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Obesity is a recognized public health epidemic with a prevalence that continues to increase dramatically in nearly all populations, impeding progress in reducing incidence rates of cardiovascular disease. Over the past decade, obesity science has evolved to improve knowledge of its multifactorial causes, identifying important biological causes and sociological determinants of obesity. Treatments for obesity have also continued to develop, with more evidence-based programs for lifestyle modification, new pharmacotherapies, and robust data to support bariatric surgery. Despite these advancements, there continues to be a substantial gap between the scientific evidence and the implementation of research into clinical practice for effective obesity management. Addressing barriers to obesity science implementation requires adopting feasible methodologies and targeting multiple levels (eg, clinician, community, system, policy) to facilitate the delivery of obesity-targeted therapies and maximize the effectiveness of guideline-driven care to at-need patient populations. This scientific statement (1) describes strategies shown to be effective or promising for enhancing translation and clinical application of obesity-based research; (2) identifies key gaps in the implementation of obesity science into clinical practice; and (3) provides guidance and resources for health care professionals, health care systems, and other stakeholders to promote broader implementation and uptake of obesity science for improved population-level obesity management. In addition, advances in implementation science that hold promise to bridge the know-do gap in obesity prevention and treatment are discussed. Last, this scientific statement highlights implications for health research policy and future research to improve patient care models and optimize the delivery and sustainability of equitable obesity-related care.

Excess muscle fat is observed in obesity and associated with greater burden of cardiovascular risk factors and higher risk of mortality. Liraglutide reduces total body weight and visceral fat but its effect on muscle fat and adverse muscle composition is unknown. This is a pre‐specified secondary analysis of a randomized, double‐blind, placebo‐controlled trial that examined the effects of liraglutide plus a lifestyle intervention on visceral adipose tissue and ectopic fat among adults without diabetes with body mass index ≥30 kg/m2or ≥27 kg/m2and metabolic syndrome. Participants were randomly assigned to a once‐daily subcutaneous injection of liraglutide (target dose 3.0 mg) or matching placebo for 40 weeks. Body fat distribution and muscle composition was assessed by magnetic resonance imaging at baseline and 40‐week follow‐up. Muscle composition was described by the combination of thigh muscle fat and muscle volume. Treatment difference (95% confidence intervals [CI]) was calculated by least‐square means adjusted for baseline thigh muscle fat. The association between changes in thigh muscle fat and changes in body weight were assessed using Spearman correlation coefficients. The effect of liraglutide versus placebo on adverse muscle composition, denoted by high thigh muscle fat and low thigh muscle volume, was explored. Among the 128 participants with follow‐up imaging (92.2% women, 36.7% Black), median muscle fat at baseline was 7.8%. The mean percent change in thigh muscle fat over median follow‐up of 36 weeks was −2.87% among participants randomized to liraglutide (n= 73) and 0.05% in the placebo group (absolute change: −0.23% vs. 0.01%). The estimated treatment difference adjusted for baseline thigh muscle fat was −0.24% (95% CI, −0.41 to −0.06, P‐value 0.009). Longitudinal change in thigh muscle fat was significantly associated with change in body weight in the placebo group but not the liraglutide group. The proportion of participants with adverse muscle composition decreased from 11.0% to 8.2% over follow‐up with liraglutide, but there was no change with placebo. In a cohort of predominantly women with overweight or obesity in the absence of diabetes, once‐daily subcutaneous liraglutide was associated with a reduction in thigh muscle fat and adverse muscle composition compared with placebo. The contribution of muscle fat improvement to the cardiometabolic benefits of liraglutide requires further study.

