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PubMed1987

Surgical treatment of renovascular hypertension caused by arteriosclerosis. I. Influence of preoperative factors on blood pressure control early and late after reconstructive surgery.

This study evaluates the long-term efficacy of reconstructive surgery for renovascular hypertension caused by arteriosclerosis, which was performed on 112 patients from 1959 to 1983. Despite medical therapy, all patients had persistent hypertension, with a mean preoperative blood pressure of 188/113 mm Hg. Their median age was 49 years, and the median duration of objectively documented hypertension was 21 months at the time of surgery. Manifestations of extrarenal arteriosclerosis (ERA) were present in 57 patients (51%). Results were evaluated both at a short-term (ST) interval (mean: 8.4 months) and at a long-term (LT) interval (mean: 8.9 years) postoperatively. Patients were classified by means of strict criteria as cured, improved, or unsuccessfully treated. If a patient was cured or if his condition improved, this was considered a beneficial blood pressure response. Beneficial responses were maintained during LT follow-up, since the respective percentages for cure and improvement were 24% and 50% at the ST interval and 18% and 61% at the LT interval. These results had not been influenced by either older age or the presence of ERA, since results were similar in patients older and younger than the median age and in those with and without ERA. The preoperative duration of hypertension was the only pertinent clinical feature that influenced the LT interval results, LT beneficial responses were observed in 95% of the patients with a shorter duration and in 78% of those with a longer duration of preoperative hypertension than the median (p = 0.01). We conclude that surgical therapy for renovascular hypertension caused by arteriosclerosis can effectively reduce blood pressure and that this result is maintained during LT follow-up. In terms of anticipated blood pressure response, older age, longer duration of hypertension, and the presence of ERA do not exclude surgical therapy.

Adult↗

PubMed1986

[Parameters of normal and disordered lipid metabolism in the progression and regression of arteriosclerosis].

The processes of normal lipid metabolism in peripheral cells are regulated predominantly by LDL receptors (supply of the cells with cholesterol and essential fatty acids). Conceptions about foam cell formation in arteriosclerosis, derived from findings in cell cultures, are discussed (modified LDL lipid peroxides etc.). In prevention and regression of arteriosclerosis intracellular hydrolysis of cholesterol esters and the removal of cholesterol from the cells and the vessel wall by HDL play an important role. Further, the content of polyunsaturated fatty acids in cholesterol esters and phospholipids seems to influence the largeness of arterial lipid depositions. The manifold functions of the phospholipids within the vessel wall and the blood plasma involved in prevention and regression of arteriosclerosis (including the effect of phosphatidylcholine liposomes) are reviewed.

Arteriosclerosis↗

PubMed1986

Arteriosclerosis risk. The roles of oral contraceptives and postmenopausal estrogens.

Recent studies are reviewed to obtain a perspective on the risk of arteriosclerotic heart disease in women using various oral contraceptive formulations and postmenopausal estrogens. The evidence points to an increasing risk of arteriosclerosis in women after age 40 at a rate parallel to that of men. Arteriosclerosis risk is altered by small changes in lipoprotein concentration--in low-density lipoprotein (LDL) and high-density lipoprotein (HDL) and in a subfraction of HDL, HDL2. There are indications that oral contraceptives alter LDL, HDL and HDL2 concentrations relative to the potency of their estrogen and progestin components and also to the progestin component's associated androgenic effect, with estrogen producing reputedly favorable changes and progestin, unfavorable ones. The risk of arteriosclerosis and myocardial infarction in young women using oral contraceptive steroids is associated with increasing progestin dose, but in most studies, postmenopausal women experience no change or reduced mortality from all causes, including myocardial infarction, with it related in part to increased HDL cholesterol concentrations. It is wise to screen all women patients for hypercholesterolemia, especially those contemplating the use of oral contraceptives. Oral contraceptive steroids should be used cautiously by women with cardiovascular disease risk factors. Formulations must be selected to minimize their potentially adverse effects on lipoprotein physiology.

Adult↗

PubMedDate not supplied

Chronic progressive leukoencephalopathy with systemic arteriosclerosis in young adults.

