The survival of patients in group B, who presented late, was found to be significantly better than the survival of patients in group A, who presented early. This finding is consistent with the. view that the onset of AIDS is delayed in patients who receive early medical intervention in HIV infection.""'2 However, the finding suggests that the subsequent survival of these patients when they develop AIDS may be commensurately decreased. We believe that our data are compatible with the results of the Concorde and other studies, in which early intervention with zidovudine delayed the development of AIDS but did not affect survival overall.'0 1213In conclusion, this study highlights the scale of the public health problem posed by patients presenting with AIDS coincidental with their first positive result in an HIV test. It also contributes to the debate on the effects of medical intervention on survival after an AIDS defining illness has developed.
Objectives To determine whether specialist nurse intervention improves outcome in patients with chronic heart failure. Design Randomised controlled trial. Setting Acute medical admissions unit in a teaching hospital. Participants 165 patients admitted with heart failure due to left ventricular systolic dysfunction. The intervention started before discharge and continued thereafter with home visits for up to 1 year. Main outcome measures Time to first event analysis of death from all causes or readmission to hospital with worsening heart failure. Results 31 patients (37%) in the intervention group died or were readmitted with heart failure compared with 45 (53%) in the usual care group (hazard ratio = 0.61, 95% confidence interval 0.33 to 0.96).Compared with usual care, patients in the intervention group had fewer readmissions for any reason (86 v 114, P = 0.018), fewer admissions for heart failure (19 v 45, P < 0.001) and spent fewer days in hospital for heart failure (mean 3.43 v 7.46 days, P = 0.0051). Conclusions Specially trained nurses can improve the outcome of patients admitted to hospital with heart failure.
We identify the SLC22A3-LPAL2-LPA gene cluster as a strong susceptibility locus for coronary artery disease (CAD) through a genome-wide haplotype association (GWHA) study. This locus was not identified from previous genome-wide association (GWA) studies focused on univariate analyses of SNPs. The proposed approach may have wide utility for analyzing GWA data for other complex traits.
34) for women. The only age/sex group in which BMI was under-estimated from self reports (mean 0.2) was the 55-64 year old women. Prediction equations that explained 90% (men) and 88% (women) of the diVerence between self reported and measured height included age and self reported weight. The equivalent prediction equations for weight explained 93% of the diVerence between self reported and measured weight for men and included smoking and diabetic status, while for women 96% of the variance was explained with no further variables being significant. Sensitivity and specificity for determining clinical obesity (BMI>30) were 83% and 96% respectively for men, and 89% and 97% for women. Conclusions-This Scottish population was unique in the under-reporting of height as well as weight, which resulted in BMI estimates with low error. These data suggest that self reported weights and heights would be satisfactory for the monitoring of obesity prevalence in Scotland.
Objective-To estimate the fall in coronary heart disease (CHD) mortality in Scotland attributable to medical and surgical treatments, and risk factor changes, between 1975 and 1994. Design-A cohort model combining eVectiveness data from meta-analyses with information on treatment uptake in all patient categories in Scotland. Setting and patients-The whole Scottish population of 5.1 million, including all patients with recognised CHD. Interventions-All cardiological, medical, and surgical treatments, and all risk factor changes between 1975 and 1994. Data were obtained from epidemiological surveys, routine National Health Service sources, and local audits. Main outcome measures-Deaths from CHD in 1975 and 1994.Results-There were 15 234 deaths from CHD in 1994, 6205 fewer deaths than expected if there had been no decline from 1975 mortality rates. In 1994, the total number of deaths prevented or postponed by all treatments and risk factor reductions was estimated at 6747 (minimum 4790, maximum 10 695). Forty per cent of this benefit was attributed to treatments (initial treatments for acute myocardial infarction 10%, treatments for hypertension 9%, for secondary prevention 8%, for heart failure 8%, aspirin for angina 2%, coronary artery bypass grafting surgery 2%, and angioplasty 0.1%). Fifty one per cent of the reduction in deaths was attributed to