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

Ischemic optic neuropathy and retinal arterial occlusion are 2 forms of arterial occlusive disease affecting the eye. Reports in the literature suggest platelet hyperactivity in acute arterial occlusive diseases affecting other organ systems. Therefore, 14 patients with ischemic optic neuropathy and 17 patients with central or branch retinal artery occlusion were studied to determine whether platelets have a role in the pathogenesis of these vascular occlusive disorders. The results of the following investigations were no different in these patients compared with those in 18 control patients with non-vascular eye diseases: prothrombin times, partial thromboplastin times, plasma fibrinogen, factor V, factor VIII, platelet counts and threshold concentrations of ADP, epinephrine and collagen resulting in secondary platelet aggregation and serotonin release. In contrast, platelet coagulant activities concerned with the early stages of intrinsic coagulation were significantly increased in patients with retinal artery occlusion without hypertension or type IV hyperlipoproteinemia, but generally normal in patients with ischemic optic neuropathy and in patients with retinal artery occlusion associated with hypertension, type IV hyperlipoproteinemia, diabetes mellitus and generalized atherosclerosis. These results are consistent with a platelet contribution to retinal arterial occlusive disease in patients without other known contributing factors such as hypertension, serum lipid abnormalities, diabetes mellitus and generalized atherosclerosis and may have implications regarding prophylaxis.
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PMID:Platelet coagulant activities in arterial occlusive disease of the eye. 50 1

The authors have investigated risk factors associated with the occurrence of nonarteritic anterior ischemic optic neuropathy (AION) in 83 patients and 124 eyes. 12% of the patients with nonarteritic AION had diabetes mellitus, 37.3% hypertension, 14.5% atherosclerosis, while the rest (36.2%) were classified as idiopathic. The incidence of bilateral AION was slightly less than 50%. The period in which both eyes get affected is usually 1-2 months or longer. Nonarteritic AION can occur at any age, therefore it is seen in young people as well. The role of arterial hypertension and diabetes in pathogenesis of AION is still to be determined.
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PMID:Risk factors in nonarteritic anterior ischemic optic neuropathy. 207 25

Electroretinograms (ERG), oscillatory potentials (OP) and pattern reversal visual evoked potentials (VEP) were performed in nine patients (mean age 66 years) with unilateral long-standing anterior ischemic optic neuropathy (AION) and in an age matched control group. Normal ERGs but bilateral impaired OPs were observed in virtually all AION affected patients. Regardless of visual acuity, VEP amplitude reduction was found in all eyes with AION and in controlateral eyes of patients with associated systemic conditions such as diabetes mellitus, arterial hypertension and atherosclerosis. A normal latency of VEP was found bilaterally in AION affected patients; however no correlation between VEP latency and visual acuity or fields could be established. Our results seem to indicate moderate ischemic damage to the retina and to the axons of the optic pathways in patients with AION.
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PMID:Electrophysiological findings in anterior ischemic optic neuropathy. 277 May 27

Based on the method of person-years, the morality rate of 155 patients with circulatory disorders was calculated and compared with the death rate of an age-matched general population. No excess mortality was found among 53 patients with central retinal vein occlusion and among 58 patients with ischemic optic neuropathy. On the other hand, 44 patients with central retinal or branch artery occlusion showed a statistically significant increased mortality rate. Patients with arterial circulatory disorders were subdivided into hypertensives and normotensives; an increased mortality rate was seen only among patients with hypertension but not among patients with normal blood pressure. Hypertension is one of the main cardiovascular risk factors. The increased mortality risk among our patients with hypertension may be indicative of a progressive atherosclerosis.
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PMID:[Life expectancy of patients with circulatory disorders of the posterior eyeball segment]. 687 59

The optic nerve and chiasm, obtained at autopsy, from 53 cases with clinical histories of cerebrovascular disturbances were histopathologically investigated, and ischemic changes in the posterior portion of the optic nerve were revealed in 12 cases. The progress of posterior ischemic optic neuropathy might be divided into necrotic, liquefactive and scar stages. The lesions were located in the transverse, peripheral, altitudinal and axial areas of the optic nerve. Occlusive changes of the vascular lumina due to atherosclerosis, arteriolosclerosis, capillosclerosis and emboli were demonstrated in association with the ischemic changes in the optic nerve parenchyma.
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PMID:Posterior ischemic optic neuropathy. II. Histopathology of the idiopathic form. 687 61

An acute loss of vision accompanied by signs of optic nerve head ischemia in an elderly patient should alert the examiner to suspect the presence of temporal arteritis until it can be proven otherwise. The patient presented here had ischemic optic neuropathy that was initially thought to be due to temporal arteritis, but eventually was proven to be associated with pronounced atherosclerotic aortic arch disease. The diagnosis was complicated by the severe loss of vision and by an elevated erythrocyte sedimentation rate (ESR). A temporal artery biopsy was normal, and other findings implicated the pronounced diffuse atherosclerosis as the cause of the ischemia of the optic nerve head. Therapy was directed toward the vascular occlusive disease, and involved an aortoinnominate bypass graft.
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PMID:Complicated aortic arch syndrome and ischemic optic neuropathy presenting as giant cell (temporal) arteritis. 703 43

