Impact of Non-HIV Related Comorbidities on Retention in HIV Medical Care: Does Retention Improve Over Time?

The purpose of this study was to understand how the presence of comorbid conditions affects retention in HIV medical care over time. A retrospective cohort design employing a medical chart review was conducted. A generalized linear mixed model was used to determine the predictors that affect retention over time. The mean follow-up for the study population was 5.75 years, and only 48.6 % achieved optimal retention. During the study period, 882 non-HIV related comorbidities were diagnosed in 610 (44.9 %) patients of whom, approximately 31 % had ≥2 comorbidities diagnosed. In the mixed model, the number of comorbidities diagnosed during the study period was associated with improved retention over time (odds ratio = 2.28; 95 % confidence interval = 1.83–2.71). Having a non-HIV related comorbid condition was associated with improved retention, while those patients who were ‘healthier’ had worse retention. More research is needed to identify factors that improve retention and to quantify the impact of these factors.     

The number of cardiac myocytes in the hypertrophic and hypotrophic left ventricle of the obese and calorie-restricted mouse heart

Changes in body mass due to varying amounts of calorie intake occur frequently with obesity and anorexia/cachexia being at opposite sides of the scale. Here, we tested whether a high-fat diet or calorie restriction (CR) decreases the number of cardiac myocytes and affects their volume. Ten 6–8-week-old mice were randomly assigned to a normal (control group, n = 5) or high-fat diet (obesity group, n = 5) for 28 weeks. Ten 8-week-old mice were randomly assigned to a normal (control group, n = 5) or CR diet (CR group, n = 5) for 7 days. The left ventricles of the hearts were prepared for light and electron microscopy, and analysed by design-based stereology. In CR, neither the number of cardiac myocytes, the relationship between one- and multinucleate myocytes nor their mean volume were significantly different between the groups. In contrast, in the obese mice we observed a significant increase in cell size combined with a lower number of cardiomyocytes (P < 0.05 in the one-sided U-test) and an increase in the mean number of nuclei per myocyte. The mean volume of myofibrils and mitochondria per cardiac myocyte reflected the hypertrophic and hypotrophic remodelling in obesity and CR, respectively, but were only significant in the obese mice, indicating a more profound effect of the obesity protocol than in the CR experiments. Taken together, our data indicate that long-lasting obesity is associated with a loss of cardiomyocytes of the left ventricle, but that short-term CR does not alter the number of cardiomyocytes.