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)

A 68 year-old woman presented with a two-week history of amaurosis fugax, ipsilateral fronto-temporal headache and jaw claudication suggesting carotid giant cell arteritis. However, this syndrome proved to be due to atherosclerosis causing complete occlusion of the external carotid artery at its origin and narrowing of the internal carotid artery. Combined external and internal carotid endarterectomy relieved the symptoms. The symptom complex of temporal arteritis may be rarely mimicked by carotid atherosclerotic occlusive disease.
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PMID:Temporal arteritis-like presentation of carotid atherosclerosis. 396 42

Risk factors for the development and rupture of intracranial saccular (berry) aneurysms were identified in a case-control study of autopsy subjects. The development of berry aneurysms was positively correlated with increased frequencies of systemic arterial hypertension (p less than 0.001), cerebral artery atherosclerosis (p less than 0.05), and marked asymmetry of the cerebral vessels comprising the circle of Willis (p less than 0.005). In addition, patients with berry aneurysms more frequently had histories of persistent headache (p less than 0.001), pregnancy-induced hypertension (p less than 0.01), long-term use of analgesics (p less than 0.001), especially aspirin (p less than 0.05), and a family history of stroke (p less than 0.05). Factors associated with a decreased risk of berry aneurysms included treatment with insulin to control diabetes mellitus (p less than 0.005), leanness (p less than 0.05), chronic pancreatitis (p less than 0.001), malignant tumors (p less than 0.001), and moderate or severe coronary or renal atherosclerosis (p less than 0.05). Rupture of berry aneurysms was positively correlated with size (p less than 0.05) and the presence of multiple aneurysms (p less than 0.005), but also with long-term analgesic usage (p less than 0.05), excessive ethanol consumption (p less than 0.01), and fatty metamorphosis of the liver (p less than 0.01). The factors that predispose to rupture of berry aneurysms are interrelated in the sense that several of them are known to cause a decrease in the synthesis of prostaglandin E, whereas one of the factors that appears to be protective has the opposite effect. Marked and abrupt lowering of serum prostaglandin levels would cause dilatation of cerebral vasculature and increased cerebral blood flow; in the setting of hypertension, focal defects in cerebral arteries could develop, leading to the formation and subsequent rupture of berry aneurysms.
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PMID:Risk factors for the development and rupture of intracranial berry aneurysms. 401 70

Sulocton effect was evaluated in 33 patients with symptoms of brain ischaemia during atherosclerosis. Thirty patients received the drug orally for 2 months in doses of 100 mg thrice daily. Three patients discontinued the treatment earlier (two of them discontinued it because of side effects). After two months of treatment a significant improvement was observed in such disturbances important for wellbeing and social contacts as: anxiety and fear, mood depression, disequilibrium of emotion, motivation and initiative. In many patients headaches, dizziness and gait disturbances disappeared or diminished. Sulocton was useful in the treatment of patients with cerebral atherosclerosis.
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PMID:[Evaluation of sulocton action in patients with atherosclerotic brain ischemia]. 629 59

Two cases of the spontaneous dissecting aneurysm (SDA) of the cervical carotid artery (ICA) were reported. Case 1: A 36 years old man was admitted with a sudden onset of right hemiparesis, aphasia and a one-week history of headache and neck pain. Serological examinations were normal. Angiography showed a severe stenosis with two intimal flaps of the left cervical ICA. Four weeks later, left STA-MCA anastomosis was performed. After six weeks from the onset, re-angiography showed the resolution of the left cervical ICA stenosis. Case 2: A 26 years old man experienced the transient monoocular blindness a week before admission. He was admitted with a sudden onset of right hemiparesis and aphasia. Serological examinations were normal. Angiography showed a postsinus tapering occlusion of the left cervical ICA. Four weeks later, left STA-MCA anastmosis was performed. After the operation, left hemiparesis improved remarkably. After two weeks from the operation, re-angiography showed the complete resolution of the left cervical ICA stenosis. As the differential diagnoses, spasm, arteritis, embolism and thrombosis with atherosclerosis were listed. But from the reason reported, we diagnosed the two cases as the resolution of the SDA of the ICA. From the previous literature, 129 cases of SDA of the ICA were reviewed and discussed about the symptom, angiographic findings and treatment. Some specific findings (high frequency of resolution, 87%, etc.) were found. SDA of the ICA occurs in the non-atherosclerotic age and causes the ischemic brain damage. SDA of the ICA should be paid more attention and will probably be identified more frequently.
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PMID:[Spontaneous dissecting aneurysm of the cervical internal carotid artery. Report of 2 cases and review of literature]. 652 29