Clinicopathological studies of four cases of chronic progressive leukoencephalopathy with systemic arteriosclerosis are reported. Two patients were siblings. In all of our patients, the illness began in early adulthood (25-29 years of age), with gait and speech disturbance as the first symptoms. At about the same time, the patients complained of lumbago, caused by intervertebral disc hernia, and had a tendency toward baldness. They gradually developed disturbance of memory, dementia, spastic paraplegia, and positive pathological reflexes. After a few years, they could neither stand nor walk and became decerebrate. Blood pressures ranged from 120/60 to 140/80 mm Hg. Laboratory data were within normal limits, including serum cholesterol. EEG showed a generalized slowing. The illness ended in death after 9 years in one case and 3-4 years in the other three cases. A general autopsy was done in three cases and only the brain was autopsied in one case. The visceral organs and the brains were fixed in 10% formalin for macroscopic and histological studies. The general autopsies revealed arteriosclerosis in the small arteries of the heart, spleen, and kidneys in three cases and in addition, moderate arteriosclerosis of the coronary arteries in one. Remarkably uniform changes were found in the brains of all four cases, involving diffuse demyelination of the cerebral white matter, with some preservation of U-fibers, and small cystic and softening foci in the white matter and the basal ganglia. The cytoarchitecture of the cerebral cortex was well-preserved. The degeneration of the white matter was caused by arteriosclerotic changes of the small arteries: fibrous intimal proliferation and hyaline degeneration and splitting of the internal elastic membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1983

[The medico-social problem of arteriosclerosis].

After defining arteriosclerosis and emphasising the need to accept the multiplicity of factors producing it, the present article shows that the disease has all the classic features of a social disease. The various risk factors involved are then analysed. Effective medical treatment of any disease must be based on knowledge of its epidemiology and aetiopathogenesis. Unfortunately in the case of arteriosclerosis not enough is known of either. It is concluded that current prevention of arteriosclerosis must be based essentially on combating the risk factors from childhood. In addition we need a combined approach covering health education, certain social factors, the design and function of the health service and the training and briefing of health service personnel.

Aged↗

PubMed1978

[The initial stage of thrombus formation in early stages of arteriosclerosis].

An arterial thrombosis develops via a lesion of the vascular wall. By the contact of the flowing blood with subendothelial collagen and basal membrane proportions the adhesion and aggregation of platelets develop which, depending on flowing conditions and local conditions, such as ADP-concentration, may lead to manifest thromboses. The prostaglandines have an essential influence on these processes. The relations of thrombosis to arteriosclerosis consist in the stimulation of the smooth muscle cells to proliferation by a factor of thrombocytes, in the organisation of experimental arterial thromboses with formation of an intima proliferation and in the complications of manifest arteriosclerosis by secondary thromboses. Methods for the proff of an increased inclination to thrombosis on the basis of an increased platelet function are critically discussed as to their clinical usability. A spontaneously increased aggregation of platelets is regarded as a reference to progressing arteriosclerosis. In these cases the significant increase of the spontaneous aggregation is of special importance in diabetics.

Adenosine Diphosphate↗

PubMed1995

[Significance of clinical examination concerning arteriosclerosis].

According to the number of deaths by major cause, Malignant neoplasma takes the first rank as the cause of death and then heart disease as a second and next rank to cerebrovascular disease since 1985, instead of top rank of cerebrovascular by that time. However, heart disease and cerebrovascular could be supposed as a arteriosclerosis disease fundamentally, arteriosclerosis disease (heart disease plus cerebrovascular) is usually top of rank in the cause of death since the Showa era. Therefore, it is great significance to make studies of risk factor on the arteriosclerosis in the laboratory medicine.

Arteriosclerosis↗

PubMed1994

[Juvenile arteriosclerosis: rare cause of generalized dilatative and stenosing vascular disease].

In addition to generalized arteriosclerosis connective tissue disease, systemic vasculitis as well as genetic metabolic disease are described to be the cause of stenotic and aneurysmatic vessel wall alteration. Although these causes are rather unusual, they must be considered for the diagnosis of a generalized vascular disease with arterial occlusion as well as aneurysm formation to determine the appropriate procedure for the individual. Whereas operative treatment should be avoided as far as possible for patients with Behçet's disease or Marfan syndrome, it is rather indicated for any kind of juvenile arteriosclerosis with arterial stenosis as well as dilatation. In this way the patient described in the following could be treated successfully by operation even though the cause of the juvenile arteriosclerosis was inexplicable, and in addition to local complications also the threatening rupture of the aneurysm could be controlled.

