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The escalating prevalence of obesity has been linked to substantial increases in both metabolic and cardiovascular disease. Nevertheless, the direct effects of obesity on cardiovascular health and function require further exploration. In particular, the relationship between obesity and cardiac function has received intense scrutiny. Although obesity increases the risk for development of heart failure (HF), it appears to exert a protective effect in patients in whom HF has already been diagnosed (the “obesity paradox”). The protective effects of obesity in patients with previously diagnosed HF are the focus of particularly intense research. Several explanations have been proposed, but most studies are limited by the use of body mass index to classify obesity. Because body mass index does not distinguish between fat mass, fat-free mass, and lean mass, individuals with similar body mass indices may have vastly different body composition. This article discusses the roles of body composition, diet, cardiorespiratory fitness, and weight loss in the development of cardiac dysfunction and HF and the potential protective role that body composition compartments might play in improving HF prognosis. Based on an intensive literature search (Pubmed, Google Scholar) and critical review of the literature, we also discuss how a multidisciplinary approach including a nutritional intervention targeted to reduce systemic inflammation and lean mass–targeted exercise training could potentially exert beneficial effects for patients with HF.

Obesity has reached epidemic proportions in the United States and in much of the westernized world, contributing to considerable morbidity. Several of these obesity-related morbidities are associated with greater risk for death with coronavirus disease 2019 (COVID-19). Severe acute respiratory syndrome coronavirus 2 penetrates human cells through direct binding with angiotensin-converting enzyme 2 receptors on the cell surface. Angiotensin-converting enzyme 2 expression in adipose tissue is higher than that in lung tissue, which means that adipose tissue may be vulnerable to COVID-19 infection. Obese patients also have worse outcomes with COVID-19 infection, including respiratory failure, need for mechanical ventilation, and higher mortality. Clinicians need to be more aggressive when treating obese, especially severely obese, patients with COVID-19 infection.

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.

The Scientific Report of the 2015 Dietary Guidelines Advisory Committee was primarily informed by memory-based dietary assessment methods (M-BMs) (eg, interviews and surveys). The reliance on M-BMs to inform dietary policy continues despite decades of unequivocal evidence that M-BM data bear little relation to actual energy and nutrient consumption. Data from M-BMs are defended as valid and valuable despite no empirical support and no examination of the foundational assumptions regarding the validity of human memory and retrospective recall in dietary assessment. We assert that uncritical faith in the validity and value of M-BMs has wasted substantial resources and constitutes the greatest impediment to scientific progress in obesity and nutrition research. Herein, we present evidence that M-BMs are fundamentally and fatally flawed owing to well-established scientific facts and analytic truths. First, the assumption that human memory can provide accurate or precise reproductions of past ingestive behavior is indisputably false. Second, M-BMs require participants to submit to protocols that mimic procedures known to induce false recall. Third, the subjective (ie, not publicly accessible) mental phenomena (ie, memories) from which M-BM data are derived cannot be independently observed, quantified, or falsified; as such, these data are pseudoscientific and inadmissible in scientific research. Fourth, the failure to objectively measure physical activity in analyses renders inferences regarding diet-health relationships equivocal. Given the overwhelming evidence in support of our position, we conclude that M-BM data cannot be used to inform national dietary guidelines and that the continued funding of M-BMs constitutes an unscientific and major misuse of research resources.

Purpose of Review Sleep is an important component of cardiovascular (CV) health. This review summarizes the complex relationship between sleep and CV disease (CVD). Additionally, we describe the data supporting the treatment of sleep disturbances in preventing and treating CVD. Recent Findings Recent guidelines recommend screening for obstructive sleep apnea in patients with atrial fibrillation. New data continues to demonstrate the importance of sleep quality and duration for CV health. Summary There is a complex bidirectional relationship between sleep health and CVD. Sleep disturbances have systemic effects that contribute to the development of CVD, including hypertension, coronary artery disease, heart failure, and arrhythmias. Additionally, CVD contributes to the development of sleep disturbances. However, more data are needed to support the role of screening for and treatment of sleep disorders for the prevention of CVD.

