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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1) In 113 patients with cerebral infarction, the cause of infarction was cardiac embolism in 35, atherosclerotic thromboembolism in 45. It was either cardiac embolism or atherosclerosis but undetermined in 30. 2) Seven risk factors have been analysed. Eight patients (7 p.cent) had none of these factors. In the 105 remaining patients risk factors were: a) atrial fibrillation in 36, diagnosed in 21. Efficient treatment was applied in 1 or perhaps in 2 patients; b) High blood pressure in 39, diagnosed in 32, efficiently treated in 5; c) dyslipidemia in 42, diagnosed in 9, efficiently treated in 3; d) obesity in 50, efficiently tackled in 2; e) diabetes in 24, diagnosed in 11, efficiently treated in 2; f) hyperuricemia in 28, diagnosed in 1 with no efficient treatment; g) smoking in 44, abandonned by 1 only. 3) The high frequency of cardiac embolism is briefly commented. 4) Non diagnosis or unefficient treatment was present in a high proportion of cases. Realizing this regrettable state of affairs should result in better preventive diagnosis and treatment which, is assumed, could significantly reduce cerebral infarction.
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PMID:[Cerebral infarctions. Study of their prevention]. 120 32

Thromboxane A2 (TXA2) biosynthesis was studied in healthy subjects, patients with chronic cerebral infarction, patients under chronic aspirin treatment and patients with atrial fibrillation. Urinary 11-dehydro-TXB2, as a major metabolite of TXA2, was measured by radioimmunoassay. The extent of carotid atherosclerosis was determined by B-mode ultrasonography. The mean +/- SD urinary excretion in patients with cerebral infarction and distinct carotid-atherosclerotic lesions (1,725 +/- 239 ng/g creatinine, n = 6) was significantly higher (p less than 0.01) than in healthy subjects (911 +/- 239 ng/g creatinine, n = 44) and patients with cerebral infarction who had no distinct carotid lesion (1,050 +/- 191 ng/g creatinine, n = 6). The urinary excretion of healthy subjects was higher (p less than 0.01) in smokers (1,063 +/- 244 ng/g creatinine, n = 17) than in non-smokers (815 +/- 183 ng/g creatinine, n = 27). Aspirin largely suppressed 11-dehydro-TXB2 excretion (266 +/- 114 ng/g creatinine, n = 7). Three of 5 patients with atrial fibrillation showed very high values. Our results indicated that platelet activation occurs in the atherosclerotic lesions, and that urinary 11-dehydro-TXB2 is the appropriate analytic target for detecting platelet activation.
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PMID:Urinary 11-dehydro-thromboxane B2: a quantitative index of platelet activation in cerebral infarction. 139 73

The study is to evaluate the relationship between extracranial carotid atherosclerosis and ischemic cerebrovascular disease using noninvasive B-mode ultrasonography and X-ray computed tomography. The sensitivity of bruits for diagnosing severe carotid stenosis was also evaluated. A total of 229 consecutive Japanese patients were recruited for this study, of which 97 had chronic-stage ischemic cerebrovascular disease and remaining 132 patients had at least one risk factor for atherosclerosis. Carotid atherosclerosis was evaluated by B-mode ultrasonography. Ischemic cerebrovascular disease was assessed by history taking, neurological findings and X-ray CT examination. The severity of carotid atherosclerosis was assessed by using two indices; plaque score and maximum percentage diameter stenosis. We also evaluated whether it was ulcerated plaque or not. Plaque score was computed by summing up all carotid plaque thicknesses (mm) on both sides. According to the CT findings, cerebral infarction was divided into two types; deep subcortical infarction and cortical infarction. The incidence of cerebral infarction increased in relation to plaque score and maximum percentage stenosis. Although the incidence of cerebral infarction in patients without carotid atherosclerosis was only 33% (38/116), it in patients with moderate carotid atherosclerosis (plaque score > 5) was 59% (26/44) (p < 0.05, chi-square test). The incidence of ipsilateral infarction was revealed to be higher in patients with severe (50% or more) carotid stenosis (61%) than in cases of mild stenosis (28%) (p < 0.05). Thirteen patients had ulcerated plaques and they suffered more frequently cerebral infarction than patients without ulcerated lesions. Cortical infarction was more frequent in patients with severe carotid stenosis than in patients without carotid atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An ultrasonic study of the relationship between extracranial carotid atherosclerosis and ischemic cerebrovascular disease in Japanese]. 146 Jul 77