Aneurysm↗

PubMed1994

[Hypothetical connection between diabetes mellitus and free radical reactions in arteriosclerosis].

Diabetic patients develop arteriosclerosis at an early age. Their disease progresses more rapidly than that of nondiabetics, due to the underlying cause of arteriosclerosis of which the origin is still unknown. Much attention has been paid recently to the causative role of glycosilated lipoproteins, free radical reactions and hyperinsulinaemia--insulin resistance. Disturbances of the carbohydrate metabolism are accompanied by disorders in lipid metabolism and in the antioxidant system. While proteins undergo glycosilation, free radicals are being released from inflamed cells and, during the course of glycosilation with subsequent lipid peroxidation. Oxidation of lipids and proteins form the basis of pathological processes that might initiate the development of arteriosclerosis. There are attempts to influence the above processes by scavengers--e.g. vitamins, Ca-antagonists, angiotensin converting enzyme inhibitors and antilipaemic agents.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1994

Triple drug immunosuppression significantly reduces immune activation and allograft arteriosclerosis in cytomegalovirus-infected rat aortic allografts and induces early latency of viral infection.

The effect of triple drug immunosuppression (cyclosporine A 10 mg/kg/day+methylprednisolone 0.5 mg/kg/day+azathioprine 2 mg/kg/day) on rat cytomegalovirus (RCMV)-enhanced allograft arteriosclerosis was investigated applying WF (AG-B2, RT1v) recipients of DA (AG-B4, RT1a) aortic allografts. The recipients were inoculated intraperitoneally with 10(5) plaque-forming units of RCMV 1 day after transplantation or left noninfected. The grafts were removed on 7 and 14 days, and at 1, 3, and 6 months after transplantation. The presence of viral infection was demonstrated by plaque assays, cell proliferation by [3H]thymidine autoradiography, and vascular wall alterations by quantitative histology and immunohistochemistry. Triple drug immunosuppression reduced the presence of infectious virus in plaque assays and induced early latency of viral infection. It significantly reduced the peak adventitial inflammatory response (P < 0.05) and reduced and delayed intimal nuclear intensity and intimal thickening (P < 0.05) in RCMV-infected allografts. The proliferative response of smooth muscle cells was reduced by triple drug immunosuppression to 50% of that observed in nonimmunosuppressed RCMV-infected allografts, but still the proliferative peak response was seen at 1 month. Only low level immune activation, ie, the expression of interleukin-2 receptor (P < 0.05) and MHC class II, was observed under triple drug immunosuppression in the adventitia of RCMV-infected allografts, whereas there was no substantial change in the phenotypic distribution of inflammatory cells. In conclusion, although RCMV infection significantly enhances allograft arteriosclerosis also in immunosuppressed allografts, triple drug immunosuppression has no additional detrimental effect but rather a protective one on vascular wall histology. These results further suggest that RCMV-enhanced allograft arteriosclerosis may be an immunopathological condition linked to the host immune response toward the graft and/or the virus rather than a direct virus-induced phenomenon.

Animals↗

PubMed1993

Vitamin B6 and arteriosclerosis.

In 1949, Rinehart and Greenberg reported that marked arteriosclerosis occurs in vitamin-B6-deficient monkeys. The present study investigates the relationship between vitamin B6 and arteriosclerosis and summarizes the results. I found that thrombogenesis, disorder of collagen metabolism and production of free radicals may be the processes that cause arteriosclerosis in human and experimental animals with vitamin B6 deficiency.

Animals↗

PubMed1996

[An autopsy case of "diffuse neurofibrillary tangles with calcification", multiple infarctions and hyaline arteriosclerosis].

"Diffuse neurofibrillary tangles with calcification (DNTC)" is a slowly progressive form of presenile dementia characterized by localized temporal atrophy, pronounced calcareous deposits and numerous neurofibrillary tangles (NFTs) without senile plaques. We report a 70-year-old woman with DNTC, multiple infarctions and hyaline arteriosclerosis. This case was clinically characterized by persistent delusional ideas and personality changes. Intellectual deterioration was mild, and no focal manifestations were noted. Neuropathologically, numerous NFTs were seen distributed primarily in the hippocampal region, and massive calcareous deposits were observed in the cerebrum, basal ganglia and cerebellum. There were no senile plaques. Although the findings in this case were compatible with a diagnosis of DNTC, certain additional findings were also noted. The first was the presence of multiple infarctions in the basal ganglia and hyaline arteriosclerosis. Although these lesions may have been induced by hypertension, our review of previous reports of DNTC revealed a high incidence of arteriosclerosis. The second was the absence of lobar atrophy, which may have been due to the cerebral edema caused by the subdural hemorrhage or related to the relatively short duration of the illness. The dilatation of the temporal horn of the lateral ventricle and prominent NFTs in the hippocampal region indicate the initial occurrence of the disease in this region.