Urban environments contribute substantially to the rising burden of cardiometabolic diseases worldwide. Cities are complex adaptive systems that continually exchange resources, shaping exposures relevant to human health such as air pollution, noise, and chemical exposures. In addition, urban infrastructure and provisioning systems influence multiple domains of health risk, including behaviors, psychological stress, pollution, and nutrition through various pathways (eg, physical inactivity, air pollution, noise, heat stress, food systems, the availability of green space, and contaminant exposures). Beyond cardiometabolic health, city design may also affect climate change through energy and material consumption that share many of the same drivers with cardiometabolic diseases. Integrated spatial planning focusing on developing sustainable compact cities could simultaneously create heart-healthy and environmentally healthy city designs. This article reviews current evidence on the associations between the urban exposome (totality of exposures a person experiences, including environmental, occupational, lifestyle, social, and psychological factors) and cardiometabolic diseases within a systems science framework, and examines urban planning principles (eg, connectivity, density, diversity of land use, destination accessibility, and distance to transit). We highlight critical knowledge gaps regarding built-environment feature thresholds for optimizing cardiometabolic health outcomes. Last, we discuss emerging models and metrics to align urban development with the dual goals of mitigating cardiometabolic diseases while reducing climate change through cross-sector collaboration, governance, and community engagement. This review demonstrates that cities represent crucial settings for implementing policies and interventions to simultaneously tackle the global epidemics of cardiovascular disease and climate change.

Cardiovascular-kidney-metabolic (CKM) syndrome is a novel construct recently defined by the American Heart Association in response to the high prevalence of metabolic and kidney disease. Epidemiological data demonstrate higher absolute risk of both atherosclerotic cardiovascular disease (CVD) and heart failure as an individual progresses from CKM stage 0 to stage 3, but optimal strategies for risk assessment need to be refined. Absolute risk assessment with the goal to match type and intensity of interventions with predicted risk and expected treatment benefit remains the cornerstone of primary prevention. Given the growing number of therapies in our armamentarium that simultaneously address all 3 CKM axes, novel risk prediction equations are needed that incorporate predictors and outcomes relevant to the CKM context. This should also include social determinants of health, which are key upstream drivers of CVD, to more equitably estimate and address risk. This scientific statement summarizes the background, rationale, and clinical implications for the newly developed sex-specific, race-free risk equations: PREVENT (AHA Predicting Risk of CVD Events). The PREVENT equations enable 10- and 30-year risk estimates for total CVD (composite of atherosclerotic CVD and heart failure), include estimated glomerular filtration rate as a predictor, and adjust for competing risk of non-CVD death among adults 30 to 79 years of age. Additional models accommodate enhanced predictive utility with the addition of CKM factors when clinically indicated for measurement (urine albumin-to-creatinine ratio and hemoglobin A1c) or social determinants of health (social deprivation index) when available. Approaches to implement risk-based prevention using PREVENT across various settings are discussed.

Cardiovascular-kidney-metabolic health reflects the interplay among metabolic risk factors, chronic kidney disease, and the cardiovascular system and has profound impacts on morbidity and mortality. There are multisystem consequences of poor cardiovascular-kidney-metabolic health, with the most significant clinical impact being the high associated incidence of cardiovascular disease events and cardiovascular mortality. There is a high prevalence of poor cardiovascular-kidney-metabolic health in the population, with a disproportionate burden seen among those with adverse social determinants of health. However, there is also a growing number of therapeutic options that favorably affect metabolic risk factors, kidney function, or both that also have cardioprotective effects. To improve cardiovascular-kidney-metabolic health and related outcomes in the population, there is a critical need for (1) more clarity on the definition of cardiovascular-kidney-metabolic syndrome; (2) an approach to cardiovascular-kidney-metabolic staging that promotes prevention across the life course; (3) prediction algorithms that include the exposures and outcomes most relevant to cardiovascular-kidney-metabolic health; and (4) strategies for the prevention and management of cardiovascular disease in relation to cardiovascular-kidney-metabolic health that reflect harmonization across major subspecialty guidelines and emerging scientific evidence. It is also critical to incorporate considerations of social determinants of health into care models for cardiovascular-kidney-metabolic syndrome and to reduce care fragmentation by facilitating approaches for patient-centered interdisciplinary care. This presidential advisory provides guidance on the definition, staging, prediction paradigms, and holistic approaches to care for patients with cardiovascular-kidney-metabolic syndrome and details a multicomponent vision for effectively and equitably enhancing cardiovascular-kidney-metabolic health in the population.