A 54 year old man without pathologic past history but mild hypertension, obesity and gastric ulcer, presented with a syndrome of Wallenberg. He had complained for five days of progressive and diffuse headache. The neurological condition improved initially, but the patient died suddenly two weeks later. Pathological examination showed no significant alteration except for left ventricular enlargement and mild arteriosclerosis. There was a hemodissection (dissecting aneurysm) of the left vertebral artery next to the inferior oliva. It induced a lateral infarct and a limited dorsal infarct at the middle third level of medulla oblongata. Although the location of the arterial changes is usual, their nature is exceptional. The cause of the arterial hemodissection could not be ascertained: fibrous arterial dysplasia, atherosclerosis or congenital abnormalities of internal elastic layer may be discussed. But no definite conclusion can be reached.
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PMID:[Wallenberg's syndrome due to a dissecting aneurysm of the vertebral artery]. 713 26

This study included 125 cases of cerebellar infarction followed during an average period of 4.3 years. The diagnosis was made by CT or MRI. Infarctions localized to the territory of the superior cerebellar artery (SCA) and the territory of the posterior inferior cerebellar artery (PICA) occurred with the same frequency. Transient ischemic attacks preceded infarction in 26% of cases. Symptoms and signs were usual with sudden association of headache, dizziness, unsteadiness and vomiting. Vestibular signs were more important in infarctions of the PICA territory; cerebellar signs and dysarthria were more frequent in infarction of the SCA territory. A decreased level of consciousness developed in only 21% of cases. Surgical operation was required in 9 cases. Investigations have showed the large responsibility of cardiac embolisms and atherosclerosis. Short term outcome was more often favourable: 116 patients were alive at the end of the first month; 80% of survivors were independent one year later. At 5 years, 73% of patients were alive. After the acute period, mortality was mainly due to cerebro-vascular and cardiac events.
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PMID:[Clinical and evolutive aspects of cerebellar infarction]. 786 66

A total of 123 patients with primary hypercholesterolemia were randomized on a 2:1 ratio to receive either fluvastatin at 20 mg once daily at night (n = 82) or gemfibrozil at 600 mg twice daily (n = 41) in a double-blind, double-dummy comparison of the effects on plasma lipid parameters and tolerability over 8 weeks. All patients had either low-density lipoprotein cholesterol (LDL-C) concentrations > or = 160 mg/dL (4.1 mmol/L) in association with definite coronary artery disease (CAD) or > or = 2 risk factors, or LDL-C > or = 190 mg/dL (4.9 mmol/L) with no CAD and < 2 risk factors. All had triglyceride (TG) levels < or = 350 mg/dL (4.0 mmol/L). After 8 weeks of treatment, fluvastatin produced significant reductions from baseline of 17.4% (p < 0.001) in LDL-C, 13.2% (p < 0.001) in total cholesterol (TC), 13.8% (p < 0.001) in very low-density lipoprotein cholesterol (VLDL-C), and 6.4% (NS) in TG. High-density lipoprotein cholesterol (HDL-C) was increased by 5.6% (p < 0.001), and the ratio of LDL-C:HDL-C (Friedewald) was decreased by 21.2% (p < 0.001). Gemfibrozil reduced LDL-C by 15.8%, TC by 13.4%, VLDL-C by 32.2%, LDL-C:HDL-C by 24.8%, and TG by 34.2%, and increased HDL-C by 13.9% (all changes were statistically significant, p < 0.001) compared with baseline. Gemfibrozil produced significantly greater changes in VLDL-C (p < 0.01), HDL-C (p < 0.001), and TG (p < 0.001), but not in LDL-C: HDL-C, compared with fluvastatin. Both drugs significantly reduced apolipoprotein (apo) B and lipoparticles (Lp) E:B, and increased apo A-I but had divergent effects on LpA-I (increased with fluvastatin and reduced with gemfibrozil; p < 0.05). At the end of the study, 43.8% of fluvastatin patients and 45% of gemfibrozil patients achieved a reduction of > 20% in LDL-C levels. Normalization of LDL-C levels was achieved (according to European Atherosclerosis Society guidelines) by 13.4% of fluvastatin- and 14.6% of gemfibrozil-treated patients. Both drugs were well tolerated; adverse events occurred in 36.6% of fluvastatin recipients compared with 58.5% of patients taking gemfibrozil. No clinically notable elevations of aspartate or alanine aminotransferases, alkaline phosphatase, or creatine phosphokinase occurred. No patient developed new or worsening lens opacities associated with a reduction in optically corrected visual acuity. The most commonly reported adverse events were headache and gastrointestinal upset. There were no serious drug-related adverse events.
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PMID:Comparison of lipid-lowering effects of low-dose fluvastatin and conventional-dose gemfibrozil in patients with primary hypercholesterolemia. 801 67

