Epigenomes in Cardiovascular Disease.

If unifying principles could be revealed for how the same genome encodes different eukaryotic cells and for how genetic variability and environmental input are integrated to impact cardiovascular health, grand challenges in basic cell biology and translational medicine may succumb to experimental dissection. A rich body of work in model systems has implicated chromatin-modifying enzymes, DNA methylation, noncoding RNAs, and other transcriptome-shaping factors in adult health and in the development, progression, and mitigation of cardiovascular disease. Meanwhile, deployment of epigenomic tools, powered by next-generation sequencing technologies in cardiovascular models and human populations, has enabled description of epigenomic landscapes underpinning cellular function in the cardiovascular system. This essay aims to unpack the conceptual framework in which epigenomes are studied and to stimulate discussion on how principles of chromatin function may inform investigations of cardiovascular disease and the development of new therapies

COPD and cardiovascular disease

COPD is one of the major public health problems in people aged 40 years or above. It is currently the 4th leading cause of death in the world and projected to be the 3rd leading cause of death by 2020. COPD and cardiac comorbidities are frequently associated. They share common risk factors, pathophysiological processes, signs and symptoms, and act synergistically as negative prognostic factors. Cardiac disease includes a broad spectrum of entities with distinct pathophysiology, treatment and prognosis. From an epidemiological point of view, patients with COPD are particularly vulnerable to cardiac disease. Indeed, mortality due to cardiac disease in patients with moderate COPD is higher than mortality related to respiratory failure. Guidelines reinforce that the control of comorbidities in COPD has a clear benefit over the potential risk associated with the majority of the drugs utilized. On the other hand, the true survival benefits of aggressive treatment of cardiac disease and COPD in patients with both conditions have still not been clarified. Given their relevance in terms of prevalence and prognosis, we will focus in this paper on the management of COPD patients with ischemic coronary disease, heart failure and dysrhythmia.Novartis Portugal Novartisinfo:eu-repo/semantics/publishedVersio

Walks4work: Rationale and study design to investigate walking at lunchtime in the workplace setting

Background: Following recruitment of a private sector company, an 8week lunchtime walking intervention was implemented to examine the effect of the intervention on modifiable cardiovascular disease risk factors, and further to see if walking environment had any further effect on the cardiovascular disease risk factors. Methods. For phase 1 of the study participants were divided into three groups, two lunchtime walking intervention groups to walk around either an urban or natural environment twice a week during their lunch break over an 8week period. The third group was a waiting-list control who would be invited to join the walking groups after phase 1. In phase 2 all participants were encouraged to walk during their lunch break on self-selecting routes. Health checks were completed at baseline, end of phase 1 and end of phase 2 in order to measure the impact of the intervention on cardiovascular disease risk. The primary outcome variables of heart rate and heart rate variability were measured to assess autonomic function associated with cardiovascular disease. Secondary outcome variables (Body mass index, blood pressure, fitness, autonomic response to a stressor) related to cardiovascular disease were also measured. The efficacy of the intervention in increasing physical activity was objectively monitored throughout the 8-weeks using an accelerometer device. Discussion. The results of this study will help in developing interventions with low researcher input with high participant output that may be implemented in the workplace. If effective, this study will highlight the contribution that natural environments can make in the reduction of modifiable cardiovascular disease risk factors within the workplace. © 2012 Brown et al.; licensee BioMed Central Ltd

Gene Therapy for Cardiovascular Disease

The last decade has seen substantial advances in the development of gene therapy strategies and vector technology for the treatment of a diverse number of diseases, with a view to translating the successes observed in animal models into the clinic. Perhaps the overwhelming drive for the increase in vascular gene transfer studies is the current lack of successful long-term pharmacological treatments for complex cardiovascular diseases. The increase in cardiovascular disease to epidemic proportions has also led many to conclude that drug therapy may have reached a plateau in its efficacy and that gene therapy may represent a realistic solution to a long-term problem. Here, we discuss gene delivery approaches and target diseases