A growing appreciation of the pathophysiological interrelatedness of metabolic risk factors such as obesity and diabetes, chronic kidney disease, and cardiovascular disease has led to the conceptualization of cardiovascular-kidney-metabolic syndrome. The confluence of metabolic risk factors and chronic kidney disease within cardiovascular-kidney-metabolic syndrome is strongly linked to risk for adverse cardiovascular and kidney outcomes. In addition, there are unique management considerations for individuals with established cardiovascular disease and coexisting metabolic risk factors, chronic kidney disease, or both. An extensive body of literature supports our scientific understanding of, and approach to, prevention and management for individuals with cardiovascular-kidney-metabolic syndrome. However, there are critical gaps in knowledge related to cardiovascular-kidney-metabolic syndrome in terms of mechanisms of disease development, heterogeneity within clinical phenotypes, interplay between social determinants of health and biological risk factors, and accurate assessments of disease incidence in the context of competing risks. There are also key limitations in the data supporting the clinical care for cardiovascular-kidney-metabolic syndrome, particularly in terms of early-life prevention, screening for risk factors, interdisciplinary care models, optimal strategies for supporting lifestyle modification and weight loss, targeting of emerging cardioprotective and kidney-protective therapies, management of patients with both cardiovascular disease and chronic kidney disease, and the impact of systematically assessing and addressing social determinants of health. This scientific statement uses a crosswalk of major guidelines, in addition to a review of the scientific literature, to summarize the evidence and fundamental gaps related to the science, screening, prevention, and management of cardiovascular-kidney-metabolic syndrome.

Visceral and ectopic fat are key drivers of adverse cardiometabolic outcomes in obesity. We aimed to evaluate the effects of injectable liraglutide 3·0 mg daily on body fat distribution in adults with overweight or obesity without type 2 diabetes at high cardiovascular disease risk.

The care for patients with type 2 diabetes mellitus (T2DM) necessitates a multidisciplinary team approach to reduce cardiovascular (CV) risk but implementation of effective integrated strategies has been limited.

To evaluate the association between TMAO and related metabolites with adverse cardiovascular events in a multiethnic urban primary prevention population.

Despite decades of unequivocal evidence that waist circumference provides both independent and additive information to BMI for predicting morbidity and risk of death, this measurement is not routinely obtained in clinical practice. This Consensus Statement proposes that measurements of waist circumference afford practitioners with an important opportunity to improve the management and health of patients. We argue that BMI alone is not sufficient to properly assess or manage the cardiometabolic risk associated with increased adiposity in adults and provide a thorough review of the evidence that will empower health practitioners and professional societies to routinely include waist circumference in the evaluation and management of patients with overweight or obesity. We recommend that decreases in waist circumference are a critically important treatment target for reducing adverse health risks for both men and women. Moreover, we describe evidence that clinically relevant reductions in waist circumference can be achieved by routine, moderate-intensity exercise and/or dietary interventions. We identify gaps in the knowledge, including the refinement of waist circumference threshold values for a given BMI category, to optimize obesity risk stratification across age, sex and ethnicity. We recommend that health professionals are trained to properly perform this simple measurement and consider it as an important ‘vital sign’ in clinical practice.

The Epitomee Capsule (EC) is an, oral, self‐use, bio-degradable device for weight management, composed of absorbent polymers that self-expands in the stomach (pH-sensitive) and creates a triangular shape, space-occupying super-absorbent gel structure. A recent study reported that 42 % of study completers obtained >5 % weight reduction at 12 weeks. We performed exploratory analyses of this study to evaluate its effect on cardiovascular risk factors and on self-reported satiety, between-meal snacking and meal-size.

