These findings suggested that virologic failure may be due to suboptimal antiviral potency, and selection of a predominantly indinavir-resistant virus population may be delayed for months even in the presence of ongoing indinavir therapy. The most obvious interpretation is that patients simply stopped taking their drugs. However, after qualitative examination for the presence or absence of drug, it was concluded that this was probably not the case. Patients developed viral rebound despite drug exposure, and the virus was still sensitive to indinavir. Instead of changing a regimen entirely, it may be possible to modify and intensify it to regain viral suppression.
Full publications are in preparation.
In the study, data were reanalyzed from the Framingham Study by using logistic splines to map the relationship between risk of cardiovascular and all-cause death and systolic blood pressure. Specifically, the study tested for the independence of the slope parameters from age and sex and the validity of the linear logistic regression model. It was reported that risk was independent of systolic blood pressure for all pressure lower than a threshold at the 70th percentile for a person of a given age and sex, but that risk sharply increased with pressure higher than the 80th percentile. Because systolic blood pressure increases with age, and more so in women than men, a pressure of 140 mm Hg cannot be considered an absolute cut-off. Consequently, a substantial proportion of the population who would currently be thought to be at increased risk are, therefore, at no increased risk.