Physical activity (PA) and exercise training (ET) have great potential in the prevention, management, and rehabilitation of a variety of diseases, but this potential has not been fully realized in clinical practice. The health care system (HCS) could do much more to support patients in increasing their PA and ET. However, counseling on ET is not used widely by the HCS owing partly to attitudes but mainly to practical obstacles. Extensive searches of MEDLINE, the Cochrane Library, the Database of Abstracts of Reviews of Effects, and ScienceDirect for literature published between January 1, 2000, and January 31, 2013, provided data to assess the critical characteristics of ET counseling. The evidence reveals that especially brief ET counseling is an efficient, effective, and cost-effective means to increase PA and ET and to bring considerable clinical benefits to various patient groups. Furthermore, it can be practiced as part of the routine work of the HCS. However, there is a need and feasible means to increase the use and improve the quality of ET counseling. To include PA and ET promotion as important means of comprehensive health care and disease management, a fundamental change is needed. Because exercise is medicine, it should be seen and dealt with in the same ways as pharmaceuticals and other medical interventions regarding the basic and continuing education and training of health care personnel and processes to assess its needs and to prescribe and deliver it, to reimburse the services related to it, and to fund research on its efficacy, effectiveness, feasibility, and interactions and comparability with other preventive, therapeutic, and rehabilitative modalities. This change requires credible, strong, and skillful advocacy inside the medical community and the HCS.

Habitual light to moderate alcohol intake (up to 1 drink per day for women and 1 or 2 drinks per day for men) is associated with decreased risks for total mortality, coronary artery disease, diabetes mellitus, congestive heart failure, and stroke. However, higher levels of alcohol consumption are associated with increased cardiovascular risk. Indeed, behind only smoking and obesity, excessive alcohol consumption is the third leading cause of premature death in the United States. Heavy alcohol use (1) is one of the most common causes of reversible hypertension, (2) accounts for about one-third of all cases of nonischemic dilated cardiomyopathy, (3) is a frequent cause of atrial fibrillation, and (4) markedly increases risks of stroke—both ischemic and hemorrhagic. The risk-to-benefit ratio of drinking appears higher in younger individuals, who also have higher rates of excessive or binge drinking and more frequently have adverse consequences of acute intoxication (for example, accidents, violence, and social strife). In fact, among males aged 15 to 59 years, alcohol abuse is the leading risk factor for premature death. Of the various drinking patterns, daily low- to moderate-dose alcohol intake, ideally red wine before or during the evening meal, is associated with the strongest reduction in adverse cardiovascular outcomes. Health care professionals should not recommend alcohol to nondrinkers because of the paucity of randomized outcome data and the potential for problem drinking even among individuals at apparently low risk. The findings in this review were based on a literature search of PubMed for the 15-year period 1997 through 2012 using the search terms alcohol, ethanol, cardiovascular disease, coronary artery disease, heart failure, hypertension, stroke, and mortality. Studies were considered if they were deemed to be of high quality, objective, and methodologically sound.

To evaluate the effects of L-carnitine compared with placebo or control on morbidity and mortality in the setting of acute myocardial infarction. A systematic review and meta-analysis of 13 controlled trials (N=3629) was conducted to determine the effects of L-carnitine vs placebo or control on mortality, ventricular arrhythmias (VAs), angina, heart failure, and reinfarction. These trials were identified via searches of the Ovid MEDLINE, PubMed, and Excerpta Medica (Embase) databases between May 1, 2012, and August 31, 2012. Compared with placebo or control, L-carnitine was associated with a significant 27% reduction in all-cause mortality (odds ratio, 0.73; 95% CI, 0.54-0.99; P=.05; risk ratio [RR], 0.78; 95% CI, 0.60-1.00; P=.05), a highly significant 65% reduction in VAs (RR, 0.35; 95% CI, 0.21-0.58; P<.0001), and a significant 40% reduction in the development of angina (RR, 0.60; 95% CI, 0.50-0.72; P<.00001), with no reduction in the development of heart failure (RR, 0.85; 95% CI, 0.67-1.09; P=.21) or myocardial reinfarction (RR, 0.78; 95% CI, 0.41-1.48; P=.45). Compared with placebo or control, L-carnitine is associated with a 27% reduction in all-cause mortality, a 65% reduction in VAs, and a 40% reduction in anginal symptoms in patients experiencing an acute myocardial infarction. Further study with large randomized controlled trials of this inexpensive and safe therapy in the modern era is warranted.

