Obesity management for cardiovascular disease prevention

Background: Obesity is a complex disease that leads to higher morbidity and mortality and its rate in the United States is rapidly rising. Targeting obesity management is one of the cornerstones of preventive medicine. Early intervention can significantly reduce the risk of developing cardiovascular disease. While it is well known that lifestyle interventions such as healthful nutrition and routine physical activity are the first and most important step in management, some do not achieve the desired results and require further therapies. Methods: A literature review was conducted, that included clinical documents, public scientific citations and peer review articles to evaluate anti-obesity medications, endoscopic procedures and bariatric surgeries in the management of obesity. We also included effects of these interventions on weight loss, cardiovascular disease risk reduction and side effects. Results: This clinical review summarizes recent evidence for the different approaches in obesity management including medications, common endoscopic procedures and bariatric surgeries. For more detailed review on the different management options discussed, we recommend reviewing Obesity Medicine Association Clinical Practice Statement [1]. Conclusion: Management of obesity reduces cardiovascular risk, improves metabolic parameters and other important health outcomes. Different management approaches are available, hence, a high level of awareness of the growing epidemic of obesity is needed to ensure timely referrals to obesity medicine specialists.</p

Salt and cardiovascular disease

Blood pressure is the most powerful predictor of stroke and other cardiovascular events. The importance of salt (sodium chloride) intake in determining blood pressure and the incidence of hypertension is well established. Furthermore, randomised controlled clinical trials of moderate reductions in salt intake show a dose dependent cause-effect relation and lack of a threshold effect within usual levels of salt intake in populations worldwide. The effect is independent of age, sex, ethnic origin, baseline blood pressure, and body mass. Prospective studies,2 3 4 5 with one exception,6 also indicate that higher salt intake predicts the incidence of cardiovascular events. While widespread support exists for reducing salt intake to prevent cardiovascular disease, the lack of large and long randomised trials on the effects of salt reduction on clinical outcomes has encouraged some people to argue against a policy of salt reduction in populations

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

Application of non-HDL cholesterol for population-based cardiovascular risk stratification: results from the Multinational Cardiovascular Risk Consortium.

BACKGROUND: The relevance of blood lipid concentrations to long-term incidence of cardiovascular disease and the relevance of lipid-lowering therapy for cardiovascular disease outcomes is unclear. We investigated the cardiovascular disease risk associated with the full spectrum of bloodstream non-HDL cholesterol concentrations. We also created an easy-to-use tool to estimate the long-term probabilities for a cardiovascular disease event associated with non-HDL cholesterol and modelled its risk reduction by lipid-lowering treatment. METHODS: In this risk-evaluation and risk-modelling study, we used Multinational Cardiovascular Risk Consortium data from 19 countries across Europe, Australia, and North America. Individuals without prevalent cardiovascular disease at baseline and with robust available data on cardiovascular disease outcomes were included. The primary composite endpoint of atherosclerotic cardiovascular disease was defined as the occurrence of the coronary heart disease event or ischaemic stroke. Sex-specific multivariable analyses were computed using non-HDL cholesterol categories according to the European guideline thresholds, adjusted for age, sex, cohort, and classical modifiable cardiovascular risk factors. In a derivation and validation design, we created a tool to estimate the probabilities of a cardiovascular disease event by the age of 75 years, dependent on age, sex, and risk factors, and the associated modelled risk reduction, assuming a 50% reduction of non-HDL cholesterol. FINDINGS: Of the 524 444 individuals in the 44 cohorts in the Consortium database, we identified 398 846 individuals belonging to 38 cohorts (184 055 [48·7%] women; median age 51·0 years [IQR 40·7-59·7]). 199 415 individuals were included in the derivation cohort (91 786 [48·4%] women) and 199 431 (92 269 [49·1%] women) in the validation cohort. During a maximum follow-up of 43·6 years (median 13·5 years, IQR 7·0-20·1), 54 542 cardiovascular endpoints occurred. Incidence curve analyses showed progressively higher 30-year cardiovascular disease event-rates for increasing non-HDL cholesterol categories (from 7·7% for non-HDL cholesterol <2·6 mmol/L to 33·7% for ≥5·7 mmol/L in women and from 12·8% to 43·6% in men; p<0·0001). Multivariable adjusted Cox models with non-HDL cholesterol lower than 2·6 mmol/L as reference showed an increase in the association between non-HDL cholesterol concentration and cardiovascular disease for both sexes (from hazard ratio 1·1, 95% CI 1·0-1·3 for non-HDL cholesterol 2·6 to <3·7 mmol/L to 1·9, 1·6-2·2 for ≥5·7 mmol/L in women and from 1·1, 1·0-1·3 to 2·3, 2·0-2·5 in men). The derived tool allowed the estimation of cardiovascular disease event probabilities specific for non-HDL cholesterol with high comparability between the derivation and validation cohorts as reflected by smooth calibration curves analyses and a root mean square error lower than 1% for the estimated probabilities of cardiovascular disease. A 50% reduction of non-HDL cholesterol concentrations was associated with reduced risk of a cardiovascular disease event by the age of 75 years, and this risk reduction was greater the earlier cholesterol concentrations were reduced. INTERPRETATION: Non-HDL cholesterol concentrations in blood are strongly associated with long-term risk of atherosclerotic cardiovascular disease. We provide a simple tool for individual long-term risk assessment and the potential benefit of early lipid-lowering intervention. These data could be useful for physician-patient communication about primary prevention strategies. FUNDING: EU Framework Programme, UK Medical Research Council, and German Centre for Cardiovascular Research

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

The genetics of cardiovascular disease

Recent advances in genotyping technology and insights into disease mechanisms have increased interest in the genetics of cardiovascular disease. Several candidate genes involved in cardiovascular diseases were identified from studies using animal models, and the translation of these findings to human disease is an exciting challenge. There is a trend towards large-scale genome-wide association studies that are subject to strict quality criteria with regard to both genotyping and phenotyping. Here, we review some of the strategies that have been developed to translate findings from experimental models to human disease and outline the need for optimizing global approaches to analyze such results. Findings from ongoing studies are interpreted in the context of disease pathways instead of the more traditional focus on single genetic variants

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