Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with stages I and II of vascular encephalopathy developing on the background of atherosclerosis were treated with ascovertin during 21 days. Ascovertin is a complex of flavonoid dihydroquercetin and ascorbic acid. The study group included 21 patients aged 45-65 years and a comparison group consisted of 10 age-matched patients un treated with ascovertin. The ascovertin treatment relieved headache, reduced vertigo and fatigability, improved cognitive functions. The reliable diminishing of whole blood viscosity due to improvement of cellular rheology indices (decrease of aggregation and increase of erythrocyte deformability as well as decrease of indices of lipid peroxidation in erythrocyte membrane and blood plasma) was observed in the stydy group but not in the comparison one.
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PMID:[Clinical efficacy of a novel hemorheological drug ascovertin in patients with vascular encephalopathy]. 1584 24

Using clinical, psychological methods and MRI, 199 patients with vascular (VE) and posttraumatic encephalopathy (PE) have been studied. It is shown that atherosclerosis, essential hypertension and their combination become relevant at the age of 40 years. Multiple microfocal white matter lesions, leukoaraiosis, extensive bilateral atrophic changes and dilatation of subarachnoid spaces were characteristic of patients with VE (mean age 67+/-10 years). In patients with PE, mean age 22+/-7 years, the local dilatation of subarachnoid space, unilateral dilatation of lateral ventricle and cystic changes in subarachnoid spaces were detected.
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PMID:[The results of brain MRI in patients with vascular and posttraumatic encephalopathy: a comparative study]. 1598 18

The aim of the work was to assess extra- and intracranial venous hemodynamics in patients with circulatory disorder-induced encephalopathy (DE). Altogether 114 DE patients were examined. There were 46 women and 68 men aged 43 to 78 years (mean age 59.6+/-12.5 years). As dependent on the clinical manifestations the patients were distributed into groups: stage 1 DE was present in 36 patients, stage 2 DE in 47>> and stage 3 DE was identified in 31 patients. 82.78% of the examined had arterial hypertension (AH), the mean standing of which accounted for 9.7+/-7.2 years. The control group accrued 36 practically normal persons aged 36 to 62 years (mean age 47.6+/-11.3 years). All the patients were provided standard neurologic examination, magnetic resonance tomography (MRT) of the brain with venography of the brachiocephalic veins and venous sinuses of the brain, Color Doppler Imaging of the extracranial vessels, and transcranial Doppler. The patients complained primarily of headache, dizziness, instability and staggering on walking, memory and work fitness decrease, and irritability. Atherosclerotic plaques which were primarily homogeneous (types IV and V according to the classification by Geroulakos et al., 1993) were identified in the carotid arteries in 76 (62%) patients. In 48 (42%) patients, stenoses were bilateral. Hemodynamically significant (>50%) stenoses were present in 42 (34%) persons. In most cases, the patients showed dilatation of the jugular veins and a mean reduction of the flow intensity to 14+/-8.1 cm/s as compared to the control group (20.6+/-11.3 cm/s). The tendency toward flow intensity lowering associated with its phasic nature disorder was particularly well-defined in patients with stage 3 DE and a long-term history of AH. On examination of the parameters of cerebral venous circulation the patients with stage 1 DE tended to the rise of the linear flow velocity (LFV) in the basal veins of Rozenthal and in the direct sinus. However, no significant changes in the PI parameters were recorded. In the patient group with stages 2 and 3 DE, there was an appreciable rise of the LFV in the deep veins in the presence of a remarkable PI lowering (the flow velocity in the vein of Rozenthal 21.8+/-7.2 cm/s in stage 2 DE, and 24.4+/-7.2 cm/s in stage 1 DE). In 87 (79%) cases, MRT revealed the signs of diffuse ischemic lesion of the brain. Fifty-five (48%) patients were diagnosed to have leukoarayos whereas in 48 (42%) cases, there were identified multiple lacunar infarctions, primarily of the deep cerebral segments. Ten (8%) patients demonstrated type 1 Arnold-Chiari abnormalities -- hypoplasia of the large cerebral cistern and 4 patients had porto-cerebellar atrophy (megacysterna magna). Analysis of the MRV revealed, in the majority of cases (in 67 or 59%), developmental abnormality of the drainage system of the brain. Thus, 42 (37%) patients were diagnosed to have hypoplasia of one of the transverse sinuses (of the right one in 23 cases and of the left one in 19 cases); 17 (15%) persons had aplasia of the transverse sinus. Eight patients showed hypoplasia of the sigmoid sinuses (of the right one in 5 cases and of the left one in 3 cases). In all the cases of developmental abnormalities of the venous sinuses, there was a compensatory dilatation of the contralateral sinus and in some cases, there were visualized the upper and lower sinuses, the identification of which in health is difficult. So, atherosclerosis of AH-induced lesion of the brachiocephalic arteries interferes with the action of the physiological "arteriovenous pump" thereby provoking venous congestion. Progression of the process is associated with depletion of the compensatory adaptive potentialities of the collateral venous outflow which (especially in concomitant developmental abnormality in the region of the posterior cranial fossa and venous sinuses) favours aggravation of venous circulatory distress, the rise of the CSF pulse pressure and the emergence of benign intracranial hypertension and hydrocephalus followed by cerebral atrophy.
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PMID:[Cerebral venous hemodynamics in chronic disorders of cerebral circulation]. 1603 1

