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N Qizilbash

Publications and source records attributed to N Qizilbash.

11 recordsLinked to original sources
PubMed1998

Are risk factors for stroke and coronary disease the same?

Many risk factors operate in both coronary heart disease and stroke, especially ischaemic stroke--age, sex, social class, blood pressure, pre-existing vascular disease (angina, myocardial infarction, cardiac failure, diabetes and peripheral vascular disease, transient ischaemic attack and stroke), atrial fibrillation and fibrinogen, smoking, alcohol and height. Total cholesterol has also recently been recruited to this list. The various mechanisms involved in stroke and its subtypes and the epidemiological problems in evaluating aetiological factors in stroke make the comparison with coronary heart disease more difficult. The recent discrepancy between much of the epidemiology and the clinical trials evaluating the role of lipids in stroke has spurred the systematic review (meta-analysis) of major prospective observational studies. These will provide a clearer assessment about the quantitative comparison of some of the more important risk factors for stroke and coronary heart disease in the near future.

Humans↗
PubMed1997

Repeat measurement of case-control data: corrections for measurement error in a study of ischaemic stroke and haemostatic factors.

BACKGROUND: Haemostatic factors are suspected to be involved in the aetiology of cerebrovascular events. METHODS: In a case-control study of 105 cases of transient ischaemic attack and minor ischaemic stroke, and 241 controls, data were available on levels of the haemostatic factors-von Willebrand factor (vWF), plasminogen activator inhibitor-1 (PAI), tissue plasminogen activator (TPA) and factor VII (FVII). These are subject to measurement error and within-person fluctuation of true levels, which may bias relative risk estimates. For all subjects, two determinations were performed on the same blood sample, which allowed estimation of pure measurement error. For estimation of within-person fluctuation, levels were measured from a repeat blood sample on 81 of the controls one year later. RESULTS: The pure measurement error accounted for a very small proportion of the total variation in all cases. Uncorrected for within-person fluctuation, the odds ratio estimates associated with exceeding the median of vWF, PAI, TPA and FVII respectively were 1.88, 0.87, 1.30 and 0.93. After correction for within-person fluctuation odds ratios were 3.56, 0.80, 1.41 and 0.91. Because the PAI determination was not robust to storage conditions, it was estimated that 75% of the variation in this factor was within-person rather than between-persons. Thus, estimates of relative risk relation to PAI cannot be regarded as reliable in this study. CONCLUSIONS: It is likely that elevated levels of vWF are associated with increased risk of ischaemic stroke, but interpretation must be tentative, due to relatively large within-person fluctuation of vWF levels.

Analysis of Variance↗
PubMed1997

Von Willebrand factor and risk of ischemic stroke.

We carried out a case-control study to determine whether von Willebrand factor (vWF) antigen (and factor VII and tissue plasminogen activator [tPA] antigens) are associated with ischemic stroke. Ninety-five patients with transient ischemic attack or minor ischemic stroke recruited from the Oxfordshire Community Stroke Project and one neurology clinic were compared with 236 controls, group-matched for age and sex, from the same general practitioners as the incident cases. In crude analyses, concentrations of vWF antigen were significantly higher in cases than in controls (p = 0.004). The age- and sex-adjusted odds ratios from lowest (referent) to highest quartile of vWF antigen were 1.00, 1.15, 2.34, and 2.36 (trend test, p = 0.006). Factor VII antigen and tPA antigen were not significantly different between cases and controls. Although adjustment for other potential risk factors abolished the statistical significance of the association between vWF and disease, this was largely due to the influence of history of ischemic heart disease. We conclude that vWF is a potent and independent risk factor for transient ischemic attack, minor ischemic stroke, and, by extrapolation, ischemic stroke in general. The data also suggest that vWF may be a risk factor for both ischemic stroke and ischemic heart disease. We found no evidence to implicate factor VII and tPA as risk factors for ischemic stroke.

Adult↗
PubMed1995

Fibrinogen and cerebrovascular disease.

The importance of fibrinogen has been identified in two prospective observational studies. Reactive elevations in fibrinogen levels that occur within hours of a major stroke invalidate most cross-sectional case-control studies evaluating fibrinogen as a risk factor. However, as no elevation is seen following fresh episodes of transient ischaemic attacks, reliable conclusions drawn from a case-control study using such patients support the findings of the prospective studies. The association is related to occlusive stroke, but the relationship with intracerebral haemorrhage is unclear. The relationship has been found to be independent of other haemostatic and haemorheological factors (e.g. von Willebrand factor, tissue plasminogen activator and packed cell volume). Adjustment for regression dilution bias would further strengthen the observed relationship. Therefore, after blood pressure, fibrinogen is the most important potentially treatable risk factor for ischaemic stroke. There are several mechanisms whereby fibrinogen could promote athero-thromboembolism: thrombosis through a hypercoagulable state; the acceleration of atherosclerosis; or the reduction of blood flow due to high blood or plasma viscosity. The mechanism, however, is unlikely to be mediated through high blood viscosity per se as secondary erythrocytosis (another major determinant of blood viscosity) has not consistently been found to be a risk factor for stroke. Studies relating fibrinogen levels to the degree of carotid artery stenosis support the accelerating influence of fibrinogen on atherosclerosis. Fibrinogen should be considered a risk factor for ischaemic stroke and included in the assessment of individual risk factors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Fibrinogen and lipid concentrations as risk factors for transient ischaemic attacks and minor ischaemic strokes.