measurable risk factor reductions (smoking 36%, cholesterol 6%, secular fall in blood pressure 6%, and changes in deprivation 3%). Other, unquantified factors apparently accounted for the remaining 9%. These proportions remained relatively consistent across a wide range of assumptions and estimates in a sensitivity analysis. Conclusions-Medical treatments and risk factor changes apparently prevented or postponed about 6750 coronary deaths in Scotland in 1994. Modest gains from individual treatments produced a large cumulative survival benefit. Reductions in major risk factors explained about half the fall in coronary mortality, emphasising the importance and future potential of prevention strategies. (Heart 1999;81:380-386)
Summary. Coagulation factor activity (fibrinogen, VII, VIII and IX), coagulation inhibitor activity (antithrombin, protein C, protein S), and coagulation activation markers (prothrombin fragment F1, 2; thrombin-antithrombin complexes) were measured in 747 men and 817 women aged 25-74 years, randomly sampled from the north Glasgow population in the Third MONICA Survey. Significant effects of age, sex, menopause and hormone use were observed and specific reference ranges are presented to illustrate these effects. Significant correlations were observed between several coagulation factors and inhibitors. Increased levels of factors VII, VIII and IX and decreased levels of protein C were associated with increased coagulation activation. In general, increases in coagulation factors with age were greater than increases in coagulation inhibitors, especially in men; this imbalance may favour increased coagulation activation and hence increased thrombotic risk with age.
Abstract-The effects of excess cortisol secretion on blood pressure and fat deposition are well documented, but the importance of this glucocorticoid in controlling these processes in normal individuals is less clear. We studied the relationship between cortisol excretion rate (tetrahydrocortisol [THF]ϩallo-THFϩtetrahydrocortisone [THE]) and a range of important cardiovascular risk factors in 439 normal subjects (238 male) sampled from the North of Glasgow (Scotland) population. There were marked gender differences: female subjects were lighter and had lower blood pressures and cortisol levels, whereas HDL cholesterol was higher. The pattern of cortisol metabolism was also different; the index of 11-hydroxysteroid dehydrogenase activity (THFϩallo-THF/THE) was lower and that of 5␣-reductase (allo-THF/THF) was higher. There was a strong correlation of blood pressure (positive), cholesterol (positive), and HDL cholesterol (negative in women, positive in men) with age. Cortisol excretion rate did not correlate with blood pressure but correlated strongly with parameters of body habitus (body mass index and waist and hip measurements [positive]) and HDL cholesterol (negative).With multiple regression analysis, there remained a significant association of cortisol excretion rate with HDL cholesterol in men and women and with body mass index in men. These results suggest that glucocorticoids regulate key components of cardiovascular risk. (Hypertension. 1999;33:1364-1368.)Key Words: glucocorticoids Ⅲ blood pressure Ⅲ body mass index Ⅲ cholesterol C linical 1 and experimental 2 cortisol excesses are associated with increases in blood pressure and profound alteration of intermediary metabolism, resulting in characteristic obesity, insulin resistance, and changes in lipid metabolism. In groups of subjects with essential hypertension, plasma 3 or urinary 4 cortisol levels may be mildly but significantly higher than those of matched normal subjects, and the efficiency of cortisol metabolism by 11-hydroxysteroid dehydrogenase (11-HSD) or 5␣-reductase may be abnormal. 5,6 Moreover, similar alterations in cortisol metabolism may contribute to obesity and to increased abdominal fat deposition in polycystic ovary disease. 7 However, in the general population, the contribution of cortisol to blood pressure and to relative obesity is less well established despite the fact that these are important predisposing factors to cardiovascular disease. A recent study of a small group of subjects concluded that differences in the level of cortisol and its metabolic disposal may be a contributory cause of obesity. 8 In the present study, we examined the association between cortisol and cardiovascular risk factors in a large sample of the middleaged population of an area with a high prevalence of cardiovascular disease. Methods PopulationA random sample of the North Glasgow, Scotland, population was selected as a stratified random sample of the patient lists of 30 general practitioners, randomly selected from all those practicing in North Gl...
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