A novel approach to cardiovascular health by optimizing risk management (ANCHOR): a primary prevention initiative examining the impact of health risk factor assessment and management on cardiac wellness

Cardiovascular disease (CVD) represents an increasing burden to health care systems. Modifiable risk factors figure prominently in the population-attributable risk for premature coronary artery disease. Primary care is well placed to facilitate CVD risk improvement. We plan to evaluate the ability of a novel primary care intervention providing systematic risk factor screening, risk-weighted behavioural counselling and pharmacological intervention to achieve 2 objectives: (1) optimized management of global CVD risk of patients and (2) increased patient adherence to lifestyle and pharmaceutical interventions aimed at decreasing global CVD risk. A pre-post longitudinal prospective design with a nonrandomized comparison group is being undertaken in 2 geographically diverse primary care practices in Nova Scotia with differing reimbursement models. Participants will complete a readiness to change and pre-post health risk assessment (HRA), that will trigger a 1-year intervention individualized around risk and readiness. The primary outcome will be the proportion of participants with Framingham moderate and high-risk strata that reduce their absolute risk by 10% and 25%, respectively. The secondary outcome will be the proportion of moderate and high-risk participants who reduce their risk category. The impact of the intervention on clinical and behavioural variables will also be examined. Low risk participants will be separately analyzed. Data from participants unable to change from the high risk category because of diabetes mellitus or established atherosclerotic disease will also be analyzed separately, with changes in clinical measures from baseline being assessed. A health economic analysis is planned.     

Dynamics of heat shock protein 60 in endothelial cells exposed to cigarette smoke extract

Heat shock protein 60 (HSP60), expressed on the surface of endothelial cells (ECs) stressed by e.g. oxidized LDL or mechanical shear, was shown to function as an auto-antigen and thus as a pro-atherosclerotic molecule. The aim of this study was to determine whether cigarette smoke chemicals can lead to the activation of the “HSP60 pathway.” It was also our aim to elucidate the dynamics of HSP60 from gene expression to endothelial surface expression and secretion. Here we show for the first time that the exposure of human umbilical vein endothelial cells (HUVECs) to cigarette smoke extract (CSE) results in an up-regulation of HSP60 mRNA. Live cell imaging analysis of a HSP60-EYFP fusion protein construct transfected into ECs revealed that mitochondrial structures collapse in response to CSE exposure. As a result, HSP60 is released from the mitochondria, transported to the cell surface, and released into the cell culture supernatant. Analysis of HSP60 in the sera of healthy young individuals exposed to secondhand smoke revealed significantly elevated levels of HSP60. Cigarette smoking is one of the most relevant risk factors for atherosclerosis. Herein, we provide evidence that cigarette smoke may initiate atherosclerosis in the sense of the “auto-immune hypothesis of atherosclerosis.”     

Placing prediction into the fear circuit

Pavlovian fear conditioning depends on synaptic plasticity at amygdala neurons. Here, we review recent electrophysiological, molecular and behavioral evidence suggesting the existence of a distributed neural circuitry regulating amygdala synaptic plasticity during fear learning. This circuitry, which involves projections from the midbrain periaqueductal gray region, can be linked to prediction error and expectation modulation of fear learning, as described by associative and computational learning models. It controls whether, and how much, fear learning occurs by signaling aversive events when they are unexpected. Functional neuroimaging and clinical studies indicate that this prediction circuit is recruited in humans during fear learning and contributes to exposure-based treatments for clinical anxiety. This aversive prediction error circuit might represent a conserved mechanism for regulating fear learning in mammals.     

Obsessive–compulsive disorder: a review of the diagnostic criteria and possible subtypes and dimensional specifiers for DSM‐V

Background: Since the publication of the DSM‐IV in 1994, research on obsessive–compulsive disorder (OCD) has continued to expand. It is timely to reconsider the nosology of this disorder, assessing whether changes to diagnostic criteria as well as subtypes and specifiers may improve diagnostic validity and clinical utility. Methods: The existing criteria were evaluated. Key issues were identified. Electronic databases of PubMed, ScienceDirect, and PsycINFO were searched for relevant studies. Results: This review presents a number of options and preliminary recommendations to be considered for DSM‐V. These include: (1) clarifying and simplifying the definition of obsessions and compulsions (criterion A); (2) possibly deleting the requirement that people recognize that their obsessions or compulsions are excessive or unreasonable (criterion B); (3) rethinking the clinical significance criterion (criterion C) and, in the interim, possibly adjusting what is considered “time‐consuming” for OCD; (4) listing additional disorders to help with the differential diagnosis (criterion D); (5) rethinking the medical exclusion criterion (criterion E) and clarifying what is meant by a “general medical condition”; (6) revising the specifiers (i.e., clarifying that OCD can involve a range of insight, in addition to “poor insight,” and adding “tic‐related OCD”); and (7) highlighting in the DSM‐V text important clinical features of OCD that are not currently mentioned in the criteria (e.g., the major symptom dimensions). Conclusions: A number of changes to the existing diagnostic criteria for OCD are proposed. These proposed criteria may change as the DSM‐V process progresses. Depression and Anxiety, 2010. © 2010 Wiley‐Liss, Inc.