Salt intake, stroke, and cardiovascular disease : meta-analysis of prospective studies

Objective: To assess the relation between the level of habitual salt intake and stroke or total cardiovascular disease outcome. Design: Systematic review and meta-analysis of prospective studies published 1966-2008. Data sources: Medline (1966-2008), Embase (from 1988), AMED (from 1985), CINAHL (from 1982), Psychinfo (from 1985), and the Cochrane Library. Review methods: For each study, relative risks and 95% confidence intervals were extracted and pooled with a random effect model, weighting for the inverse of the variance. Heterogeneity, publication bias, subgroup, and meta-regression analyses were performed. Criteria for inclusion were prospective adult population study, assessment of salt intake as baseline exposure, assessment of either stroke or total cardiovascular disease as outcome, follow-up of at least three years, indication of number of participants exposed and number of events across different salt intake categories. Results: There were 19 independent cohort samples from 13 studies, with 177 025 participants (follow-up 3.5-19 years) and over 11 000 vascular events. Higher salt intake was associated with greater risk of stroke (pooled relative risk 1.23, 95% confidence interval 1.06 to 1.43; P=0.007) and cardiovascular disease (1.14, 0.99 to 1.32; P=0.07), with no significant evidence of publication bias. For cardiovascular disease, sensitivity analysis showed that the exclusion of a single study led to a pooled estimate of 1.17 (1.02 to 1.34; P=0.02). The associations observed were greater the larger the difference in sodium intake and the longer the follow-up. Conclusions: High salt intake is associated with significantly increased risk of stroke and total cardiovascular disease. Because of imprecision in measurement of salt intake, these effect sizes are likely to be underestimated. These results support the role of a substantial population reduction in salt intake for the prevention of cardiovascular disease

Nutrigenomics: Using Sulforaphane Consumption as a Mechanism to Prevent Cardiovascular Disease through Epigenetic Regulation

Cardiovascular disease is the leading cause of death in the United States. Diet composition and reduced expression of the transcription factor Nrf2 are both possible factors contributing to cardiovascular disease. As vitamin supplementation grows in scope and popularity, it is becoming common to replace vegetable consumption with multivitamins. The purpose of this research was to investigate how sulforaphane, an isothiocyanate found in its greatest quantities in broccoli, prevents cardiovascular disease through epigenetic regulation in order to promote the understanding that vitamin supplementation does not adequately replace the health benefits of phytonutrients found in vegetables. In order to investigate sulforaphane’s ability to prevent cardiovascular disease through epigenetic regulation, I studied scholarly journal articles that focused on experiments involving sulforaphane-induced activation of Nrf2 and the effects of Nrf2 activation such as up-regulation of antioxidant genes and phase II enzymes. Additionally, I studied articles examining sulforaphane-induced reductions in blood pressure and elimination of cardiac dysfunctions such as cardiac hypertrophy and decreased fractional shortening with the goal of identifying Nrf2 activation as the underlying mechanism. The results showed that up-regulation of antioxidant genes, signaling of phase II enzymes, lowered blood pressure, and elimination of cardiac dysfunctions were all a result of sulforaphane-induced activation of Nrf2. These results indicate that people who may be at risk for cardiovascular disease could benefit from including broccoli in their diet rather than using vitamin and mineral supplementation to replace vegetables that provide valuable phytonutrients.https://scholarscompass.vcu.edu/uresposters/1284/thumbnail.jp

Cardiovascular diseases, risk factors and barriers in their prevention in Croatia [Kardiovaskularne bolesti, rizični faktori i zapreke za prevenciju u Hrvatskoj]

