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

Plasma lipid and lipoproteins levels were determined in a continuous series of 50 patients (36 males and 14 females), mean age around 50 years, with a clinical diagnosis of transient ischemic attacks (TIAs). TIA was defined as a sudden episode of focal cerebrovascular insufficiency, with complete resolution of the symptoms within 24 h. TIAs are considered an important prognostic symptom for ischemic cerebrovascular diseases, being manifest in approximately 45% of the patients later undergoing a complete stroke. Plasma total cholesterol levels did not differ in these patients, when compared with a similar series of patients of the same age and sex, free of cerebrovascular lesions. A slight elevation of mean triglyceride levels was detected in the patients of both sexes, as well as higher incidence of type IV hyperlipoproteinemia. The most significant finding, however, observed only in male TIA patients, was that of significantly reduced high density lipoprotein (HDL)-cholesterol levels. This reduction (-19.7% compared to the control group) is similar to that recently reported for patients with clear-cut ischemic cerebrovascular disease. The detection of decreased HDL-cholesterol levels in male TIA patients may be of considerable significance for a prognostic evaluation of this biochemical parameter.
Atherosclerosis 1979 Feb
PMID:Decreased high density lipoprotein-cholesterol levels in male patients with transient ischemic attacks. 22 5

Transient ischemic attacks are not only the consequence of cerebral atherosclerosis. A woman of 48 years had transient ischemic attacks because of a meningeom narrowing the internal carotid artery. A steal syndrome in tumor vessels of a glioblastoma must be presumed in a man of 67 showing initial hemisyndrome with first transient, later on remaining palsy.
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PMID:[Transient ischemic attacks with intracranial tumors (author's transl)]. 49 65

One hundred seventeen patients, 31 with TIA and 86 with cerebral infarction, had angiographically verified atherosclerosis within the relevant carotid artery territory and normal CSF. They were treated with anticoagulants for a mean of 11.1 months. No TIA but 1 cerebral infarction, appearing during inadequate anticoagulant therapy, was registered. Seventy-six of the patients, 20 with TIA and 56 with infarction, were followed for a mean of 4.4 months after cessation of anticoagulants or during inadequate antinecessitating re-institution of anticoagulant therapy. Long-term, anticoagulant treatment can be recommended in carefully selected patients with TIA, and also with infarction in the carotid territory.
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PMID:Prognosis in patients with infarction and TIA in carotid territory during and after anticoagulant therapy. 50 92

Carotid and vertebrobasilar transient ischemic attacks (TIAs) were clinically and angiographically correlated in 85 patients who had four-vessel angiography within 2 weeks after a TIA. The patients were divided into carotid and vertebrobasilar groups by clinical criteria. In the correlations of symptoms with arteriography, lesions of the contralateral internal carotid artery were observed in 54 percent of the patients. Of 39 patients with vertebrobasilar symptoms, 34 percent also had one carotid lesion and six patients had combinations of symptoms of both carotid and vertebrobasilar disease. In correlation with carotid bruits of the 85 patients, bruits were heard over one carotid artery in 42 percent. Subclavian bruits were heard in 47 percent of the patients with vertebrobasilar symptomatology. TIAs owing to arteriosclerosis of the cervical arteries occurred in 85 percent of the patients, but there was no significant difference in the incidence of atherosclerosis-induced TIA in the carotid and vertebrobasilar systems. For accurate population surveys of the prevalence of TIAs, and for clinical decisions, proper categorization of patients is necessary.
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PMID:Carotid and vertebrobasilar transient ischemic attacks: clinical and angiographic correlation. 57 96

Transient ischaemic focal cerebral attacks (TIA's) are due to: 1) atherosclerosis when embolism may take place or perhaps transient occlusion of the internal carotid artery or mural or transiently occlusive thrombus of an intracranial artery stenosis or transient systemic hypotension. In recent years embolism may have been overdiagnosed; 2) cardiac embolism due to dysrythmias, myocardial infarction, endocarditis, valvular prosthesis, etc.; 3) miscellaneous causes, often difficult to demonstrate such as tortuosity of the extracranial cerebral arteries, dissecting aneurysms, changes in cerebrovascular resistance; 4) not unfrequently no cause is found, especially in young patients.
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PMID:[Pathogenesis of focal, transitory cerebral ischemic accidents]. 60 29