Findings from epidemiological studies over the past 30 years have shown that visceral adipose tissue, accurately measured by CT or MRI, is an independent risk marker of cardiovascular and metabolic morbidity and mortality. Emerging evidence also suggests that ectopic fat deposition, including hepatic and epicardial fat, might contribute to increased atherosclerosis and cardiometabolic risk. This joint position statement from the International Atherosclerosis Society and the International Chair on Cardiometabolic Risk Working Group on Visceral Obesity summarises the evidence for visceral adiposity and ectopic fat as emerging risk factors for type 2 diabetes, atherosclerosis, and cardiovascular disease, with a focus on practical recommendations for health professionals and future directions for research and clinical practice. We discuss the measurement of visceral and ectopic fat, pathophysiology and contribution to adverse health outcomes, response to treatment, and lessons from a public health programme targeting visceral and ectopic fat. We identify knowledge gaps and note the need to develop simple, clinically applicable tools to be able to monitor changes in visceral and ectopic fat over time. Finally, we recognise the need for public health messaging to focus on visceral and ectopic fat in addition to excess bodyweight to better combat the growing epidemic of obesity worldwide.

IMPORTANCE: African Americans have a higher burden of heart failure (HF) risk factors and clinical HF than other racial/ethnic groups. However, the factors underlying the transition from at-risk to clinical HF in African Americans are not well understood. OBJECTIVE: To evaluate the contributions of left ventricular hypertrophy (LVH) and subclinical myocardial injury as determined by abnormal high-sensitivity cardiac troponin-I (hs-cTnI) measurements toward HF risk among African Americans. DESIGN, SETTING, AND PARTICIPANTS: This prospective, community-based cohort study was conducted between July 2016 and September 2018 and included African American participants from Jackson, Mississippi enrolled in the Jackson Heart Study without prevalent HF who had hs-cTnI measurements and an echocardiographic examination at baseline. Participants were stratified into categories based on the presence or absence of LVH and subclinical myocardial injury (category 1: hs-cTnI <4 ng/L in women and <6 ng/L in men; category 2: 4-10 ng/L in women and 6-12 ng/L in men; category 3: >10 ng/L in women and >12 ng/L in men). MAIN OUTCOMES AND MEASURES: Adjusted associations between LVH, subclinical myocardial injury, and the risk of incident HF hospitalization were assessed using Cox proportional hazards models. RESULTS: The study included 3987 participants (2552 women [64%]; 240 (6.0%) with LVH; 1003 (25.1%) with myocardial injury) with 285 incident HF events over a median follow-up of 9.8 years (interquartile range, 8.9-10.6 years). In adjusted analyses, higher LV mass and subclinical myocardial injury were independently associated with the risk of HF with a significant interaction between the 2 (Pint < 0.001). The highest risk of HF was noted among individuals with both LVH and myocardial injury (absolute incidence, 35%; adjusted hazard ratio [aHR; vs no LVH and no myocardial injury], 5.35; 95% CI, 3.66-7.83). A significant interaction by sex was also observed. Men with LVH and subclinical myocardial injury had an almost 15-fold higher risk of HF (aHR, 14.62; 95% CI, 7.61-28.10) vs those with neither LVH nor injuries. By contrast, women with this phenotype had a nearly 4-fold higher risk of HF (aHR, 3.81; 95% CI, 2.40-6.85). CONCLUSIONS AND RELEVANCE: The combination of LVH and subclinical myocardial injury identifies a malignant, preclinical HF phenotype in African Americans with a very high risk of HF, particularly among men. This finding could have implications for future screening strategies that are designed to prevent HF in the population.

Severe hypercholesterolemia (SH), defined as a low-density lipoprotein cholesterol (LDL-C) level ≥ 190 mg/dl, is associated with an increased risk for premature atherosclerotic cardiovascular disease. Despite guideline recommendations, many patients with severe hypercholesterolemia remain untreated. We conducted an observational analysis of a large pool of SH patients, exploring demographic and social factors contributing to disparities in the prescription of statin and other lipid-lowering therapies.

To investigate the obesity paradox and association of extreme obesity with long-term outcomes among older ST-segment elevation myocardial infarction (STEMI) patients.