Aged↗

PubMed1996

[Pathology of arteriosclerosis obliterans].

Pathomorphological aspects of arteriosclerosis obliterans were reviewed. While the morphology is basically atherosclerosis, complete occlusions by fresh or old thrombi are often observed. Obstruction with lipid-poor fibrous tissue is also recognized. Calcification of intima or media is often present, but it does not correspond with grade of atherosclerosis. Occlusion of major arteries of the lower limbs are frequently discovered in asymptomatic aged persons. The occlusive lesions usually far-advanced before initial clinical manifestation of ischemic processes becomes apparent. Before clinical manifestations, various compensatory mechanisms including arterial anastomosis and decrease of the peripheral vascular resistance react to correct the abnormal arterial circulation. Clinical initiation first appears after the failure of these compensatory mechanisms. As in other atherosclerotic diseases, etiology of arteriosclerosis obliterans must be diverse, but upright gait of man may have some influence to develop the disease. Among many aggravating factors, diabetes mellitus is the most serious and it shows several features different from ordinary arteriosclerosis oblilerans.

Arteriosclerosis Obliterans↗

PubMed1997

[Neuropathy associated with arteriosclerosis].

OBJECTIVE: To determine the frequency and characteristics of the neuropathy associated with arteriosclerosis. MATERIAL AND METHODS: A prospective clinical and electrophysiological study was made of 29 male patients with arteriosclerosis, in whom other causes of polyneuropathy had been excluded. RESULTS: Eleven patients complained of paresthesiae (mostly mild). In 11 patients there were signs of polyneuropathy on clinical examination. Neurophysiological studies were abnormal in 11 patients, suggesting the presence of predominantly sensitive axonal neuropathy. In five patients with paresthesiae both physical examination and electrophysiological studies were normal. In 17 patients there were changes in the somatosensory evoked potentials. The brainstem auditory evoked potentials of 27 patients were suggestive of diffuse changes in central nervous conduction, together with super-imposed focal lesions. There were no differences as regards age, signs of disease in the legs or of the involvement of widespread illness, whether they were smokers, ex-smokers or non-smokers, the number of cigarettes smoked daily or the total duration of the smoking habit between the patients with and without clinical or electrophysiological polyneuropathy. CONCLUSIONS: Approximately one third of the patients with arteriosclerosis have clinical or electrophysiological signs suggestive of predominantly sensitive axonal polyneuropathy. In some cases the patients had paresthesia but no changes were seen on physical or electrophysiological examination. The evoked potentials showed diffuse changes in central nervous conduction, and in some cases this was associated with signs of focal lesions.

Adult↗

PubMed1997

[The role of oxidative stress and the preventive effect of free radical scavengers in arteriosclerosis].

The role of oxidative stress in the development of arteriosclerosis is well established. This pathogenetic explanation unificates in itself the lipid and thrombotic theories. The authors summarize the most substantial literary data in this relation, they discuss in details those therapic methods, in which the natural and synthetic antioxidants are involved as preventive drugs in the development and consequences of arteriosclerosis. Thus the effects of the dihydroquinoline type antioxidants as well as those of Vitamins A, C and E are discussed partly in experimental, partly in clinical studies. The authors conclude on the basis of own and literary data that the application of antioxidants could decrease the blood vessel alterations produced by arteriosclerosis, as well as the pathological tissue alterations developed in the consequences of ischaemia.

Antioxidants↗

PubMed1994

Role of calcium in arteriosclerosis--experimental evaluation of antiarteriosclerotic potencies of Ca antagonists. Study Group for Calcium Antagonism.