We report our experience of stroke in 136 young adults aged from 18 to 45 years seen in the Eastern Province of Saudi Arabia over a 10-year period. They constituted 25% of all our stroke cases. Thirty-eight percent were Saudi nationals and 62% expatriates. Males largely outnumbered females. The frequency of cerebral infarction (54%) was not very different from that of intracranial hemorrhage (45%). Atherosclerosis and embolism of cardiac origin were the major causes of infarction. The main causes of intracranial bleeding were arterial aneurysms, arteriovenous malformations and hypertension. However, the causes of 29% of ischemic strokes and 44% of hemorrhagic ones remained undetermined. Interethnic comparison of the causes showed that hemorrhages were significantly more frequent in Far East immigrants. Sixty five percent of cerebral infarctions in Asiatic patients remained of undetermined origin. The local variant of sickle cell gene did not seem to play a major role in the pathogenesis of stroke in the Saudi young adult. These data are commented and compared with similar reported data. The influence of the demographic structures of the Saudi population and immigrants communities is analyzed.
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PMID:[Cerebrovascular disorders in young adults in Saudi Arabia. A study of 136 cases]. 149 27

The aim of this study is to describe the clinical characteristics and the pathological mechanisms of carotid transient ischemic attacks (TIA) in 117 patients which were hospitalised for such symptoms. Our results show a male predominance, except for age group under 40 and over 79 years. The principal cardiovascular index and risk factors are: arterial hypertension, smoking, hyperlipidemia, vascular intermittent claudication and hematocrit greater than 46%. Amongst our patients, 17% with hemispherical and mixed TIAs had a cerebral infarction proved by CT-Scan, the recent aspect and localisation of which were compatible with symptoms. The atherosclerotic causes are more frequently associated with mixed and retinal TIAs than hemispheric TIAs. This fact may be attributed to a larger proportion of stenotic atherosclerotic lesions by mixed TIAs than hemispheric ones. The cardiac embolic pathogenic mechanism is responsible for 11% of TIAs if considered individually; of 5% if associated with carotid atherosclerosis.
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PMID:[Transitory carotid ischemic attacks: clinical and pathogenic aspects]. 172 4

Atherosclerosis results from multiple factors, and involves several mechanisms including endothelial monocyte and smooth muscle cell changes, cholesterol accumulation, lumen stenosis, necrosis, mineralization, plaque hemorrhage, rupture, and thromboembolism. Calcium antagonists have been shown in hypercholesterolemic animal models to reduce atherosclerosis. This effect cannot be explained on the basis of changes in blood pressure, therefore suggesting that calcium channel antagonists have a direct effect on arterial wall processes associated with plaque evolution. The antiatherosclerosis properties of calcium antagonists have been tested in human subjects and suggest that these compounds inhibit new lesion development. Recent developments in B-mode ultrasonography allow investigators to detect and monitor atherosclerosis noninvasively. This method is being used in several trials within the U.S. and Europe to evaluate treatment effects on carotid atherosclerosis. Carotid artery disease is associated with transient ischemic attacks, ischemic cerebral infarction, and with risk for coronary artery disease. B-mode ultrasonography is a powerful method for monitoring atherosclerosis progression. The combination of this technology with calcium antagonist treatment will allow evaluation of the efficacy of intervention on the arterial wall during the asymptomatic stages of atherosclerosis evolution.
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PMID:Antiatherogenic properties of calcium antagonists. 172 13

Cardiovascular disease is the third most common cause of death in Tshepong Hospital in the western Transvaal, and the most common cause of death in patients older than 35 years. A prospective study was undertaken which included limited necropsies in 90 of the 167 cardiovascular disease deaths over 1 year. A reliable mortality pattern for cardiovascular deaths is described. Additionally, attention is paid to co-existing conditions. Conditions relating to cardiovascular disease, such as hypertension, benign hypertensive nephrosclerosis, atherosclerosis and obesity, were also evaluated. Cerebrovascular conditions were found in 32% of cardiovascular deaths. Intracerebral haemorrhage was found in 50% and cerebral infarction in 29% of cases. Fifty-seven per cent of cardiovascular deaths were due to cardiac conditions, the most common being pulmonary hypertension (31%), dilated cardiomyopathy and chronic rheumatic valvular disease (17% each) and hypertensive heart disease (14%). Forty-nine per cent of subjects were hypertensive, while 40% exhibited benign nephrosclerosis and only 3% of the examined vessels had signs of severe atherosclerosis. Tuberculosis was present in 13% of cases. The clinical diagnosis was the same as the final necropsy diagnosis in 38% of cases. These results emphasise the importance of performing necropsies to obtain reliable mortality statistics.
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PMID:Cardiovascular causes of death at Tshepong Hospital in 1 year, 1989-1990. A necropsy study. 173 52

