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Vascular risk factors stroke

Schulz UG, Rothwell PM (2003). Differences in vascular risk factors between aetiological subtypes of ischemic stroke in population-based incidence studies. Stroke 34 2050-2059... [Pg.27]

Schulz UG, Flossman E, Rothwell PM (2004). Heritability of ischemic stroke in relation to age, vascular risk factors and subtypes of... [Pg.27]

Non-stroke vascular disease or vascular risk factors... [Pg.124]

Vascular risk factors (Ch. 2) and diseases should be sought. It is unusual for an ischemic stroke or TIA to occur in someone with no vascular risk factors, unless they are very old, or are young with some unusual cause of stroke (Ch. 6). A history of heart disease may be relevant and cardiac symptoms should be specifically inquired about. [Pg.126]

Aortic arch atheroma is now increasingly diagnosed by transesophageal echocardiography in patients with TIAs or ischemic stroke, but so far there are no surgical, or indeed medical, treatment options over and above controlling vascular risk factors and antiplatelet drugs. One trial of medical treatment has been started, the Aortic Arch Related Cerebral Hazard (ARCH) trial (MacLeod et al. 2004). [Pg.310]

Vascular risk factors previous stroke, hypertension, diabetes, contralateral internal cerebral artery occlusion, peripheral vascular disease... [Pg.313]

Upregulation of adhesion molecules has been documented in human stroke patients [7]. It was demonstrated that leukocytes from patients suffering an ischemic stroke or transient ischemic attack showed increased CDl la expression within 72 hours of the onset of symptoms [123]. Increased ICAM-1 expression on the surface of vessels fi om cerebral cortical infarcts was detected in four patients [124]. In some studies, soluble isoforms of adhesion molecules shed fi om the surfaces of activated cells were quantified in serum. Serum endothelial-leukocyte adhesion molecule-1 (ELAM-1, E-selectin) levels increased up to 24 hours after stroke. Similar increases were observed in serum vascular cell adhesion molecule-1 (VCAM-1) levels and these increases were sustained up to 5 days [125]. In contrast, serum ICAM-1 levels in acute ischemic stroke patients have been found to be lower than or the same as those of asymptomatic control subjects matched for age, sex, and vascular risk factors [125,126]. The reason not to detect an increase in serum levels of adhesion molecules might be due to the late enrolling of patients. Once adhesion molecules bind to leukocytes and endothelial cells, they can no longer be detected in serum [7]. [Pg.193]

Several cases of intravenous immunoglobulin-related thrombosis have been reported (78,79). It can be either venous or arterial (80). It has been suggested that thrombosis can be caused by platelet activation and increased plasma viscosity (79). In patients with vascular risk factors, such as old age, hypertension, and a history of stroke or coronary artery disease, complications, such as myocardial infarction, pulmonary embolism, stroke, and acute spinal cord events, have been described (80). Intravenous immunoglobulin enhances platelet aggregation and the release of adenosine triphosphate in human platelets in vitro. In addition, there is a dose-related increase in plasma viscosity with increasing plasma immunoglobulin concentration (79,80). [Pg.1723]

Persistent and paroxysmal atrial fibrillation (AF) are potent risk factors for first and recurrent stroke. It has been estimated that AF affects more than 2,000,000 Americans and becomes more frequent with age, being the most frequent cardiac arrhythmia in the elderly [6,38], The prevalence of AF peaks at 8.8% among people over the age of 80 years, hi the Framingham Stroke Study, 14% of strokes occurred because of AF. The absolute risk of stroke in patients with AF varies 20-fold, according to age and the presence of vascular risk factors [6,7]. Several stroke risk stratification schemes have been developed and validated. Overall, patients with prior stroke or transient ischanic attack carry the highest stroke risk [6,39]. [Pg.32]

Homocysteine arises from dietary methionine. High levels of homocysteiae (hyperhomocysteinemia) are a risk factor for occlusive vascular diseases including atherosclerosis and thrombosis (81—84). In a controlled study, semm folate concentrations of <9.2 nmol/L were linked with elevated levels of plasma homocysteiae. Elevated homocysteine levels have beea associated also with ischemic stroke (9). The mechanism by which high levels of homocysteine produce vascular damage are, as of yet, aot completely uaderstood. lateractioa of homocysteiae with platelets or eadothehal cells has beea proposed as a possible mechanism. Clinically, homocysteine levels can be lowered by administration of vitamin B, vitamin B 2> foHc acid. [Pg.42]

Hypertension, or a chronic elevation in blood pressure, is a major risk factor for coronary artery disease congestive heart failure stroke kidney failure and retinopathy. An important cause of hypertension is excessive vascular smooth muscle tone or vasoconstriction. Prazosin, an aradrenergic receptor antagonist, is very effective in management of hypertension. Because oq-receptor stimulation causes vasoconstriction, drugs that block these receptors result in vasodilation and a decrease in blood pressure. [Pg.102]

A complete history and physical examination should assess (1) presence or absence of cardiovascular risk factors or definite cardiovascular disease in the individual (2) family history of premature cardiovascular disease or lipid disorders (3) presence or absence of secondary causes of hyperlipidemia, including concurrent medications and (4) presence or absence of xanthomas, abdominal pain, or history of pancreatitis, renal or liver disease, peripheral vascular disease, abdominal aortic aneurysm, or cerebral vascular disease (carotid bruits, stroke, or transient ischemic attack). [Pg.113]

