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)

Despite adequate diagnostic evaluation and prolonged follow-up, the causes of epilepsy in the elderly patient frequently remain unknown. Some of these may be of occult, degenerative or vascular central nervous system disease origin--entities which are often difficult to incriminate specifically. Unquestionably, in a few cases, seizures occur at the time of the initial cerebrovascular accident, although in some patients seizures may follow such an episode after a latent interval, particularly when cortical motor areas have been damaged by the initial vascular insult. It is important to differentiate this group from those with recurrent vascular episodes, in whom diagnostic studies and treatment may differ. Brain tumour is as prominent a cause of seizures in the seventh decade as it is in younger adults, but probably is of lower incidence thereafter. Focal, clinical and electroencephalographic findings and a progressive clinical course are particularly common in this group. A heterogeneous group of causes, a few of which are liable to affect the ageing patient, are responsible for some of the seizures in old age and should be searched for when the etiology is obscure. Diagnostic studies will vary with the individual problem and, whenever possible, should be restricted to non-invasive studies such as electroencephalography and computer-assisted tomography, after initial baseline clinical assessment and laboratory studies have been performed. Contrast procedures such as angiography are sometimes hazardous to patients with atherosclerosis and should be reserved for selected patients. Treatment follows conventional guidelines with some modifications due to the vulnerability of the ageing patient to degenerative disease and complications of immobilization.
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PMID:Seizures after the age of sixty. 99 28

Atherosclerosis is a degenerative disease responsible for the majority of deaths in the western populations. According to the idea of the reaction to injury the endothelial cells lining the vascular wall are exposed to repeated insults to their integrity. The injury results in a loss of functional attributes of endothelium and leads to a sequence of events including platelet adherence and aggregation, release of platelet granular components, migration and proliferation of medial smooth muscle cells into the intima. Examples of types of injury include chemical injury, as in hyperlipidemia, or mechanical stress associated with critical changes in vascular flow. Atherosclerosis has been considered a disease primarily concerned with lipid metabolism by regarding the intramural caseous material of atheromatous arteries as the sine qua non of the disease. The limitation of the lipid theory is that the conventional cholesterol-fed animal does not exactly reproduces the pathology of atherosclerosis. An alternative theory suggests that atherosclerosis is induced by mechanical fatigue which produces the progressive change in structure and mechanical properties of the vessel wall. In this view the lipid accumulation is a secondary phenomenon, the consequence of concomitant biochemical alterations of mural constituents. The hypothesis of reaction to injury provides a plausible explanation for the lesion formation and the different theories of atherogenesis are not mutually exclusive.
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PMID:[The vascular and metabolic mechanisms of the development of the atherosclerotic plaque]. 184 83

Neuronal intranuclear hyaline inclusion disease (NIHID) has been recognized in 14 patients. It usually occurs in the first and second decades but has been seen in the sixth. Both sexes are affected by this sporadic multisystem degenerative disorder that has involved the central and peripheral nervous systems with fibrillar and granular intranuclear inclusions. NIHID appears to be several variants of a multisystem degenerative disease as illustrated by the combination of a spontaneous, degenerative central and peripheral nervous system disorder with neuronal intranuclear inclusions and severe atherosclerotic coronary artery disease in a 23-year-old white man. Beginning at 11 years of age, this patient had experienced diffuse muscle spasms, dysarthria, dysphagia, tremors, ataxia, oculogyric crises, progressive muscle weakness, and atrophy. At autopsy, neuronal intranuclear hyaline inclusions and neuronal loss were seen in his brain, brainstem, cerebellum, spinal cord, bowel, bladder, and esophagus. These fibrillary and granular Cowdry type A and B intraneuronal inclusions were consistent with the diagnosis of NIHID associated with severe coronary atherosclerosis.
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PMID:Neuronal intranuclear hyaline inclusion disease associated with premature coronary atherosclerosis. 244 45

