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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Risk factors for primary cerebral hemorrhage remain uncertain. The population-based Stroke Registry of Dijon provides data on the risk factors. Among residents of Dijon (France), 130 cases of primary cerebral hemorrhage hospitalized from 1985 to 1992 were matched with 130 controls by age and sex. The following data were collected: history of hypertension, alcohol consumption, tobacco consumption, history of coagulation disorder, diabetes mellitus, dyslipidemia, and infectious disease in the 7 days before admission. The following parameters were measured on admission: blood pressure, blood glucose, cholesterol, triglycerides, hematocrit, fibrinogen, prothrombin levels, platelet counts, prothrombin time, bilirubin, transaminases, gamma-glutamyltransferase, and alkaline phosphatase. Electrocardiogram and Doppler ultrasound examination of cervical arteries were performed. Statistical analysis was performed by means of relative risk ratio for paired samples when dealing with proportions, and Student's t test for quantitative variables. A stepwise discriminant analysis was carried out to establish the relative weight of the different risk factors and their discriminant values. Among the qualitative data, the significant factors were history of hypertension, alcohol consumption, cardiac arrhythmia, atherosclerosis of carotid arteries and a previous infectious disease in the 7 days before admission. Among the quantitative data, the significant factors were early hypertension, high blood glucose levels, high hematocrit, and low cholesterol levels, in the acute stage of the stroke. After multifactorial analysis, only two factors were significant: hypertension and low cholesterol levels. Our population-based case-control study showed that hypertension and low cholesterol levels are the two discriminant risk factors for both lobar and basal ganglia primary cerebral hemorrhage. Therefore, treatment of hypercholesterolemia may increase risk of cerebral hemorrhage.
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PMID:Risk factors for primary cerebral hemorrhage: a population-based study--the Stroke Registry of Dijon. 789 3

The relationship of dyslipidemia, particularly hypercholesterolemia to coronary heart disease is now well established. Although ischemic heart disease and stroke share many of the same risk factors, the relationship of cholesterol to stroke remains controversial. The 6-year and 12-year follow-up of the MRFIT study showed that elevated cholesterol significantly increased the risk for fatal nonhemorrhagic stroke. Atkins found no evidence that lowering plasma cholesterol influenced the incidence of fatal or nonfatal stroke and regression analysis showed no statistical association between the magnitude of cholesterol reduction and the risk for fatal stroke. We cannot preclude the possibility that more effective cholesterol lowering over a longer period of time might be effective. Hypertension is the most powerful risk factor for stroke. The San Antonio Heart Study reported a clustering of cardiovascular risk factors in individuals who developed hypertension during an eight-year follow-up period (higher levels of BP, fasting TC and LDLC, TG, glucose and insulin, and BMI, less favourable fat deposition, and lower HDL). Insulin resistance may be the unifying factor that results in those phenomena, the so-called syndrome X. The important factor underlying syndrome X may be central or visceral obesity, suggesting that maintenance or attainment of ideal weight would be a powerful preventive factor against both CHD and nonhemorrhagic stroke. There is evidence from the Treatment of Mild Hypertension Study that nutritional/hygienic measures can reduce the syndrome X risk factors and hence the risk of coronary heart disease and stroke.
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PMID:Dyslipidemia and metabolic factors in the genesis of heart attack and stroke. 791 92

The correlation between the circulating immune complexes (CIC) and dyslipidemia was studied in a group of 150 patients with acute ischemic stroke and 50 normal controls. The object of the study was also to find out whether these two components represent a macromolecular complex with increased atherogenic capacity or only two risk factors acting separately but achieving a summation of their atherogenic power. It can be considered that in acute ischemic stroke the presence of the two risk factors constitutes a condition of acceleration of the atherogenic process, i.e., the appearance of the vascular accident. The decrease of HDL-cholesterol detected in all the subgroups studied is probably due to the decrease of the cholesterol "reverse transport" process which favours the atherogenic process. It was found that CIC and low density lipoproteins (LDL) are risk factors which act separately determining by the effects they generate a summation of their atherogenic capacity. Cholesterol and triglycerides apparently contained in the CIC structure, can be considered as a methodologic artefact due to the use of a common reagent (PEG-6000).
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PMID:Circulating immune complexes and low density lipoproteins--a molecular complex or the summation of the atherogenic risk of two separate entities? 813 Jul 57

