Behavioral Problems in Community-Dwelling People with Dementia

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73826/1/j.1547-5069.2000.00055.x.pd

The Association between Antidepressant Medications and Coronary Heart Disease in Brazil: A Cross-Sectional Analysis on the Brazilian Longitudinal Study of Adult Health (ELSA-Brazil)

Background: Recent studies have highlighted associations between use of antidepressant medications and coronary heart disease (CHD). Tricyclic antidepressants are not recommended in patients with CHD as they may increase morbidity and mortality. However, this class of antidepressants are freely prescribed in public health pharmacies, while access to other classes of antidepressants is restricted in Brazil. Here we examine the associations between antidepressant use and prevalent CHD in a large cohort from Brazil. Methods: Participants included 14,994 civil servants aged 35 to 74 from the baseline assessment of the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). CHD (n=710) included stable angina, myocardial infarction and coronary revascularization. Univariate (unadjusted) and multivariate (adjusted) logistic regression analyses were conducted to estimate odds ratios and confidence intervals. Results: After full adjustment for covariates, tricyclic antidepressants (TCA) use (n=156) was associated with a 2-fold increase in prevalent CHD, relative to non-use (n=14,076). Additional sensitivity analysis revealed a three-fold association for myocardial infarction (OR: 2.962, 95% CI: 1.413-6.210) and coronary revascularization (OR: 2.915, 95% CI: 1.275-6.662). There were no significant associations between antidepressant use and stable angina pectoris. Conclusions: Findings highlight a strong association between TCA use and prevalent CHD. While the cross-sectional design is an important limitation of the present study, findings have important implications for the treatment of cardiac patients in Brazil

Are Large Physiological Reactions to Acute Psychological Stress Always Bad for Health?

How we react physiologically to stress has long been considered to have implications for our health. There is now persuasive evidence that individuals who show large cardiovascular reactions to stress are at increased risk of developing cardiovascular disease, particularly hypertension. By implication, low reactivity is protective or benign. However, there is recent evidence that low reactivity may predict elevated risk for a range of adverse health outcomes, such as depression, obesity, poor self-reported health, and compromised immunity. In addition, low cortisol and cardiovascular reactivity may be a characteristic of individuals with addictions to tobacco and alcohol, as well as those at risk of addiction and those who relapse from abstinence. Our ideas about reactivity may have to be revised in the light of such findings

Symptoms of anxiety and depression are related to cardiovascular responses to active, but not passive, coping tasks

Objective: Anxiety and depression have been linked to blunted blood pressure (BP) and heart rate (HR) reactions to mental stress tests; however, most studies have not included indices of underlying hemodynamics nor multiple stress tasks. This study sought to examine the relationships of anxiety and depression with hemodynamic responses to acute active and passive coping tasks. Methods: A total of 104 participants completed the Hospital Anxiety and Depression Scales and mental arithmetic, speech, and cold pressor tasks while BP, HR, total peripheral resistance, and cardiac output (CO) were assessed. Results: After adjustment for traditional risk factors and baseline cardiovascular activity, depression scores were negatively associated with systolic BP, HR, and CO responses to the mental arithmetic task, while anxiety scores were inversely related to the systolic BP response to mental arithmetic. Conclusion: High anxiety or depression scores appear to be associated with blunted cardiac reactions to mental arithmetic (an active coping task), but not to the cold pressor test or speech tasks. Future research should further examine potential mechanisms and longitudinal pathways relating depression and anxiety to cardiovascular reactivity

Effects of antidepressant treatment on heart rate variability in major depression: A quantitative review

<p>Abstract</p> <p>Background</p> <p>The literature measuring effects of antidepressant and electroconvulsive therapy (ECT) for major depression on heart rate variability (HRV) in medically well individuals was reviewed.</p> <p>Methods</p> <p>Fourteen studies evaluating HRV were included. Twenty three pre-post or within group comparisons were available. Treatment impact on measures of HRV was pooled over studies. We examined different classes of antidepressants, and for short and long electrocardiogram (ECG) recordings separately.</p> <p>Results</p> <p>Tricyclic antidepressants (TCAs) were associated with declines in most measures of HRV and significant increase in heart rate (HR) in studies with short recording intervals. No significant changes were found for longer recording times.</p> <p>Treatment effects with selective serotonin reuptake inhibitors (SSRIs) were more variable. Short-recording studies revealed a significant decrease in HR and an increase in one HRV measure. In two 24-hour recording studies no significant changes were observed. No relationship between ECT and HRV has been established in the literature. The effects of other drugs are reported.</p> <p>Limitations</p> <p>Few studies measure the effects of treatment of depression on HRV. Existing studies have generally used very small samples, employing a variety of measurements and methodologies.</p> <p>Conclusion</p> <p>We confirm that TCAs are associated with a large decrease in HRV and increase HR. However, data for SSRIs is not clear. Although the effect of SSRIs on HRV is weaker than for TCAs, evidence shows that SSRIs are associated with a small decrease in HR, and an increase in one measure of HRV. The use of TCAs in depression leads to changes in HRV that are associated with increased risk of mortality.</p

Thrombocytogenesis by megakaryocyte; Interpretation by protoplatelet hypothesis

Serial transmission electron microscopy of human megakaryocytes (MKs) revealed their polyploidization and gradual maturation through consecutive transition in characteristics of various organelles and others. At the beginning of differentiation, MK with ploidy 32N, e.g., has 16 centrosomes in the cell center surrounded by 32N nucleus. Each bundle of microtubules (MTs) emanated from the respective centrosome supports and organizes 16 equally volumed cytoplasmic compartments which together compose one single 32N MK. During the differentiation, single centriole separated from the centriole pair, i.e., centrosome, migrates to the most periphery of the cell through MT bundle, corresponding to a half of the interphase array originated from one centrosome, supporting one “putative cytoplasmic compartment” (PCC). Platelet demarcation membrane (DM) is constructed on the boundary surface between neighbouring PCCs. Matured PCC, composing of a tandem array of platelet territories covered by a sheet of DM is designated as protoplatelet. Eventually, the rupture of MK results in release of platelets from protoplatelets

How to Develop and Sustain a Peer-Mentored Research Work Group

Most collaborative research models in nursing focus on hierarchical structures in which an identified expert or leader directs and/or guides others in conducting research. The authors propose a peer-mentored model of collaborative research that promotes collegial participation, maximizes the use of each member\u27s expertise, and enhances skill development within the group. This article is a description of the evolution of the Dementia Research Work Group within the Decker School of Nursing at Binghamton University. Emphasis is placed on how to create and nurture a peer-mentored research work group as well as what has been learned from the process