The main neurological complications after cardiac surgery and non-surgical cardiac procedures include stroke, encephalopathy and neuropsychological deficits. Embolism from aortic atherosclerosis is the most common pathogenic mechanism. This article reviews the incidence, risk factors, and mechanisms of these complications.
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PMID:Management of the elderly cardiac surgical patient: neurological sequelae. 1635 34

Several studies report that blood pressure is increased in victims of Alzheimer's disease (AD) decades before the onset of the disease. Years before onset of Alzheimer's disease, blood pressure start to decrease and continues to decrease during the disease process. High blood pressure has also been related to pathological manifestations of Alzheimer's disease (senile plaques, neurofibrillary tangles, hippocampal atrophy). The exact mechanism behind these associations is not clear. Hypertension is also a risk factor for stroke, ischemic white matter lesions, silent infarcts, general atherosclerosis, myocardial infarction and cardiovascular diseases, and often clusters with other vascular risk factors, including diabetes mellitus, obesity and hypercholesterolemia. Also these risk factors have been related to Alzheimer's disease. Hypertension may thus cause cerebrovascular disease that may increase the possibility for individuals with AD encephalopathy to express a dementia syndrome. Hypertension may also lead to vessel wall changes in the brain, leading to hypoperfusion, ischemia and hypoxia which may initiate the pathological process of AD. Finally, subclinical AD may lead to increased blood pressure, and similar biological mechanisms may be involved in the pathogenesis of both disorders. Hypertension is a common disorder and often untreated. Several observational studies have reported that use of antihypertensives decreases risk of AD. Even though hypertension only results in a moderately increased risk of AD, or overall dementia, better treatment of hypertension may have an immense effect on the total number of demented individuals.
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PMID:Update on hypertension and Alzheimer's disease. 1694 11

During the last decade, scientific evidence is mounting that elevated plasma levels of homocysteine are associated with an increased risk of atherosclerosis and cardiovascular ischemic events. Despite this evidence, however, there are still concerns about the mechanisms(s) by which homocysteine exerts its pro-atherogenic effect, and it is unclear whether the decreased plasma levels of homocysteine through diet or drugs may be paralleled by a reduction in cardiovascular risk. Experimental studies have shown that many possible mechanisms are implicated in the pro-atherogenic effect of homocysteine. Endothelial function is altered in subjects with hyperhomocysteinemia, and endothelial dysfunction is correlated with plasma levels of homocysteine. Exercise training reduces plasma levels of homocysteine and improves endothelial function, however without evidence of a better outcome. Larger studies are needed in order to demonstrate that the reduction of plasma levels of homocysteine by oral supplementation with folates and vitamins B6 and B12 translates into a decreased incidence of ischemic events, in particular in patients with documented coronary artery disease and ischemic encephalopathy.
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PMID:[Hyperhomocysteinemia in pediatric age and nutritional aspects of folates: an early cardiovascular risk factor]. 1731 47