During the first year the Austrian Stroke Prevention Study enrolled 599 volunteers without clinical signs or symptoms of cerebrovascular disease aged 50 to 70 years. Study participants were randomly selected from the official register of the city of Graz. The rate of positive response was 26.9 percent. All subjects underwent an extensive risk factor screening with Duplex scanning of the carotid arteries obtained from a subset of 176 individuals. The prevalence of well-documented cerebrovascular risk factors was 40.6% for arterial hypertension, 35.4% for cardiac disease, 8.5% for diabetes mellitus und 3% for elevated haematocrit. The less well-documented cerebrovascular risk factors dyslipidemia, overweight, physical inactivity, hyperfibrinogenemia and smoking were noted in 75%, 33.7%, 27.2%, 14.9% and 12.2% of subjects, respectively. Multiple well-documented risk factors were noted in 23.7% of the examined volunteers. Multiple linear regression analysis revealed body mass index (p < 0.0001) and age (p < 0.0001) as independent predictors of the frequency of well-documented risk factors observed in any individual. Atherosclerotic carotid disease occurred in 61.9% of study participants investigated by Doppler sonography and was significantly associated with age (p < 0.00001), life-time tobacco consumption (p < 0.0001) and the concentration of apolipoprotein B (p < 0.05). This study demonstrates high prevalence rates of vascular risk factors in an elderly Austrian community. Implications for stroke prevention result from the conjunction of overweight and frequency of risk factors noted in any study participant, as well as from the relationship of carotid atherosclerosis to smoking and dyslipidemia.
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PMID:Cerebrovascular risk factors in an elderly Austrian population: first year results of the Austrian Stroke Prevention Study (ASPS). 836 75

Abdominal (truncal) fat distribution reflected by an elevated waist to hip ratio (WHR) predicts metabolic abnormalities such as diabetes and dyslipidemia as well as hypertension and stroke, all of which are associated with obesity. The pathogenesis is not known, although elevated splanchnic serum free fatty acid levels and reduced hepatic insulin clearance have been implicated. WHR and body fat (BF) by 40K-counting and 3H2O were measured before liver biopsy during antiobesity surgery in 68 severely obese women (body mass index [BMI], 48.9 +/- 1.1 SEM) and 15 men (BMI, 49.0 +/- 3.1) without histories of liver disease, diabetes, or hepatotoxic exposure. Biopsies were graded for fat content semiquantitatively (0 to 4+) by the hepatologist who was blinded to the patients' clinical characteristics. All 15 men had fatty infiltration (score, 2.5 +/- 0.3 v 1.4 +/- 0.1 in women; P < .001). The correlation between WHR and liver fat was .44 (P < .0005), while BF (-.16), weight (.15), or BMI (.04) did not correlate significantly with steatosis (all NS). As expected, percentage body fat (BF%) was greater in women than in men (40.3 +/- 0.8 kg v 33.9 +/- 2.0, P < .007), and accordingly liver fat was inversely related to BF% (r = -.32, P < .002). Steatosis was significantly greater in 14 men (2.5 +/- 0.3) than in 20 women (1.7 +/- 0.3, P < .04) matched for BF%. In multiple regression analysis R2 = .49, P < .0001), WHR and sex accounted for the variance in liver fat content without any further contribution from weight, BMI, BF, or BF%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Body fat topography as an independent predictor of fatty liver. 849 7

Despite selectivity in prescriptions and changes in formulations, combined oral contraceptives still increase the relative risk of thrombo-embolic accidents. The main mechanism implies ethinyloestradiol accumulation in the liver and related consequences, not for circulating lipoproteins, but for coagulation/fibrinolysis balance. Most serious concerns should be directed to subjects having preexisting arterial or venous wall alterations or hemostatic disorders. Restriction of oral contraceptive use extended to all subjects suspected of carrying these risks has been highly effective for prevention of coronary accidents but less for prevention of stroke or venous thrombosis. The crude number of vascular accidents remains very low in women below 35 years old, non smokers, without hypertension, diabetes, dyslipidemia nor cardiac valve disease, without personal or familial history of thrombosis, and without any significant increase in weight, blood pressure and triglycerides while using pills.
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PMID:[Metabolic and vascular risks with oral contraceptives]. 857 Oct 54

The fibrinolytic system is thought to be impaired in older hypertensive adults, thus contributing to the elevated risk of atherothrombosis, stroke, and acute myocardial infarction in this population. However, studies that have examined the fibrinolytic system in hypertensive individuals have failed to control for the confounding effects of other metabolic risk factors, making it difficult for one to determine the independent effect of hypertension on the fibrinolytic system. The purpose of the present study was to test the hypothesis that the fibrinolytic system is not impaired in older sedentary hypertensive men when the confounding effects of cardiovascular disease, diabetes, and dyslipidemia are controlled. Plasma concentrations of tissue-type plasminogen activator antigen and activity as well as plasminogen activator inhibitor-1 antigen and activity were measured under resting conditions in 12 hypertensive (69.4 +/- 1.4 years) and 11 normotensive 65.2 +/- 1.3 years) older men. The hypertensive and normotensive subjects had similar anthropometric and metabolic characteristics. There were no significant differences between the hypertensive and normotensive men in tissue-type plasminogen antigen (7.3 +/- 0.5 versus 6.1 +/- 0.6 ng/mL) and activity (1.8 +/- 0.3 versus 1.7 +/- 0.2 IU/mL) or plasminogen activator inhibitor-1 antigen (14.1 +/- 2.3 versus 10.8 +/- 2.2 ng/mL) and activity (17.4 +/- 1.2 versus 17.5 +/- 1.8 arbitrary units [AU]/mL) levels. In addition, the molar concentration ratio of active tissue type plasminogen activator to active plasminogen activator inhibitor-1 did not differ between the hypertensive (1:9.7 +/- 2.3) mmol/L) and normotensive (1:10.5 +/- 2.2 mmol/L) subjects, indicative of no impairment in fibrinolytic potential in either group. These results support the hypothesis that hypertension does not directly result in impaired fibrinolytic function in older adults. Furthermore, our findings suggest that abnormalities in fibrinolytic function in older hypertensive men are likely due to the primary effects of other metabolic disorders that usually accompany hypertension, such as hyperinsulinemia and dyslipidemia.
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PMID:The fibrinolytic system is not impaired in older men with hypertension. 862 Nov 96