Cardiovascular and cerebrovascular disorders associated with lipid metabolism disturbance and atherosclerosis represent major risk factors for dementia (3,25,59). Atherosclerosis is the primary cause of heart disease and stroke in which genetic and environmental factors converge (553). More than 90% of patients older than 70-80 yr with dementia show signs of atherosclerosis in their arteries and a clear cerebrovascular component in their dementia process. It is very likely that pure AD is practically absent in octogenarians, in whom the prevalent diagnosis is vascular or mixed dementia (3,25,59), in which the APOE-4 allele also accumulates (18-20,554). [Pg.308]

The risk factors for vascular dementia are essentially the same as those for stroke and heart attack. They include high blood pressure, heart disease, diabetes mellitus, sickle cell disease, obesity, smoking, alcohol use, depression, and high cholesterol levels. [Pg.288]

Reduction in risk of Ml, stroke, and death from cardiovascular causes - In patients 55 years of age or older at high risk of developing a major cardiovascular event because of a history of coronary artery disease, stroke, peripheral vascular disease, or diabetes that is accompanied by at least 1 other cardiovascular risk factor (eg, hypertension, elevated total cholesterol levels, low FIDL levels, cigarette smoking, documented microalbuminuria). [Pg.574]

Although atherosclerosis exerts its most important effects on the coronary vessels, other vascular beds are frequently affected, such as the carotid arteries, the aorta, and the vessels of the legs. However, the possibility that effective lipid lowering could have beneficial effects on atherosclerotic diseases other than CHD has received relatively little attention. Although there is some evidence that hypercholesterolemia is a risk factor for stroke, especially in younger patients (Prospective Studies Collaboration, 1995), the epidemiologic data are not nearly as extensive or unequivocal as for CHD. The first evidence that HMG-CoA reductase inhibitors could reduce the risk of cerebrovascular effects was provided by 4S, in which there was a significant 28% reduction in the... [Pg.106]

Many individuals with LA also harbor lacunar and/or cortical infarcts. Presence of LA serves as an intermediate surrogate both for ischemic stroke and intracerebral hemorrhage as they all share similar risk factors and similar pathophysiological mechanisms (Inzitari 2003). LA is widely found in dementing illnesses, such as Alzheimer s disease, vascular dementia, and cerebral autosomal dominant arteri-opathy with subcortical infarcts and leukoencepha-lopathy (CADASIL). Failure of blood supply in the... [Pg.151]

Other groups have emphasized that previous infections are an independent risk factor for acute stroke. This phenomenon might be at least in part attributable to the activation of cytokines and adhesion molecules such as the vascular cell adhesion molecule (VCAM) and intercellular adhesion molecule (ICAM) (5). [Pg.146]

Previous ischaemic stroke/ transient ischaemic attack or thromboembolic event Age > 75 years with hypertension, diabetes, or vascular disease (coronary artery disease or peripheral artery disease) Age > 65 years with no high risk factors Age < 75 years with hypertension, diabetes, or vascular disease (coronary artery disease or peripheral artery disease) Age less than 65 years with no moderate or high risk factors... [Pg.437]

Rothwell PM, Coull AJ, Giles MF et al. (2004). Change in stroke incidence, mortality, case-fatality, severity and risk factors in Oxfordshire, UK from 1981 to 2004 (Oxford Vascular Study). Lancet 363 1925-1933 Rothwell PM, Coull AJ, Silver LE et al. (2005). Population-based study of event-rate, incidence, case fatality and mortality for all acute vascular events in all arterial territories (Oxford Vascular Study). [Pg.15]

Schmahmann JD (2003). Vascular syndromes of the thalamus. Stroke 34 2264-2278 Schulz UG, Rothwell PM (2001). Major variation in carotid bifurcation anatomy a possible risk factor for plaque development Stroke 32 2522-2529 Scott BL, Jankovic J (1996). Delayed-onset progressive movement disorders after static brain lesions. Neurology 46 68-74 Wardlaw JM, Merrick MV, Ferrington CM et al. (1996). Comparison of a simple isotope method of predicting likely middle cerebral artery occlusion with transcranial Doppler ultrasound in acute ischaemic stroke. Cerebrovascular Diseases 6 32-39 Wardlaw JM, Lewsi SC, Dennis MS etal. (1999). Is it reasonable to assume a particular embolic source from the type of stroke Cerebrovascular Diseases 9(Supp 1) 14... [Pg.131]

Cl, confidence interval Ml, myocardial infarction PVD, peripheral vascular disease TIA, transient ischemic attack. Hazard ratios derived from the model are used for the scoring system. The score for the five-year risk of stroke is the product the individual scores for each of the risk factors present. The score is converted into a risk with a graph. Source. Rothwell et at. (2005). [Pg.182]

However, there is only one report specifically on which patients with a previous TIA or stroke and NRAF are at high (and low) risk, based on 375 patients with NRAF and TIA or non-disabling stroke treated in the placebo arm of the European Atrial Fibrillation Trial (van Latum et al. 1995). Independent risk factors for vascular death, stroke and other major vascular events included increasing age, previous thromboembolism, ischemic heart disease,... [Pg.220]


See other pages where Vascular risk factors stroke is mentioned: [Pg.66]    [Pg.197]    [Pg.477]    [Pg.32]    [Pg.32]    [Pg.144]    [Pg.362]    [Pg.362]    [Pg.367]    [Pg.369]    [Pg.821]    [Pg.490]    [Pg.74]    [Pg.200]    [Pg.263]    [Pg.242]    [Pg.145]    [Pg.233]    [Pg.164]    [Pg.14]    [Pg.28]    [Pg.108]    [Pg.218]    [Pg.221]   
See also in sourсe #XX -- [ Pg.126 ]




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