Ischemic disorders of the retina and optic nerve head (OPH) constitute a common cause of visual loss in the middle-aged and elderly population. These disorders have a high association with atherosclerosis. This review has considered the various aspects of atherosclerosis and its role, as well as that of serotonin, in the development of ischemic disorders of the retina and ONH. It is known that when platelets aggregate on an atheromatous plaque, serotonin is one of the agents released. Studies in experimental atherosclerotic monkeys have shown that, although serotonin has no effect on ocular vasculature in normal monkeys, in atherosclerotic monkeys it produces vasopasm of the central retinal artery (CRA) and/or posterior ciliary artery (PCA) in various combinations but not vasopasm of the arterioles in the retina; vasospasm of the CRA and/or PCA(s) can consequently cause transient, complete occlusion or impaired blood flow in these arteries. It is postulated that in some atherosclerotic individuals this mechanism may play an important role in the development of ischemic disorders of the retina and ONH, including amaurosis fugax, (CRA) occlusion and anterior ischemic optic neuropathy, and possibly also glaucomatous optic neuropathy, particularly in normal tension glaucoma. Studies have also shown that dietary treatment of atherosclerosis abolishes or markedly improves the serotonin induced vasoconstriction within a few months. All these considerations may have important implications for our understanding of the pathogenesis and management of these blinding disorders.
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PMID:Retinal and optic nerve head ischemic disorders and atherosclerosis: role of serotonin. 993 83

The pathogenesis of anterior ischemic optic neuropathy (AION) primarily involves interference with the posterior ciliary artery blood supply to the prelaminar optic nerve. Uremic patients often have coexisting pathology such as hypotension (decreased blood delivery), or hypertension, atherosclerosis (increased resistance to blood supply), and anemia (low blood oxygen carrying capacity), predisposing them to AION. We describe a 49-year-old patient on dialysis for many years. He had long-standing hypotension, worsened during each dialysis treatment. He awoke one morning at age 48 complaining of blurred vision in the left inferior field. Based on the clinical course, funduscopic and fluorangiographic examination and visual field defects, AION was diagnosed. Nine months after the loss of vision in the left eye, vision in the right eye became blurred and worsened over the next 24 hours. The diagnosis of AION in the right eye was made. At the last examination ten months later, the patient, still amaurotic, was given a very poor prognosis for further recovery of the visual defects. Surprisingly, very few cases of AION have been reported in chronic uremic patients on dialysis: to the best of our knowledge, only 12 including ours. Most of these cases share some features, including hypotension above all and anemia as common risk factors. Neither the type of dialysis treatment (hemo-, peritoneal dialysis) nor sex seem to have any influence on the occurrence of AION. Uremic children can be affected. What is striking in the three published pediatric cases is that they all had polycystic kidney disease. Treatment of AION in all 12 cases consisted of a combination of steroids, i.v. saline, blood transfusions and rhEpo. AION was more frequently bilateral and irreversible, ending in permanent amaurosis. In conclusion, this study aims to stress that most cases of AION occurring in chronic uremic patients on dialysis have some common features, including hypotension above all and anemia as common risk factors.
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PMID:Anterior ischemic optic neuropathy and dialysis: role of hypotension and anemia. 1173 Feb 78

There is an increasing body of evidence linking the common respiratory human pathogen Chlamydia pneumoniae with atherosclerosis and other vascular disorders. Our research was designed to investigate the association of this organism with anterior ischemic optic neuropathy (AION), representing an acute ischemic disorder of the optic nerve head. Sera were examined of 14 consecutive patients with AION and of 14 age- and sex-matched control subjects with noncardiovascular, nonpulmonary disorders. Antibodies against chlamydial lipopolysaccharide (LPS) and outer membrane proteins of C. pneumoniae were determined by ELISA. Further, nucleic acid amplification tests were done in order to detect C. pneumoniae-specific nucleotide sequences. Four patients (29%) were IgA positive, 11 (79%) were IgG positive and 1 (7%) was IgM positive for chlamydial LPS antibodies. In the control group, 36, 79 and 7% were IgA, IgG and IgM positive and showed no significant difference. IgA, IgG and IgM antibodies to C. pneumoniae were found in 43, 79 and 0% and did not differ from matched controls. By the nucleic acid amplification test, specific C. pneumo niae sequences were neither detected in the AION patients nor in the control group. These data do not support the association of AION with previous C. pneumoniae infection. However, it remains unclear whether Chlamydia actually initiates atherosclerotic injury, facilitates its progression or plays another role in other vascular disorders.
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PMID:Chlamydia in anterior ischemic optic neuropathy. 1206 60

Based on histopathology, electron microscopic corrosion cast studies, optic nerve blood flow studies, and clinical data, the pathogenesis of idiopathic nonarteritic ischemic optic neuropathy includes the following features: (1) structurally crowded optic discs are predisposed; (2) laminar and retrolaminar regions are the most common locations for infarction; (3) there is flow impairment in the prelaminar optic disc during the acute phase; (4) lack of consistent choroidal flow impairment and the retrolaminar location of infarcts suggest vasculopathy within or distal to the paraoptic branches of the posterior choroidal arteries; (5) diabetes is the most consistently identified vasculopathic risk factor; (6) impaired autoregulation of the disc circulation by atherosclerosis, with a possible contribution from serotonin and endothelin-mediated vasospasm, may play a role; and (7) progression may be caused by secondary cell death after the initial ischemic insult or compression from cavernous degeneration and mechanical axonal distortion.
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PMID:Pathogenesis of nonarteritic anterior ischemic optic neuropathy. 1278 32


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