We systematically investigated clinical, laboratory, radiologic, and pathologic features, including treatment and prognosis, of stroke syndromes in 30 patients, six from our institution and 24 from the literature, with systemic lupus erythematosus (SLE) and symptomatic large cerebral vessel occlusive disease, documented by angiography or autopsy. The average age at stroke onset was 35 years, and the diagnosis of SLE was made on average 4.4 years prior to that. At least 86% had active SLE at the time of their stroke. Headache was common at onset. We found major intracranial or extracranial vessel occlusive process by (1) thrombus, (2) dissection, (3) fibromuscular dysplasia or vasculitis, and (4) atherosclerosis. The presumed mechanisms were coagulopathy, cardiogenic embolism, large cerebral vessel vasculitis or occlusive vasculopathy, cervical arterial dissection, and premature atherosclerosis. The short-term death rate was 40% and the recurrent stroke rate was 13%. We conclude that symptomatic large cerebral vessel occlusive disease in SLE generally occurs several years after the diagnosis of SLE, usually during the active phase of the disease, is related to heterogeneous mechanisms, and carries a relatively poor short-term outcome.
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PMID:Large cerebral vessel occlusive disease in systemic lupus erythematosus. 814 3

Fifteen consecutive patients with a diagnostic problem of ischaemia-induced migraine with aura (symptomatic migraine) or migraine-associated ischaemia (migrainous infarction) were studied in order to elucidate the mechanisms. Three had a 1 month flurry of daily attacks of migraine auras with or without headache. A severe internal carotid stenosis/occlusion and reduced regional cerebral blood flow (rCBF) was demonstrated. Borderline ischaemia may thus prime the brain for developing migrainous aura with or without migraine (symptomatic migraine). Four patients had a combination of permanent deficits after the very first migraine attack, severe atherosclerosis, risk factors for stroke, high age and no family history of migraine. In these cases the evidence indicates that thromboembolic ischaemia had triggered an attack of migraine with aura (likely symptomatic migraine). Three young females presented long-lasting typical and severe idiopathic migraine with aura. Attack-associated rCBF reduction was likely to have caused permanent, mild, visual or somatosensory deficits (migrainous infarction). In five patients the relationship between migraine and stroke remained unresolved. It seems that ischaemia-induced migraine attacks may be more frequent than migraine-induced ischaemic insults. Therefore, migraine is not as strong a risk factor for stroke as indicated by the mere coincidence of the two disorders.
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PMID:Ischaemia-induced (symptomatic) migraine attacks may be more frequent than migraine-induced ischaemic insults. 845 56

There have been few reports concerning the characteristics of cerebral infarction associated with migraine (CIAM), and especially about the subsequent fate of these patients. We studied 14 patients (9 female) with CIAM. In all these patients the onset of cerebral infarction was accompanied by a unilateral throbbing headache, in 8 also with a gradual build-up of neurological deficits. No other cause of cerebral infarction could be found in these patients. Twelve patients had had previous attacks of migraine, with auras in 6. The nature of the neurological deficit was similar to previous auras in only 3 of these patients. The 2 patients without a history of migraine both developed migraine attacks afterwards. During the same period we also studied 14 patients (8 female) with a cerebral infarct of unknown origin (CIUO). The infarct involved the occipital lobe in 11 of the 14 patients with CIAM, whereas this occurred in 4 patients with CIUO [relative risk (RR): 2.8; 95% confidence interval (CI): 1.2-6.6]. Patients with CIAM had risk factors for atherosclerosis significantly less often than patients with CIUO (RR: 0.1; 95% CI: 0.02-0.9). The functional outcome of patients with CIAM was better than in patients with CIUO: all 14 patients with CIAM were independent in their daily activities, compared with 9 patients with CIUO (RR: 1.6; 95% CI: 1.1-2.3). No patient in either group had a recurrent stroke during a median follow-up period of 5.8 years. In conclusion, CIAM is a stroke entity causing mostly infarcts in the occipital lobe; vascular risk factors are uncommon and prognosis is generally good.
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PMID:Cerebral infarcts associated with migraine: clinical features, risk factors and follow-up. 883 40


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