Clinical studies have indicated the existence of an “obesity paradox” in patients with chronic heart failure (HF), that is, reduced mortality in patients who have elevated body mass index (BMI) scores compared with normal-weight reference groups. The aim of this study was to investigate the relation of BMI with all-cause and cardiovascular (CV) mortality and hospitalization in patients with chronic HF though a systematic review and meta-analysis of published research. PubMed, the Cumulative Index to Nursing and Allied Health Literature, Cochrane Central, Scopus, web of science and Embase were searched for studies reporting rates of total mortality, cardiac mortality, and risk for hospitalization in patients with HF in various BMI categories (<20 kg/m2 [low], 20 to 24.9 kg/m2 [normal reference], 25 to 29.9 kg/m2 [overweight], 30 to 34.9 [obese], and ≥35 kg/m2 [severely obese]). Event rates were compared using a forest plot of relative risk (RR) using a random-effects model assuming interstudy heterogeneity. Two study investigators independently reviewed the 124 reports retrieved and identified 6 for final analyses (n = 22,807). After a mean follow-up period of 2.85 years, the risk for adverse events was highest in patients with low BMIs: total mortality RR 1.27 (95% confidence interval [CI] 1.17 to 1.37), CV mortality RR 1.20 (95% CI 1.01 to 1.43), and hospitalization RR 1.19 (95% CI 1.09 to 1.30). Risk for CV mortality and hospitalization was lowest in overweight patients (RR 0.79, 95% CI 0.70 to 0.90, and RR 0.92, 95% CI 0.86 to 0.97, respectively). Increasing degree of obesity failed to achieve a statistically significant effect on CV mortality (RR 0.82, 95% CI 0.64 to 1.05, and RR 0.71, 95% CI 0.50 to 1.01, for obese and severely obese, respectively) and on hospitalization (RR 0.99, 95% CI 0.92 to 1.07, and RR 1.28, 95% CI 0.88 to 1.87, for obese and severely obese, respectively). In conclusion, risk for total mortality and CV mortality and hospitalization was highest in patients with chronic HF who were underweight as defined by low BMI, whereas risk for CV mortality and hospitalization was lowest in overweight subjects.

Physical inactivity and psychosocial stress are prevalent in residents of the United States. The purpose of this article is to review the interaction between these 2 conditions and examine the effects of exercise on stress and cardiovascular (CV) health. A query of scientific references between 1974 to 2018 was performed using the PubMed search engine accessing the MEDLINE database using the search terms psychosocial stress, CV disease (CVD), physical activity, exercise, cardiac rehabilitation, and team sports. Psychosocial stress is a strong independent risk factor for adverse CV events. Conversely, people who experience CV events subsequently have drastically elevated rates of new-onset mental health disorders, including depression and anxiety. Psychosocial stress and CVD often trigger self-reinforcing feedback loops that can worsen mental health and cardiac prognosis. Exercise predictably improves CV health and prognosis and also is effective at lowering levels of psychosocial stress. Group exercise in particular seems to provide social support while at the same time boosting fitness levels and, thus, may be the single most important intervention for patients with concomitant CVD and emotional stress. Collaborative physical activity, such as group exercise, team sports, interactive physical play, and cardiac rehabilitation programs, have the potential to improve mental health and CV prognosis.