This study evaluated the contributions of obesity and changes in body mass index (BMI) in mid-life to long-term heart failure (HF) risk independent of cardiorespiratory fitness (CRF) levels.

To examine the association between specific adipose tissue depots and the risk of incident cancer in the Dallas Heart Study.

Severe Hypercholesterolemia, Lipid Management

Prior studies have suggested significant underutilization of statins in women and worse cardiovascular outcomes. Data examining the impact of real-world coronary artery calcium (CAC) scoring to improve utilization of preventive therapies and outcomes is limited.

ABSTRACTIntroduction: Empagliflozin is a sodium glucose co-transporter 2 inhibitor used to improve glycemic control in adults with type 2 diabetes mellitus (T2DM) by enhancing urinary glucose excretion. Empagliflozin is effective at lowering glycosylated hemoglobin and was recently proven superior to placebo for reduction of cardiovascular disease (CVD) risk. As with any new drug, there are safety considerations that inform its potential use in patients with T2DM.Areas Covered: Here, we evaluate the safety of empagliflozin and provide an expert opinion as to its current and future role in the treatment of patients with T2DM. A search of the English language literature was performed using PubMed search terms: “empagliflozin”, “sodium glucose cotransporter 2 inhibitors”, and “drug safety”. Articles and bibliographies relevant to the subject were reviewed and additional references known to the authors were included.Expert Opinion: The evidence for empagliflozin is robust with regard to glycemic efficacy and safety. Low risk of hypoglycemia, absence of weight gain, and demonstrated cardiovascular risk reduction support its consideration as a first line medication in addition to metformin for patients with T2DM and CVD. Ongoing trials will continue to address the safety and efficacy of empagliflozin and expand our clinical knowledge of this medication.

This study hypothesized that biomarkers of subclinical myocardial injury (high-sensitivity cardiac troponin T [hs-cTnT]) and hemodynamic stress (N-terminal pro-B-type natriuretic peptide [NT-proBNP]) would differentiate heart failure (HF) risk among older adults with left ventricular hypertrophy (LVH).

The relation of body fat distribution to left ventricular (LV) structure and function is poorly defined.

Introduction:While it is well-known that Type 2 Diabetes (T2D) has a disproportionate impact on healthcare expenditure, the precise extent to which cardiorenal and mental health complications of diabetes in accountable care organizations (ACO) influence cost is not clear. We sought to investigate the association between these factors and medical spend in patients with T2D in a large ACO.Methods:We identified all patients (≥ 18 years) with T2D (defined as HbA1c ≥ 6.5% and by ICD10 codes) within our ACO population and linked their total medical spend (inpatient and ambulatory visits) for the year 2020. We investigated the association between medical spend and medical comorbidities (figure A), body mass index (BMI), glycated hemoglobin (HbA1c), and glomerular filtration rate (GFR).Results:A total of 28,566 patients with T2D were included. Mean age was 65 years, 50% were female, and 20% were Black. Comorbid conditions were common: 88% had hypertension, 33% had CAD, 19% had cerebrovascular disease, 19% had HF, 20% had CKD, 32% had OSA, 34% had anxiety, 10% had depression. Median annual spend was $754 per patient. Comorbidities associated with increased spend are shown in figure A. Patients with cardiorenal comorbidities had 723% increase in medical spend. Medical spend was weakly associated with HbA1c and BMI but increased sharply at GFR <25 ml/min/1.73 m2 (figure c). Patients with cardiorenal comorbidities accounted for 50% of all patients with T2D and 79% of the medical spend in T2D.Conclusions:In a contemporary large ACO population, cardiorenal comorbidities are associated with medical spend. Interventions to promote value in ACOs may need to focus on these high-risk groups.