Factors released from platelets deposited on injured endothelium have lately been increasingly implicated in the pathogenesis of atherosclerosis and neointimal hyperplasia. Inhibition of platelet activity has therefore been postulated to protect injured vessels from progressive degenerative disease. The objective of this study was to evaluate the effectiveness of platelet inhibiting drugs in decreasing the deposition of platelets after a standardized endothelial injury of the rabbit aorta. The aortic endothelium of 53 rabbits was denuded with a balloon catheter. Morphological changes were studied with light and electron microscopy in five rabbits. The influence of ibuprofen, acetylsalicylic acid, dipyridamole, verapamil, and prostacyclin upon the deposition of indium-111-labeled autogenous platelets 1 hr after injury was evaluated in 48 animals. The morphological studies demonstrated that platelets were deposited on the denuded aorta but no major platelet aggregation or thrombus formation occurred. The radionuclide studies showed that none of the drugs tested had any significant influence on the deposition of platelets. It is concluded that platelets immediately adhere to injured vessels but that the secondary platelet aggregation is minimal if the injury is limited to the endothelium. Conventional drugs mainly affecting platelet aggregation are ineffective in these circumstances.
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PMID:Drug effects on platelet deposition after endothelial injury of the rabbit aorta. 389 13

Atherosclerosis is a progressive and degenerative disease of the artery wall which begins relatively early in life, years if not decades prior to the onset of clinical signs and symptoms. One of the major challenges which face investigators in this field of research is to establish the validity and reliability of noninvasive methods which can detect atherosclerotic plaques before they become severe enough to result in tissue ischemia, and to determine whether or not atherosclerotic lesions can be monitored both in terms of rate and direction over time. Although several methods of direct arterial visualization are available currently, high-resolution B-mode ultrasound imaging appears to have the most advantages. This technique is noninvasive, relatively inexpensive, and can visualize not only lumen contour and configuration, but also the atherosclerotic plaque in the underlying wall. Preliminary experiments in animal models suggest that lesions as small as 0.5 mm in the carotid arteries can be detected using this method. Whether or not atherosclerotic plaques can be monitored over time, however, has not been demonstrated.
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PMID:Noninvasive assessment of atherosclerosis in nonhuman primates. 389 44

Aneurysms caused by atherosclerosis are relatively frequent, as a consequence of the high incidence of this degenerative disease of the arteries. Other types of aneurysm, for example, those of infectious etiology, are more uncommon. Bacterias and fungi are able to cause aneurysms in several parts of the arterial tree. Stengel et al (1943), in a review of world literature described 217 cases of mycotic aneurysms. The Stedman's Medical Dictionary refers to a special type of aneurysm observed in horses, caused by intra-vascular migration of a worm, the Strongylus vulgaris. It has been named verminous aneurysm and generally involves the mesenteric arteries. We haven't found in medical literature any similar observations refering to human cases. The purpose of this paper is to describe a case of aneurysm the etiology of which we have imputed to the filaria (Wuchereria bancrofti). This case was observed in Marcilio Dias Naval Hospital, Rio de Janeiro, Brazil.
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PMID:Verminous aneurysm caused by filaria. 634 61

Micronutrients are the key to optimal macronutrient metabolism because of their essential role in metabolism. Invariably, metabolic steps require the concomitant involvement of one or more vitamins and minerals. Chronic degenerative disease etiology and rate of pathogenesis are intimately associated with micronutrient imbalances. Although precise mechanisms remain to be identified, antioxidant status is critical in atherosclerosis and cancer pathogenesis. While elucidating estimates and establishing "singular" values by sex and age for parameters such as estimated average requirements, RDA, and RDI, it is imperative to arrive at these estimates in the light of their interdependent role in metabolism.
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PMID:Overview of key nutrients: micronutrient aspects. 958 6