Chemical microanalyses of conventional human coronary artery plaques (stages I-III [WHO]) revealed the correlation between progressive mural Ca overload up to excessive degrees, and the severity of plaque formation, whereas only small amounts of cholesterol were found, even in complicated lesions. The pathogenetic role of Ca was tested in three types of experimental arteriosclerosis and atheromatosis, using Ca antagonists (verapamil, nitrendipine, diltiazem) as research tools: 1) The Ca type, in vitamin D3 plus nicotine-treated rats; 2) the cholesterol type, in cholesterol-fed New Zealand rabbits; 3) mixed types, in SHRs and NaCl-fed Dahl-S rats. Types (1) and (3) were demonstrated to be governed by a progressive arterial Ca uptake that could be established already in early lesions. The increased mural Ca supply promoted cellular necroses, migration, and proliferation, as well as calcification and degradation of elastic fibers. Ca antagonists prevented the increased Ca incorporation into arterial walls and inhibited the development of experimental arterioscleroses of types (1) and (3). Ca antagonists did not protect coronary arteries of cholesterol-fed rabbits (type [2]) from occlusive cholesterol accumulation. The data suggest an important pathogenetic role of Ca and pronounced antiarteriosclerotic potencies of Ca antagonists in Ca-dominated types of experimental arteriosclerosis. The significance of the present results for pathophysiology and therapy of conventional human arteriosclerosis remains to be clarified.

Adult↗

PubMed2002

Effect of vitamins C and E on progression of transplant-associated arteriosclerosis: a randomised trial.

BACKGROUND: Cardiac transplantation is associated with oxidant stress, which may contribute to the development of accelerated coronary arteriosclerosis. We postulated that treatment with antioxidant vitamins C and E would retard the progression of transplant-associated arteriosclerosis. METHODS: In a double-blind prospective study, 40 patients (0-2 years after cardiac transplantation) were randomly assigned vitamin C 500 mg plus vitamin E 400 IU, each twice daily (n=19), or placebo (n=21) for 1 year. The primary endpoint was the change in average intimal index (plaque area divided by vessel area) measured by intravascular ultrasonography (IVUS). Coronary endothelium-dependent vasoreactivity was assessed with intracoronary acetylcholine infusions. IVUS, coronary vasoreactivity, and vitamin C and E plasma concentrations were assessed at baseline and at 1 year follow-up. All patients received pravastatin. Analyses were by intention to treat. FINDINGS: Vitamin C and E concentrations increased in the vitamin group (vitamin C 43 [SD 21] to 103 [43] mmol/L; vitamin E 24 [14] to 65 [27] mmol/L) but did not change in the placebo group (vitamin C 45 [15] vs 43 [16] mmol/L; vitamin E 27 [14] vs 27 [9] mmol/L; p<0.0001 for difference between groups). During 1 year of treatment, the intimal index increased in the placebo group by 8% (SE 2) but did not change significantly in the treatment group (0.8% [1]; p=0.008). Coronary endothelial function remained stable in both groups. INTERPRETATION: Supplementation with antioxidant vitamins C and E retards the early progression of transplant-associated coronary arteriosclerosis.

Antioxidants↗

PubMed1997

Essential initial immunostimulation in graft coronary arteriosclerosis induction detected by retransplantation technique in rats: the participation of T cell subsets.

Graft coronary arteriosclerosis occurs as chronic rejection after heart transplantation. In the previous studies, we have examined the minimum period of allogeneic stimulation to induce this change, using heterotopic rat heart transplantation and a retransplantation model. Retransplantation of allografts back into the donor strain did not prevent graft arteriosclerosis if the grafts had resided in the primary recipient for up to five days. In this study, the participation of the T cell subset causing graft coronary arteriosclerotic change was assessed using the same model. The transplanted rats in fully allogeneic or non-MHC antigen mismatch combinations were treated with a short-course administration of FK506. The graft was removed and retransplanted into the donor strain rats to escape from further immunological stimulation. CD4+ T cells and/or CD8+ T cells of first recipient rats in both combinations were eliminated by monoclonal antibodies. The grade of arteriosclerosis in the retransplanted hearts was evaluated on a basis of a scale from 0-4 according to the histological appearance of the vessel injury on day 40 after initial engraftment. While neither anti-CD4 nor anti-CD8 monoclonal antibody alone had little effect, the administration of both mAbs reduced this arteriosclerotic change and development. In conclusion, the T cell subsets, CD4+ T cell and CD8+ T cell play a certain role in the induction of the graft coronary arteriosclerotic change.

Animals↗