Stroke is a major cause of mortality and morbidity in black Africans. The MEDUNSA Stroke Data Bank (MSDB) was established in 1984. Its goal is to gather data on all aspects of cerebrovascular disease in South African blacks, and it is supported by modern investigative techniques such as computed tomography (utilised in 82.2% of cases). The majority of the patients (71.2%) had cerebral infarction. Certain features, such as the importance of hypertension and increasing age as risk factors, were found to be similar to Western stroke populations; also, probable or definite cardiac source for cerebral embolism was present in 46% of the patients. In contrast, however, other features, such as transient ischaemic attacks, peripheral vascular disease, coronary artery disease and lacunar strokes, occurred far less frequently than is reported in Western patients. It is hoped that the MSDB will lead to a better understanding of cerebrovascular disease in blacks and possibly to in-depth comparative studies of the ubiquitous problem of atherosclerosis.
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PMID:The MEDUNSA Stroke Data Bank. An analysis of 304 patients seen between 1986 and 1987. 174 43

A study is presented of a 48-year-old female patient and her three siblings with familial hypercholesterolemia. The family members had episodes of cerebral infarction and apparently had atherosclerosis of the internal carotid artery, but no coronary heart disease due to their almost normal level of cholesterol. The laboratory studies of the family members revealed the elevations of serum lipid peroxides, serum lipoprotein(a), leukotriene C4 in blood, the thromboxane B2/6-keto-prostaglandin F1 alpha ratio in plasma and serum hydroxyl radical. Therefore, it is suspected that these factors accelerating atherosclerotic process caused the cerebral infarction. The patient demonstrated corneal opacities, palpebral xanthomas, thickened Achilles tendons, polyneuropathy and the carpal tunnel syndrome. Laboratory studies revealed an elevation in the OKT4/8 ratio, monocyte dysfunction with respect to phagocytosis and chemotaxis, and the presence of the 46XX/45XO mosaic chromosome. Lipid deposits were observed in the Achilles tendon, the transverse carpal ligament, the Schwann's cells and axons of the sural nerve, and in the keratocytes and stroma of the cornea. Following the administration of tocopherol nicotinate and probucol, the patient's serum lipid peroxide normalized and there was improvement in her palpebral xanthomas, thickening of the Achilles tendons and polyneuropathy. We conclude that the lipid deposits in this patient were due to the abnormal oxidative metabolism of low-density lipoprotein and a disturbance of the scavenger pathway due to the monocyte dysfunction.
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PMID:A family of familial hypercholesterolemia with cerebral infarction and without coronary heart disease. An unusual case with corneal opacity, polyneuropathy and carpal tunnel syndrome in the family: therapy with probucol and tocopherol nicotinate. 177 33

Several erythrocyte biophysical properties (erythrocyte deformability, erythrocyte aggregation and erythrocyte electrophoretic mobility) were investigated in patients with cerebral infarction and in individuals with risk factors of stroke (RFS population; RFSP). Blood viscosity, plasma viscosity, hematocrit, plasma fibrinogen level and yield shear stress (YSS) were also tested. In comparison with the results in a control group, erythrocyte deformability (erythrocyte length under a certain constant shear stress and erythrocyte filterability) was less in both the patient group and the group of RFSP and there is an accompanying increase of erythrocyte aggregation. Blood viscosity and fibrinogen level were higher in the patient groups. There was no correlation between erythrocyte deformability and other hemorheological parameters. Our results suggest that significant alteration of erythrocyte biophysical properties may be implicated in the pathogenesis of ischemic stroke. These abnormalities are associated with some of the risk factors of stroke such as hypertension, atherosclerosis and cardiovascular disorders.
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PMID:[Alteration of erythrocyte biophysical properties in patients with ischemic cerebrovascular disorders]. 181 80


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