Secondary hyperlipoproteinemias are found in connection with other primary organic diseases. Typical examples are those seen with diabetes mellitus, liver and kidney diseases. In addition there are changes induced by hormonal dysfunctions such as hypothyroidism, by the use of oral contraceptives or in postmenopausal women. During pregnancy there is a physiological transient increase in lipoproteins. In addition to primary organic diseases there are a number of exogenous factors such as obesity, malnutrition and alcohol abuse causing hyperlipidemia. The relation between hypertension and hyperlipidemia described as familial dyslipidemic hypertension is less well known. Obesity, hypertension, dyslipidemia, hyperuricemia and impaired glucose tolerance are the basic conditions of the metabolic syndrome. Familial combined hyperlipidemia is a genetically determined, dyslipidemic syndrome with a high prevalence among patients with coronary artery disease and stroke. As there are some links between familial combined hyperlipidemia and secondary hyperlipoproteinemias, this disease entity is discussed together in this paper. Familial combined hyperlipidemia is metabolically, genetically and by this on a molecular level closely linked to familial dyslipidemic hypertension as well as the metabolic syndrome. The exact mechanism of this disease is currently unknown.
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PMID:[Secondary disorders of lipid metabolism, metabolic syndrome and familial combined hyperlipidemia]. 865 Sep 33

Hypertension directly predisposes to all of the major atherosclerotic cardiovascular disease outcomes, including coronary artery disease, stroke, cardiac failure, and peripheral artery disease. Coronary artery disease deserves a high priority in treatment of hypertension because it is the most common and lethal sequela. However, reduction of blood pressure as the sole therapeutic goal of antihypertensive therapy is no longer appropriate. Hypertension tends to cluster with other atherogenic risk factors, including dyslipidemia, glucose intolerance, insulin resistance, obesity, and elevated uric acid. Hypertension is only one of the many risk factors for atherosclerotic cardiovascular disease and is variably hazardous, depending on the number and severity of these coexistent metabolically linked risk factors. The presence of coexistent, already overt cardiovascular disease and left ventricular hypertrophy also greatly influence the hazard and choice of therapy. The urgency for, and choice of, therapy should be based on the multivariate cardiovascular risk profile rather than relying solely on the character and severity of the blood pressure elevation. In this way at-risk hypertensive persons can be more appropriately targeted for treatment designed to improve their multivariate risk profile and to provide maximum benefit and cost effectiveness.
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PMID:Cardioprotection and antihypertensive therapy: the key importance of addressing the associated coronary risk factors (the Framingham experience). 884 93

The aim of this review is to assess the prevalence of complications and responses to various antihypertensive drug therapies in ethnic minority groups in the United States. In some instances, these comments are extended to responses of citizens in their countries of origin. The incidence of hypertension, mortality from hypertensive heart disease, stroke, and hypertensive renal disease are higher in African Americans. Although some Hispanic Americans have a lesser risk for hypertension, they have a greater risk for other risk factors such as diabetes and dyslipidemia. There is a similar association between income and mortality for both African Americans and Hispanic Americans. When compared to European Americans and other ethnic minorities, African Americans respond less favorably to beta blockers and angiotensin-converting enzyme (ACE) inhibitors. Nevertheless, the observed response in African Americans to ACE inhibitors and beta blockers is clinically significant. The available literature indicates that Asian American responses to calcium antagonists seem to be more favorable than responses to ACE inhibitors and equivalent to their responses to diuretic and beta blocker therapy. Although there are few published studies of drug efficacy in Hispanic Americans, there appears to be no hierarchy in response to the various antihypertensive drug classes. Ethnicity is not an accurate criterion for predicting poor response to any class of antihypertensive therapy. Thus, there is little justification to use racial profiling as a criterion for the avoidance of selected drug classes because of presumed lack of efficacy. Observed differences in the incidence of hypertension and its poor outcomes have led some investigators to postulate that the etiology of hypertension in ethnic minority groups is intrinsically different from whites. Awareness of racial differences in hypertension outcomes evolved in the United States within a historical context that does not fully appreciate that race is often a surrogate for many social and economic factors that influence health status and healthcare delivery. Poor outcomes in ethnic minority groups occur in many diseases, not only hypertension. The goal of ethnicity-related research should be to describe the diversity of disease expression in humans and to target at-risk groups for prevention and early intervention. The use of racial descriptors to explain genetic differences in ethnic groups should take a lesser priority.
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PMID:The impact of ethnicity on response to antihypertensive therapy. 887 72


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