OBJECTIVES: To determine whether fibrinogen and lipid concentrations are risk factors for ischaemic stroke. DESIGN: Case-control study with a population based comparison within the overall study. SETTING: Oxfordshire community stroke project and a neurology clinic. SUBJECTS: 105 patients who had a transient ischaemic attack or minor ischaemic stroke and 352 randomly chosen controls matched for age and sex from the same general practitioners as the incident cases. 52 controls were ineligible or refused interview. 104 cases and 241 controls gave blood samples for analysis. MAIN OUTCOME MEASURES: Response to structured questionnaire, height, weight, blood pressure, and serum concentrations of fibrinogen and lipids. RESULTS: Adjusted for other variables, odds ratios of ischaemic stroke were 1.78 (95% confidence interval 0.91 to 3.48; p = 0.09) [corrected] for fibrinogen concentrations greater than 3.6 g/l; 1.73 (0.90 to 3.29; p = 0.09) [corrected] for total cholesterol concentrations greater than 6.0 mmol/l; 1.34 (0.69 to 2.61; p greater than 0.4) for low density lipoprotein cholesterol concentrations greater than 3.5 mmol/l; and 0.32 (0.15 to 0.69; p = 0.002) for high density lipoprotein cholesterol concentration greater than 1.2 mmol/l. Similar results emerged comparing only community derived cases with transient ischaemic attacks and controls. The effects of fibrinogen, total cholesterol, and high density lipoprotein cholesterol were significant in a test of trend after adjusting for all other variables in the study (chi 2 = 4.14, p less than 0.05; chi 2 = 4.31, p less than 0.05, and chi 2 = 12.15, p greater than 0.001, respectively). History of ischaemic heart disease and hypertension were the only other variables that showed significance, though both lost significance after adjustment (2.06, p = 0.08 and 1.53, p = 0.2, respectively). CONCLUSIONS: Fibrinogen and lipids are important risk factors for ischaemic stroke. The pattern of changes mirrors that found in ischaemic heart disease.

Adult↗
PubMed1991

Repeat measurement of case-control data: correcting risk estimates for misclassification due to regression dilution of lipids in transient ischemic attacks and minor ischemic strokes.

In a case-control study to determine the role of lipids as risk factors for ischemic cerebrovascular disease, 105 cases of transient ischemic attacks and minor ischemic strokes were compared with 241 controls. Recruitment to the study took place in Oxford, United Kingdom, in 1986 and 1987. In a random subset of 100 of the original controls, repeat assays of total cholesterol, low density lipoprotein cholesterol, (LDL cholesterol), and high density lipoprotein cholesterol (HDL cholesterol) were performed. With maximum likelihood theory, the repeat data were used to produce odds ratio estimates of relative risk corrected for mismeasurement. Uncorrected odds ratios associated with total cholesterol of more than 6 mmol/liter, LDL cholesterol of more than 3.5 mmol/liter, and HDL cholesterol of more than 1.2 mmol/liter were, respectively, 2.06 (95% confidence interval (CI) 1.26-3.37), 2.02 (95% CI 1.24-3.30), and 0.46 (95% CI 0.28-0.74). Corrected for mismeasurement, the corresponding odds ratios were 2.90 (95% CI 1.42-5.93), 2.57 (95% CI 1.24-5.32), and 0.36 (95% CI 0.17-0.71), respectively. The attributable risks changed from 34 to 48% for total cholesterol, from 34 to 43% for LDL cholesterol, and from 35 to 45% for HDL cholesterol. The maximum likelihood procedure described here corrects for substantial underestimation of the strength of an association and indicates the need to obtain repeat measurements on variables which are subject to random fluctuation.

Case-Control Studies↗
PubMed1990

Blood pressure, stroke, and coronary heart disease. Part 2, Short-term reductions in blood pressure: overview of randomised drug trials in their epidemiological context.

There are 14 unconfounded randomised trials of antihypertensive drugs (chiefly diuretics or beta-blockers): total 37,000 individuals, mean treatment duration 5 years, mean diastolic blood pressure (DBP) difference 5-6 mm Hg. In prospective observational studies, a long-term difference of 5-6 mm Hg in usual DBP is associated with about 35-40% less stroke and 20-25% less coronary heart disease (CHD). For those dying in the trials, the DBP difference had persisted only 2-3 years, yet an overview showed that vascular mortality was significantly reduced (2p less than 0.0002); non-vascular mortality appeared unchanged. Stroke was reduced by 42% SD 6 (95% confidence interval 35-50%; 289 vs 484 events, 2p less than 0.0001), suggesting that virtually all the epidemiologically expected stroke reduction appears rapidly. CHD was reduced by 14% SD 5 (95% CI 4-22%; 671 vs 771 events, 2p less than 0.01), suggesting that just over half the epidemiologically expected CHD reduction appears rapidly. Although this significant CHD reduction could well be worthwhile, its size remains indefinite for most circumstances (though beta-blockers after myocardial infarction are of substantial benefit). At present, therefore, a sufficiently high risk of stroke (perhaps because of age, blood pressure, or, in particular, history of cerebrovascular disease) may be the clearest indication for antihypertensive treatment.

Antihypertensive Agents↗
PubMed1987

Incidence of motor neurone disease in the northern region.

The incidence of motor neurone disease in the Northern Region was studied for the year 1981 by means of hospital activity analysis records and questionnaire. The crude incidence rate was 2.2 per 100,000. This was not significantly different from the rate determined by using death certification. The age standardised incidence ratio for the region was 163 using the 1976 population and deaths from motor neurone disease in England and Wales as the reference. The female to male ratio was 1:1.8 and the average age of diagnosis was 63 years. No meaningful intraregional variation was observed. Thus mortality appears to reflect incidence fairly accurately.

Adult↗