Background Population-based studies have found that black patients with congestive heart failure have a higher mortality rate than white patients with the same condition.
This finding has been attributed to differences in the severity, causes, and management of heart failure, the prevalence of coexisting conditions, and socioeconomic factors.
Although these factors probably account for some of the higher mortality due to congestive heart failure among blacks, we hypothesized that racial differences in the natural history of left ventricular dysfunction might also have a role.
Methods Using data from the Studies of Left Ventricular Dysfunction (SOLVD) prevention and treatment trials, in which all patients received standardized therapy and follow-up, we conducted a retrospective analysis of the outcomes of asymptomatic and symptomatic left ventricular systolic dysfunction among black and white participants.
The mean (±SD) follow-up was 34.2±14.0 months in the prevention trial and 32.3±14.8 months in the treatment trial among the black and white participants.
Results The overall mortality rates in the prevention trial were 8.1 per 100 person-years for blacks and 5.1 per 100 person years for whites.
In the treatment trial, the rates were 16.7 per 100 person-years and 13.4 per 100 person-years, respectively. (...)
Mots-clés Pascal : Insuffisance ventriculaire gauche, Randomisation, Prévalence, Mortalité, Noir américain, Etiopathogénie, Ethnie, Analyse statistique, Caucasoïde, Etats Unis, Amérique du Nord, Amérique, Homme, Analyse multivariable, Ventricule cardiaque, Appareil circulatoire pathologie, Cardiopathie
Mots-clés Pascal anglais : Left ventricular failure, Randomization, Prevalence, Mortality, Black American, Etiopathogenesis, Ethnic group, Statistical analysis, Caucasoid, United States, North America, America, Human, Multivariate analysis, Heart ventricle, Cardiovascular disease, Heart disease
Notice produite par :
Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 99-0154246
Code Inist : 002B12A01. Création : 16/11/1999.