Objectives: To compare various measures of adiposity with risk for incident hospitalized heart failure (HF) with preserved ejection fraction (HFpEF) and reduced ejection fraction (HFrEF). Background: Obesity is a risk factor for HF, particularly HFpEF. It is unknown which measures of adiposity, including anthropometrics and computed tomography (CT)-measured fat area, are most predictive of HF sub-types. Methods: We studied 1,806 participants of the Multi-Ethnic Study of Atherosclerosis without baseline cardiovascular disease (CVD) who underwent anthropometrics [Body Mass Index (BMI) and Waist Circumference (WC)] and an abdominal CT. Subcutaneous and visceral adipose tissue (SAT and VAT) were measured from a single CT slice at L2-L3. Cox hazard models were used to examine associations of adiposity with incident hospitalized HFpEF and HFrEF events. Fully-adjusted models included demographics, HF risk factors, and NT-proBNP Results: Over mean follow-up of 11 years, there were 34 HFpEF and 36 HFrEF events. The fully-adjusted Hazard Ratios (95% CI) per 1-SD higher of each anthropometric and CT-measured adiposity measures for incident HFpEF were as follows: BMI [1.66 (1.12–2.45)]; WC [1.59 (1.05–2.40)]; VAT [2.24 (1.44–3.49)]. None of these adiposity measures were associated with HFrEF. Even among overweight/obese adults (BMI≥25 kg/m2), assessment of VAT (per 1-SD) was strongly associated with HFpEF [2.78 (1.62–4.76)]. SAT was not associated with HFpEF nor HFrEF. Conclusions: In a multiethnic cohort free of CVD, CT-measured VAT was independently associated with incident hospitalized HFpEF but not HFrEF. Measuring visceral fat at the time of CT imaging for other indications may offer additional prognostication of HF risk.

The role of obesity in the pathogenesis of heart failure (HF), and in particular HF with preserved ejection fraction (HFpEF), has drawn significant attention in recent years. The prevalence of both obesity and HFpEF has increased worldwide over the past decades and when present concomitantly suggests an obese-HFpEF phenotype. Anthropometrics, including body mass index, waist circumference, and waist-to-hip ratio, are associated with incident HFpEF. However, the cardiovascular effects of obesity may actually be driven by the distribution of fat, which can accumulate in the epicardial, visceral, and subcutaneous compartments. Regional fat can be quantified using non-invasive imaging techniques, including computed tomography, magnetic resonance imaging, and dual-energy X-ray absorptiometry. Regional variations in fat accumulation are associated with different HFpEF risk profiles, whereby higher epicardial and visceral fat have a much stronger association with HFpEF risk compared with elevated subcutaneous fat. Thus, regional adiposity may serve a pivotal role in the pathophysiology of HFpEF contributing to decreased cardiopulmonary fitness, impaired left ventricular compliance, upregulation of local and systemic inflammation, promotion of neurohormonal dysregulation, and increased intra-abdominal pressure and vascular congestion. Strategies to reduce total and regional adiposity have shown promise, including intensive exercise, dieting, and bariatric surgery programmes, but few studies have focused on HFpEF-related outcomes among obese. Further understanding the role these variable fat depots play in the progression of HFpEF and HFpEF-related hospitalizations may provide therapeutic targets in treating the obese-HFpEF phenotype.

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Highlights There is a bidirectional relationship between HF and liver disease. NAFLD may drive some HFpEF phenotypes. This review proposes 3 HFpEF phenotypes: obstructive HFpEF, metabolic HFpEF/NAFLD, and advanced liver disease/cirrhosis HFpEF. Additional studies are required to explore the pathophysiology and hemodynamic parameters of these phenotypes and investigate potential treatments.

Background Nonalcoholic fatty liver disease (NAFLD) and heart failure (HF) are increasing in prevalence. The independent association between NAFLD and downstream risk of HF and HF subtypes (HF with preserved ejection fraction and HF with reduced ejection fraction) is not well established. Methods and Results This was a retrospective, cohort study among Medicare beneficiaries. We selected Medicare beneficiaries without known prior diagnosis of HF. NAFLD was defined using presence of 1 inpatient or 2 outpatient claims using International Classification of Diseases, Ninth Revision, Clinical Modification ( ICD‐9‐CM ), claims codes. Incident HF was defined using at least 1 inpatient or at least 2 outpatient HF claims during the follow‐up period (October 2015–December 2016). Among 870 535 Medicare patients, 3.2% (N=27 919) had a clinical diagnosis of NAFLD. Patients with NAFLD were more commonly women, were less commonly Black patients, and had a higher burden of comorbidities, such as diabetes, obesity, and kidney disease. Over a mean 14.3 months of follow‐up, patients with (versus without) baseline NAFLD had a significantly higher risk of new‐onset HF in unadjusted (6.4% versus 5.0%; P <0.001) and adjusted (adjusted hazard ratio [HR] [95% CI], 1.23 [1.18–1.29]) analyses. Among HF subtypes, the association of NAFLD with downstream risk of HF was stronger for HF with preserved ejection fraction (adjusted HR [95% CI], 1.24 [1.14–1.34]) compared with HF with reduced ejection fraction (adjusted HR [95% CI], 1.09 [0.98–1.2]). Conclusions Patients with NAFLD are at an increased risk of incident HF, with a higher risk of developing HF with preserved ejection fraction versus HF with reduced ejection fraction. The persistence of an increased risk after adjustment for clinical and demographic factors suggests an epidemiological link between NAFLD and HF beyond the basis of shared risk factors that requires further investigation.

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Background Obesity contributes significantly to risk of atherosclerotic cardiovascular disease (ASCVD) and especially for heart failure (HF). An elevated body mass index (BMI) in older adults might not carry the same risk as in younger adults, but measured weights at other lifetime points are often not available. We determined the associations of self‐reported weights from early‐ and mid‐adulthood, after accounting for measured weight at older age, with incident HF/ASCVD risk. Methods and Results We studied 6437 MESA (Multi‐Ethnic Study of Atherosclerosis) participants (aged 45–84, free of baseline HF/ASCVD) with self‐reported weights at ages 20 and 40 years (by questionnaire), measured weights at up to 5 in‐person examinations (2000–2012), and follow‐up for adjudicated HF/ASCVD events. Participant mean±SD age at the baseline examination was 62.2±10.2 years. Over median follow‐up of 13 years, 290 HF and 828 ASCVD events occurred. After adjustment for cardiovascular risk factors and baseline BMI, higher self‐reported weights at ages 20 and 40 years were independently associated with increased risk of incident HF with hazard ratios (95% confidence interval) of 1.27 (1.07–1.50) and 1.36 (1.18–1.57), respectively, per 5‐kg/m 2 higher BMI. For incident ASCVD, only higher BMI at age 20 years was associated after accounting for current BMI (1.13 [1.01–1.26] per 5 kg/m 2 ). Obesity during follow‐up examinations was also associated with incident HF (1.72 [1.21–2.45]) but not ASCVD. Conclusions Self‐reported lifetime weight is a low‐tech tool easily utilized in any clinical encounter. Although subject to recall bias, self‐reported weights may provide prognostic information about future HF risk, incremental to current BMI, in a multiethnic cohort of middle‐aged to older adults. Clinical Trial Registration URL: http://www.clinicaltrials.gov . Unique identifier: NCT00005487.

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