cm long segments for morphometry. On consecutive cross sections of the three main branches of the coronary arteries the absolute area of lumen, intima and media as well as of the thickness of the intima and media were measured. From the numerous data of the coronary arteries different indices on coronary arteriosclerosis and by correlation to the heart weight also on coronary insufficiency had been calculated. Using these quantitative data age dependent intimal changes could be distinguished convincingly from cases with uncomplicated coronary arteriosclerosis and cases with hypertension or infarcts. Thus in forensic pathology comparative evaluations can be made in regard to the extent, severity and significance of acute and chronic coronary insufficiency.

Acute Disease↗
PubMed1977

Inhibition of spontaneously developing arteriosclerosis in female breeder rats by adrenalectomy.

In order to determine whether the adrenal glands play a primary or secondary role in the pathogenesis of the spontaneous arteriosclerosis which occurs in repeatedly bred rats, sexually mature female, Sprague-Dawley rats were adrenalectomized and maintained during four successive pregnancies. Some of the breeders were treated with deoxycorticosterone (DOCA) and 0.5% saline. The adrenalectomized breeders did not develop arteriosclerosis, beta cell degranulations, or those which has accesory or regenerated adrenal glandular tissue. Surprisingly, intact DOCA-treated breeders also showed inhibition of arterial disease but they did have fatty livers and beta cell degranulation. Body and organ weights, serum enzymes, lipids, glucose, BUN, and corticosterone were elevated in breeder rats but not to such high levels as is usual in repeatedly bred rats. These findings demonstrate that the presence of the adrenal glands is essential for the pathogenesis of the spontaneous arteriosclerosis, fatty liver, and beta cell degranulation which occurs in repeatedly bred, female rats.

Adrenal Glands↗
PubMed1992

Calcium overload--an important cellular mechanism in hypertension and arteriosclerosis.

Arterial hypertension and arteriosclerosis are dramatic consequences of vascular calcium overload. Acute intracellular calcium overload of vascular smooth muscle cells produces hypercontractility. Hypertension develops if a general increase in systemic arteriolar tone leads to a rise in peripheral flow resistance. Moreover, progressive elevation of calcium destroys the structural integrity of the arterial and arteriolar walls. Thus, in various animals models, calcium overload initiates lesions of an arteriosclerotic character. Interestingly, conventional human coronary plaques also represent a calcium-dominated type of arteriosclerosis. With the advent of specific calcium antagonists, the pathogenic effects of calcium overload and its deleterious consequences have become, for the first time, accessible to therapeutic intervention. Accordingly, adequate treatment with calcium antagonists prevents calcium overload and can thereby protect arteries and arterioles from functional disturbances and structural damage. In spontaneously hypertensive rats, specific calcium antagonists of the verapamil, nifedipine and diltiazem type normalise blood pressure (BP) by reducing transmembrane calcium influx into vascular smooth muscle cells. However, in addition to controlling BP, these drugs also act as tissue protective agents. The long term effects of calcium antagonists such as verapamil in experimental hypertension include the prevention of severe arteriosclerosis, myocardial hypertrophy, and malignant nephrosclerosis. In humans, the antihypertensive efficacy of verapamil is well documented. Further clinical studies have yet to evaluate the antiarteriosclerotic and tissue protective potential of verapamil in humans.

Animals↗
PubMed1979

[Does the concept for the prevention of chronic ischemic heart disease correspond to current ideas on etiology and pathogenesis of arteriosclerosis?].

A summarizing description of the essential relations between the existence of risk factors and the course of the morphologic changes in the arteriosclerosis in the intima is given. In this process the low density lipoproteins play an important role which together with further etiologic factors contribute to an increased permeability of the endothelium and to the stimulation of the proliferation and modulation of the smooth muscle cells, which are of central importance in the vascular reaction. Certain effects on the progression of the arteriosclerosis as well as a regression of adequate morphologic changes are to be expected from an elimination of risk factors, provided the necessary measures begin in the early stages of the arteriosclerosis, i. e. in the preatheromatous stage.

Adult↗