There is growing evidence that inflammatory processes may be involved in the development of atherosclerosis and its complications. Viral and bacterial pathogens have been implicated as possible causative factors in the pathogenesis of coronary artery disease (CAD) and restenosis after angioplasty. Antibiotic trials are now in progress to examine whether treatment of infection can prevent the complications of CAD. Atherosclerosis, the primary pathologic process in coronary artery disease (CAD), carotid artery disease, abdominal aortic aneurysm, and peripheral vascular disease, is no longer considered to be an obscure, slowly progressive, degenerative disease. Indeed, recent molecular studies on the atherosclerotic plaque have shown that the initiation, progression, and acute sequelae of atherosclerosis can be explained in part by a low-grade inflammatory process. Studies show that mediators of inflammation can be found at all stages of the life cycle of the atherosclerotic plaque. These include activated macrophages and lymphocytes, cytokines, growth factors, matrix degenerating proteinases, and tissue factor. It is hypothesized that risk factors such as hypertension, smoking, or elevated levels of low-density lipoprotein (LDL) cholesterol result in injury to the endothelial cell of the artery, and this injury initiates the inflammatory process. However, many patients with vascular disease do not have these established risk factors, and this observation has galvanized efforts to find new risk factors. Because inflammation is now considered to be an operative paradigm for atherosclerosis, it is not a major leap to the hypothesis that infectious agents, such as viral or bacterial, may play a role. Certainly this is not a new concept, and with the recent discovery that peptic ulcer disease, heretofore considered a disease of excess acid and reduced mucosal resistance, is caused by the ubiquitous bacterium Helicobacter pylori, interest in finding an infectious etiology for atherosclerosis has increased. Accordingly, the purpose of this discussion is to review in a historical manner the evidence that infectious agents-including herpes simplex virus (HSV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), Enterovirus (adenovirus, Coxsackie virus), Chlamydia pneumoniae, and H. pylori-may play a role in atherosclerosis and its manifestations, especially as they relate to CAD.
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PMID:The role of infection in atherosclerosis and coronary artery disease: a new therapeutic target. 1172 77

Risk factors for both atherosclerotic aortic wall disease and degenerative disease of the tri-leaflet aortic valve are very similar if not identical. This correlation grows even stronger as the person advances in years. Because of this, it is the prevailing view that sclerosis of the tri-leaflet aortic valve is a disease similar in etiology with sclerosis of the aortic wall. In other words, degenerative aortic valve disease is atherosclerosis of the aortic valve. Our studies challenge these views. The aortic valve is a functional assembly composed of the three cusps, corresponding sinuses, and the sinotubular junction, characterized not only by morphological features but also its functional properties, which together create an environment that is optimal for distribution of diastolic pressure load, and assures proper and timely valve opening and closure. Our experiments also demonstrate that loss of aortic wall compliance at the level of the sinuses leads to significant flexion stress in the aortic leaflets and it is likely to start a chain of events, which begins with mechanical damage to the leaflet microstructure then continues to more evident sclerosis, and finally ends in gross distortion and/or calcification of the cusps. The loss of the "pull-and-release" process may also play a part in disintegration of bioprosthetic valves and in degeneration of native aortic valves encased in non-compliant prostheses.
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PMID:Etiology of degenerative disease of the tri-leaflet aortic valve: a simple explanation for a complex problem. 1182 20

Complement (C) activation is believed to play an adverse role in several chronic degenerative disease processes, including atherosclerosis, myocardial infarction and Alzheimer's disease. We developed several in vitro quantitative assays to evaluate processes which activate C in human serum, and to assess candidates which might block that activation. Binding of C-reactive protein (CRP) to immobilized cell surfaces was used as a tissue-based method of activation, while immunoglobulin G in solution was used as a surrogate antibody method. Activation was assessed by deposition of C fragments on fixed cell surfaces, or by capture of C5b-9 from solution. We observed that several cell lines, including SH-SY5Y, U-937, THP-1 and ECV304, bound CRP and activated C following attachment of cells to a plastic surface by means of air drying. Treatment of human neuroblastoma SH-SY5Y cells with the reactive oxygen intermediates generated by xanthine (Xa) - xanthine oxidase (XaOx) prior to air drying or by hydrogen peroxide solutions after air drying, enhanced C activation, possibly through oxidation of the cell lipid membrane. Several C inhibitors were tested for their effectiveness in blocking these systems. Pentosan polysulphate (PPS), an orally active agent, blocked C activation in the same concentration range of 1-1000 microg/ml as heparin, dextran sulphate, compstatin and fucoidan. PPS may have practical application as a C inhibitor.
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PMID:Effects of C-reactive protein and pentosan polysulphate on human complement activation. 1210 Jul 26


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