An autopsy case of diffuse axonopathic leukoencephalopathy induced by drug treatment is reported. A 70-year-old woman with multiple myeloma developed encephalopathy several days after completing a course of intravenous human immunoglobulin (IVIg) and granulocyte-colony stimulating factor (G-CSF), and died within I month. T2-weighted MRI demonstrated multifocal high-signal areas in the bilateral cerebral white matter, especially in the right frontal lobe. Neuropathologically, multifocal hydropic axonal swelling with a poor glial reaction was recognized diffusely in the bilateral deep cerebral white matter, being especially marked in the frontal lobe. The cortex, subcortical U-fibers, corpus callosum, and anterior commissure were spared. The cerebellar white matter also showed similar changes, albeit less marked, but the brainstem was spared. Microscopically, the myeloma involvement of the CNS was limited to the dura, and the cerebral arteries showed slight atherosclerosis, but neither thrombi nor angitis. This case, although ultimately fatal, neurologically and neuroradiologically resembled reversible posterior leukoencephalopathy syndrome (RPLS) induced by IVIg and/or G-CSF, and the nature and selective distribution of the neuropathological changes suggested that the pathogenesis involved vasospasm of the bilateral internal carotid artery and the main trunks of the cerebral arteries, due to unknown cause, inducing ischemia in the deep white matter, which is supplied by long nutrient arteries.
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PMID:An autopsy case of drug-induced diffuse cerebral axonopathic leukoencephalopathy: the pathogenesis in relation to reversible posterior leukoencephalopathy syndrome. 1789 90

Of approximately 2,000 pathologically confirmed symptomatic CVD patients, atherothrombotic infarctions were found in 23%, lacunar infarctions in 18%, cardioembolic infarctions in 17%, hypertensive cerebral hemorrhages in 16%, lobar type hemorrhages in 3%, subarachnoid hemorrhages in 4%, progressive subcortical vascular encephalopathy of the Binswanger type (PSVE) in 8%, and others. Among 3 periods from 1975-1984, 1985-1994, 1995-2004, PSVE cases decreased during the last period, but there was no significant difference in the relative proportions of the other types of CVD during these 30 years. History of hypertension was recorded in 2/3-3/4 of the atherothrombotic infarction, in 3/4-4/5 of the lacunar infarction, and in 3/4-4/5 of the cerebral hemorrhage. Severe atherosclerosis in the main stem of cerebral arteries was found in about 3/4 of the atherothrombotic infarction, in about half of the lacunar infarction. Most frequent cardiogenic embolic source was nonvalvular atrial fibrillation showing about 3/4 of the embolic infarctions. The incidence of cerebral arterial aneurysm and of subarachnoid hemorrhage was higher in females than in males.
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PMID:[Cerebrovascular disease. Its characteristics from autopsy series in the Tokyo Metropolitan Geriatric Hospital during recent 30 years]. 1821 Jul 92

We examined 4 groups of patients younger than 70 years with atherosclerosis of coronary and/or cerebral arteries. In 98 patients the disease began as acute myocardial infarction, 65 patient from the very beginning suffered from angina of effort, 33 had ischemic cerebral stroke, and in 26 dyscirculatory encephalopathy was diagnosed. Among patients with ischemic heart disease (IHD) and cerebrovascular damages (CVD) 87 and 89%, respectively, had dyslipidemia (DLP). Disorders of lipid composition of the blood with pronounced hypercholesterolemia prevailed in patients with IHD and elevated level of triglycerides or selective decrease of antiatherogenic fraction of lipoproteides - in patients with CVD (especially in patients with stroke). When treatment is prescribed to patients with IHD and CVD at the background of DLP it is necessary to take into consideration DLP variants in order to obtain most effective action of statins and fibrates.
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PMID:[About dyslipidemic states characteristic for various forms of ischemic heart disease and cerebrovascular damages]. 1826 Sep 3

Conventional wisdom suggests that Franklin Delano Roosevelt died on 12 April 1945 aged 63 from a massive cerebral haemorrhage attributable to uncontrolled hypertension and atherosclerosis. Evidence from numerous reliable sources is presented, based largely on a constellation of previously unrecognized neurological symptoms including seizures, encephalopathy and hemianopia, supporting a scenario that, while indeed he suffered from severe cardiovascular disease, Roosevelt died from melanoma with the terminal event attributable to a metastatic lesion in the brain.
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PMID:The untold neurological disease of Franklin Delano Roosevelt (1882-1945). 2002 86


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