Cardiovascular diseases are the leading cause of death in Croatia, with significant regional differences. Despite high mortality rates, high prevalence of various cardiovascular risk factors and well organized public health network, comprehensive system for cardiovascular disease monitoring and interventions does not exist. In this study we analyzed legislation framework and responsibilities of stakeholders relevant for cardiovascular disease surveillance and prevention. According to the international experiences we analyzed characteristics of cardiovascular disease prevention in Croatia and causes of the problems appeared in the preventive programs in Croatia. Analysis showed that primary problem is not inefficiency, but the existence of barriers in preventive activities definition, responsibilities distribution and task implementation. Main cause for such situation is incompatibility of the existing practices in clinical medicine and public health with recommendations from other countries. For the successful prevention of cardiovascular disease in Croatia at least three changes need to be made--define new terms and contents of prevention, define new responsibilities distribution and provide equity in health as basic criterion for successful preventive programs

The metabolic syndrome adds utility to the prediction of mortality over its components: The Vietnam Experience Study

Background\ud The metabolic syndrome increases mortality risk. However, as “non-affected” individuals may still have up to two risk factors, the utility of using three or more components to identify the syndrome, and its predictive advantage over individual components have yet to be determined.\ud \ud Methods\ud Participants, male Vietnam-era veterans (n = 4265) from the USA, were followed-up from 1985/1986 for 14.7 years (61,498 person-years), and all-cause and cardiovascular disease deaths collated. Cox's proportional-hazards regression was used to assess the effect of the metabolic syndrome and its components on mortality adjusting for a wide range of potential confounders.\ud \ud Results\ud At baseline, 752 participants (17.9%) were identified as having metabolic syndrome. There were 231 (5.5%) deaths from all-causes, with 60 from cardiovascular disease. After adjustment for a range of covariates, the metabolic syndrome increased the risk of all-cause, HR 2.03, 95%CI 1.52, 2.71, and cardiovascular disease mortality, HR 1.92, 95%CI 1.10, 3.36. Risk increased dose-dependently with increasing numbers of components. The increased risk from possessing only one or two components was not statistically significant. The adjusted risk for four or more components was greater than for only three components for both all-cause, HR 2.30, 95%CI 1.45, 3.66 vs. HR 1.70, 95%CI 1.11, 2.61, and cardiovascular disease mortality, HR 3.34, 95%CI 1.19, 9.37 vs. HR 2.81, 95%CI 1.07, 7.35. The syndrome was more informative than the individual components for all-cause mortality, but could not be assessed for cardiovascular disease mortality due to multicollinearity. Hyperglycaemia was the individual strongest parameter associated with mortality.\ud \u

Motivational Interviewing Impact on Cardiovascular Disease

abstract: Harm reduction in cardiovascular disease is a significant problem worldwide. Providers, families, and healthcare agencies are feeling the burdens imparted by these diseases. Not to mention missed days of work and caregiver strain, the losses are insurmountable. Motivational interviewing (MI) is gaining momentum as a method of stimulating change through intrinsic motivation by resolving ambivalence toward change (Ma, Zhou, Zhou, & Huang, 2014). If practitioners can find methods of educating the public in a culturally-appropriate and sensitive manner, and if they can work with community stakeholders to organize our resources to make them more accessible to the people, we may find that simple lifestyle changes can lead to risk reduction of cardiovascular diseases. By working with our community leaders and identifying barriers unique to each population, we can make positive impacts on a wide range of issues that markedly impact our healthcare systems

Serotonin reuptake inhibitors and cardiovascular disease

Selective serotonin re-uptake inhibiting drugs (SSRIs) are widely used for endogenous depression. In addition to depleting the nerve terminals of serotonin they also lower blood platelet serotonin levels. Platelet aggregation is a major component of acute coronary syndromes, including sudden death, and also of limb ischaemia. Platelet-released serotonin causes constriction of diseased blood vessels. The recent literature has revealed a number of reports of association between the treatment of depression with SSRIs and reduced events caused by intra-arterial thrombosis. The effects of serotonin and serotonin depletion upon intracoronary thrombosis, diseased blood vessels, blood platelets and bleeding are discussed with recommendations for future research into the potential cardiovascular benefits of SSRIs and serotonin 5HT2A antagonists