No abstract

Obesity is associated with an increased risk of developing cardiovascular disease (CVD), particularly heart failure (HF) and coronary heart disease (CHD). The mechanisms through which obesity increases CVD risk involve changes in body composition that can affect hemodynamics and alters heart structure. Pro-inflammatory cytokines produced by the adipose tissue itself which can induce cardiac dysfunction and can promote the formation of atherosclerotic plaques. When obesity and HF or CHD coexist, individuals with class I obesity present a more favorable prognosis compared to individuals who are normal or underweight. This phenomenon has been termed the “obesity paradox.” Obesity is defined as an excess fat mass (FM), but individuals with obesity typically also present with an increased amount of lean mass (LM). The increase in LM may explain part of the obesity paradox as it is associated with improved cardiorespiratory fitness (CRF), a major determinant of clinical outcomes in the general population, but particularly in those with CVD, including HF. While increased LM is a stronger prognosticator in HF compared to FM, in patients with CHD excess FM can exert protective effects particularly when not associated with increased systemic inflammation. In the present review, we discuss the mechanisms through which obesity may increase the risk for CVD, and how it may exert protective effects in the setting of established CVD, with a focus on body composition. We also highlight the importance of measuring or estimating CRF, including body composition-adjusted measures of CRF (ie, lean peak oxygen consumption) for an improved risk status stratification in patients with CVD and finally, we discuss the potential non-pharmacologic therapeutics, such as exercise training and dietary interventions, aimed at improving CRF and perhaps clinical outcomes.

Interest in the potential cardiovascular (CV) benefits of omega-3 polyunsaturated fatty acids (Ω-3) began in the 1940s and was amplified by a subsequent landmark trial showing reduced CV disease (CVD) risk following acute myocardial infarction. Since that time, however, much controversy has circulated due to discordant results among several studies and even meta-analyses. Then, in 2018, three more large, randomized trials were released—these too with discordant findings regarding the overall benefits of Ω-3 therapy. Interestingly, the trial that used a higher dose (4 g/day highly purified eicosapentaenoic acid (EPA)) found a remarkable, statistically significant reduction in CVD events. It was proposed that insufficient Ω-3 dosing (<1 g/day EPA and docosahexaenoic acid (DHA)), as well as patients aggressively treated with multiple other effective medical therapies, may explain the conflicting results of Ω-3 therapy in controlled trials. We have thus reviewed the current evidence regarding Ω-3 and CV health, put forth potential reasoning for discrepant results in the literature, highlighted critical concepts such as measuring blood levels of Ω-3 with a dedicated Ω-3 index and addressed current recommendations as suggested by health care professional societies and recent significant scientific data.

No abstract

There is an ongoing debate in the medical community regarding the effects of testosterone on cardiovascular (CV) health. For decades, there has been conflicting evidence regarding the association of endogenous testosterone levels and CV disease (CVD) events that has resulted in much debate and confusion among health care providers and patients alike. Testosterone therapy has become increasingly widespread, and after the emergence of studies that reported increased CVD events in patients receiving testosterone therapy, the US Food and Drug Administration (FDA) released a warning statement about testosterone and its potential risk regarding CV health. Some of these studies were later found to be critically flawed, and some experts, including the American Association of Clinical Endocrinologists and an expert panel regarding testosterone deficiency and its treatment, reported that some of the FDA statements regarding testosterone therapy were lacking scientific evidence. This article summarizes the current evidence regarding the relationship between testosterone (endogenous and supplemental) and CV health. A literature review was conducted via search using PubMed and specific journal databases, including the New England Journal of Medicine and the Journal of the American College of Cardiology. Key search terms included testosterone and cardiovascular health, coronary artery disease, heart failure, androgen deprivation therapy, intima-media thickness, and adrenal androgens. Initial study selection was limited to publications within the past 10 years (January 1, 2007, through December 31, 2016); however, key publications outside of this time frame were selected if they provided important quantitative data or historical perspectives for the review of this topic. The search was further supplemented by reviewing references in selected articles.

The potential cardiovascular (CV) disease (CVD) benefits of Omega-3 Polyunsaturated Fatty Acids (OM3) have been intensely studied and debated for decades. Initial trials were performed in patients with low use of maximal medical therapy for CVD, and reported significant mortality benefits with the use of 1 g/day OM3 intervention following myocardial infarction (MI). More recent studies, including cohorts of patients receiving modern guideline directed medical therapy for CVD, have often not shown similar benefits with OM3 use. We conducted a literature review using PubMed, professional society guidelines, specific journal databases including New England Journal of Medicine and Journal of the American College of Cardiology from January 1, 2007 to December 31, 2017. References from selected articles were also reviewed, as well as key articles outside of the selected time-frame for their important findings or historical perspectives. Currently, there are no Class I recommendations from the American Heart Association (AHA) for the use of OM3, however, considering the safety of this therapy and beneficial findings of some modern studies (including patients with current maximal medical therapy for CVD), the AHA has recently expanded their list of Class II recommendations, in which treatment with OM3 for CVD benefit is reasonable. This review discusses the current state of the evidence, summarizes current professional recommendations, and provides recommendations for future research.

No abstract

Obesity is associated with increased prevalence of cardiovascular (CV) disease (CVD) risk factors, which may adversely impact CV structure and function and may increase the prevalence of most CVD, particularly heart failure (HF) and coronary heart disease (CHD). Physical activity (PA), exercise training (ET) and cardiorespiratory fitness (CRF) are all associated with marked reductions in most CVD, including HF and CHD. Additionally, PA/ET and, especially CRF, markedly alter the relationship between adiposity and subsequent major CVD outcomes and dramatically impact the “obesity paradox,” which are all reviewed, including attention to the debate regarding “fitness versus fatness” for long-term prognosis, including in patients with established CVD.