Introduction:Ectopic fat deposition (dysfunctional adipose tissue) is associated with atherosclerotic cardiovascular disease (ASCVD) risk. The value of adding fat distribution information to coronary artery calcium (CAC) score to predict ASCVD risk is unknown. Additionally, whether the association between fat distribution and CVD risk differs by sex is not well understood.Hypothesis:There are sex-specific relationships between adipose depots and CVD risk.Methods:We identified all participants in the Coronary Artery Risk Development in Young Adults (CARDIA) study who underwent computed tomography of the chest and abdomen. We used machine learning models (logistic regression) to evaluate associations in men and women separately between 14 fat depot measurements encompassing visceral, subcutaneous, and ectopic fat (mean liver attenuation, total visceral, epicardial, intermuscular, intramuscular [paraspinous, rectus, psoas] and subcutaneous) and sex, non-zero CAC, and CVD risk using 10-fold cross-validation.Results:A total of 3163 individuals were included (1790 women and 1373 men). A model incorporating all fat depot variables had excellent discrimination of sex (AUROC = 0.88). In the entire cohort, our fat depot model had modest discrimination of non-zero CAC (0.69) and CVD events (0.58). The performance of CAC to predict CVD improved with the addition of fat depots (0.65 to 0.71). Women had higher AUROC for fat depots to predict non-zero CAC (0.63 vs 0.58) and CVD events (0.58 vs 0.52), which remained consistent in a model that includes CAC and fat (0.69 vs 0.66). Fat improved discrimination of CAC to predict CVD events more in women vs men (0.06 vs 0.03). The strength of association between various fat depots and sex differed between men and women (Figure).Conclusions:Visceral ectopic fat depots are associated with CAC and CV risk more strongly in women vs men. Future studies should focus on the sex-specific pathophysiology of cardiometabolic disease.

To evaluate the cardiometabolic outcomes associated with discordant visceral adipose tissue (VAT) and liver fat (LF) phenotypes in 2 cohorts.

This study sought to evaluate the independent associations and interactions between high-sensitivity cardiac troponin I (hs-cTnI) and physical activity (PA) with risks of heart failure (HF) subtypes, HF with preserved ejection fraction (HFpEF) and HF with reduced ejection fraction (HFrEF).

Introduction:A ?malignant? subphenotype of left ventricular hypertrophy (LVH) has been described, in which elevations in cardiac biomarkers identify individuals with LVH at high risk for developing heart failure (HF).Hypothesis:We hypothesized that a higher prevalence of malignant LVH among blacks may contribute to racial disparities in HF risk.Methods:15,710 participants without prevalent cardiovascular disease were pooled from 3 population-based cohort studies, the ARIC Study, DHS and MESA. Participants were classified into 3 groups: those without ECG-LVH, those with ECG-LVH and normal biomarkers (hs-cTnT < 6 ng/L and NT-proBNP < 100 pg/mL), and those with ECG-LVH and abnormal levels of either biomarker (malignant LVH). The outcome was incident HF.Results:Over the 10 year follow up period, HF occurred in 512 (3.3%) participants, with rates 5.2% among black men (BM), 3.8% in white men (WM), 3.2% in black women (BW), and 2.2% in white women (WW). The prevalence of malignant LVH was 3-fold higher among BM and BW vs WM and WW. Compared with participants without LVH, the adjusted hazard ratio for HF was 2.8 (95% CI 2.1-3.5) in those with malignant LVH and 0.9 (95% CI 0.6-1.5) in those with LVH and normal biomarkers, with similar findings in each race/sex subgroup. Mediation analyses indicated that 63% of excess hazard for HF among BM and 35% of the excess hazard among BW was explained by the higher prevalence of malignant LVH in blacks. Of BM who developed HF, 30.8% had malignant LVH at baseline, with a population attributable fraction (PAF) of 0.21. The proportion of HF cases occurring among those with malignant LVH, and corresponding PAF, were intermediate and similar among BW and WM and lowest among WW.Conclusions:A higher prevalence of malignant LVH may in part explain the higher risk of HF among blacks vs whites. Strategies to prevent development or attenuate risk associated with malignant LVH should be investigated as a strategy to lower HF risk and mitigate racial disparities.

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