The treatment of TIA must be individualized. TIA is one of several manifestations of generalized atherosclerosis. While one-third of patients with TIA will suffer a stroke in five years, one-half of the same group will die of myocardial infarction. The risk of stroke is greater in carotid rather than vertebral-basilar TIA, in older patients, and in those with a cluster of TIAS, an is highest in the first month after the TIA. Treatment should reflect this knowledge.
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PMID:Transient ischemic attacks. 122 59

There is substantial evidence to support the concept that most transient ischemic attacks (TIAs) are caused by microemboli that originate in areas of atherosclerosis in the blood vessels of the neck. TIA's are important risk factors in the development of stroke. The most common clinical features of TIAs caused by carotid insufficiency are hemianesthesia and hemiparesis; other symptoms in these cases include headache, dysphasia, and visual field distrubance. By far the most common clinical manifestation of vertebrobasilar insufficiency is vertigo.
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PMID:Transient ischemic attacks: Pathophysiology and medical management. 126 82

The purpose of this study was to review data from published cerebrovascular studies to determine if it is possible to predict, based on clinical manifestations (eg, cervical bruit, transient ischemic attack, or stroke) of cerebrovascular atherosclerosis, the annual probability of having a stroke, as well as to determine and discuss the methods used in calculating and reporting vascular event rates. This overview analysis reveals that the annual stroke rates are as follows: for asymptomatic carotid stenosis, 1.3% (95% confidence interval [CI], 1.0 to 1.6); for transient monocular blindness, 2.2% (95% CI, 1.3 to 3.0); for transient ischemic attack, 3.7% (95% CI, 3.1 to 4.3); for minor stroke, 6.1% (95% CI, 5.7 to 6.6); and for major stroke, 9.0% (95% CI, 8.0 to 9.9). The data analyzed here suggest that a hierarchical profile of worsening clinical characteristics mirrors a hierarchical progression of increasing risk of stroke. These data support the idea that there is a clinical risk profile, in addition to the conventional atherosclerosis risk factor profile, for predicting subsequent stroke.
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PMID:Vascular event rates in patients with atherosclerotic cerebrovascular disease. 152 19

Patients with systemic lupus erythematosus may develop premature atherosclerosis, notably coronary artery disease. A group of 10 patients with peripheral vascular disease presenting with intermittent claudication or gangrene were studied from a group of 563 patients followed prospectively at the Wellesley Hospital Lupus Clinic. These 10 patients were compared with the next lupus clinic patient matched for age and sex, with respect to demographic characteristics and risk factors. The patients and controls did not differ significantly in lupus activity criteria count, partial thromboplastin time, the number with antibody to cardiolipin, number receiving steroids or mean steroid dose, family history of atherosclerosis, hyperlipidaemia, smoking, hypertension or use of oral contraceptives. The risk factors for developing peripheral vascular disease were a longer duration of systemic lupus erythematosus and a longer duration of use of steroids. Eight of the 10 patients had coexistent coronary artery disease or transient ischaemic attack.
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PMID:Peripheral vascular disease in patients with systemic lupus erythematosus. 154 39

Recent reports of the risk of asymptomatic carotid stenosis have been compromised by flawed patient selection or the performance of a large number of carotid endarterectomies during follow-up. We report the natural history of a randomly selected group of asymptomatic patients (n = 188; 114 males and 74 females) with documented carotid artery disease who were prospectively followed without intervention for up to 8 years. Risk factors included ischaemic heart disease in 17%, diabetes in 10%, hypertension in 46% and 88% were smokers. The degree of internal carotid stenosis was classified by duplex scanning and a total of 259 vessels had evidence of atherosclerosis. Study end-points included TIA, CVA and death. At mean follow-up of 4 years 3% of the 96 patients with internal carotid artery stenosis of less than 50% had died and 2% suffered a stroke. Six per cent of patients with a stenosis of 50-79% had died and 4% and 2% had suffered a CVA and TIA, respectively. In the 59 patients with greater than 80% stenosis 7% had suffered a TIA and an additional 7% a CVA, while 2% had died. None of the patients suffering a stroke had an antecedent TIA. Though the incidence of ischaemic events is significantly higher in patients with greater than 80% stenosis the incidence of unheralded stroke remains low. We therefore continue to recommend a conservative approach to the management of asymptomatic carotid stenosis.
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PMID:Asymptomatic carotid stenosis: a benign lesion? 155 61


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