Pericardial Fat and the Risk of Heart Failure

Kenchaiah, Satish; Ding, Jingzhong; Carr, J. Jeffrey; Allison, Matthew; Budoff, Matthew J.; Tracy, Russell P.; Burke, Gregory L.; McClelland, Robyn L.; Arai, Andrew E; Bluemke, David A.

doi:10.1016/j.jacc.2021.04.003

Cited by 85 publications

(103 citation statements)

References 40 publications

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“…[12][13][14]34,[38][39][40] EAT may have a different impact on HFpEF and HFm-rEF. The study by Kenchaiah et al 15 showed that EAT accumulation was particularly associated with new-onset HFpEF and to a lesser degree to HFmrEF. However, in an earlier study by our group, we did not observe significant differences in EAT between these patient populations.…”

Section: Discussionmentioning

confidence: 99%

Epicardial Adipose Tissue and Outcome in Heart Failure With Mid-Range and Preserved Ejection Fraction

Woerden

Veldhuisen

Manintveld

et al. 2022

Circ: Heart Failure

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Background: Epicardial adipose tissue (EAT) accumulation is thought to play a role in the pathophysiology of heart failure (HF) with mid-range and preserved ejection fraction, but its effect on outcome is unknown. We evaluated the prognostic value of EAT volume measured with cardiac magnetic resonance in patients with HF with mid-range ejection fraction and HF with preserved ejection fraction. Methods: Patients enrolled in a prospective multicenter study that investigated the value of implantable loop-recorders in HF with mid-range ejection fraction and HF with preserved ejection fraction were analyzed. EAT volume was quantified with cardiac magnetic resonance. Main outcome was the composite of all-cause mortality and first HF hospitalizations. Hazard ratios (HR) and 95% CI are described per SD increase in EAT. Results: We studied 105 patients (mean age 72±8 years, 50% women, and mean left ventricular ejection fraction 53±8%). During median follow-up of 24 (17–25) months, 31 patients (30%) died or were hospitalized for HF. In univariable analysis, EAT was significantly associated with a higher risk of the composite outcome (HR, 1.76 [95% CI, 1.24–2.50], P =0.001), and EAT remained associated with outcome after adjustment for age, sex, and body mass index (HR, 1.61 [95% CI, 1.13–2.31], P =0.009), and after adjustment for New York Heart Association functional class and N-terminal of pro-brain natriuretic peptide (HR, 1.53 [95% CI, 1.04–2.24], P =0.03). Furthermore, EAT was associated with all-cause mortality alone (HR, 2.06 [95% CI, 1.26–3.37], P =0.004) and HF hospitalizations alone (HR, 1.54 [95% CI, 1.04–2.30], P =0.03). Conclusions: EAT accumulation is associated with adverse prognosis in patients with HF with mid-range ejection fraction and HF with preserved ejection fraction. This finding supports the importance of EAT in these patients with HF. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01989299.

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Section: Discussionmentioning

confidence: 99%

Epicardial Adipose Tissue and Outcome in Heart Failure With Mid-Range and Preserved Ejection Fraction

Woerden

Veldhuisen

Manintveld

et al. 2022

Circ: Heart Failure

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“…Finally, in a recent analysis of MESA, EAT also was associated with an increased risk of incident HF ( Kenchaiah et al, 2021 ). High EAT volumes defined as > 70 cm 3 for women and > 120 cm 3 for men correlated with a twofold increased incidence of HF in women and 53% higher risk in men.…”

Section: Effects Of Obesity On the Heartmentioning

confidence: 99%

“…MESA, BMI, and VAT was significantly elevated in patients with incident HFpEF (29.9 vs. 27.8, p 0.01; 230.7 cm 3 vs. 162.6 cm 3 p < 0.001, respectively) ( Rao et al, 2018 ). Patients with EAT have elevated BMIs and increased VAT, further linking BMI as an indirect measure of VAT and EAT ( Kenchaiah et al, 2021 ).…”

Section: Effects Of Obesity On the Heartmentioning

confidence: 99%

Diabetes Mellitus and Heart Failure With Preserved Ejection Fraction: Role of Obesity

et al. 2022

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Heart failure with preserved ejection fraction is a growing epidemic and accounts for half of all patients with heart failure. Increasing prevalence, morbidity, and clinical inertia have spurred a rethinking of the pathophysiology of heart failure with preserved ejection fraction. Unlike heart failure with reduced ejection fraction, heart failure with preserved ejection fraction has distinct clinical phenotypes. The obese-diabetic phenotype is the most often encountered phenotype in clinical practice and shares the greatest burden of morbidity and mortality. Left ventricular remodeling plays a major role in its pathophysiology. Understanding the interplay of obesity, diabetes mellitus, and inflammation in the pathophysiology of left ventricular remodeling may help in the discovery of new therapeutic targets to improve clinical outcomes in heart failure with preserved ejection fraction. Anti-diabetic agents like glucagon-like-peptide 1 analogs and sodium-glucose co-transporter 2 are promising therapeutic modalities for the obese-diabetic phenotype of heart failure with preserved ejection fraction and aggressive weight loss via lifestyle or bariatric surgery is still key to reverse adverse left ventricular remodeling. This review focuses on the obese-diabetic phenotype of heart failure with preserved ejection fraction highlighting the interaction between obesity, diabetes, and coronary microvascular dysfunction in the development and progression of left ventricular remodeling. Recent therapeutic advances are reviewed.

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“…Epicardial and pericardial fat are associated with cardiovascular risk [ 142 , 143 , 144 , 145 ]. In humans, OPN expression increases in the epicardial fat of patients with CAD compared to control subjects and is associated with the presence of calcified atherosclerotic plaques.…”

Section: Immunosenescence In Cardiovascular Diseasesmentioning

confidence: 99%

T Cell Immunosenescence in Aging, Obesity, and Cardiovascular Disease

Shirakawa

Sano

2021

Cells

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Although advances in preventive medicine have greatly improved prognosis, cardiovascular disease (CVD) remains the leading cause of death worldwide. This clearly indicates that there remain residual cardiovascular risks that have not been targeted by conventional therapies. The results of multiple animal studies and clinical trials clearly indicate that inflammation is the most important residual risk and a potential target for CVD prevention. The immune cell network is intricately regulated to maintain homeostasis. Ageing associated changes to the immune system occurs in both innate and adaptive immune cells, however T cells are most susceptible to this process. T-cell changes due to thymic degeneration and homeostatic proliferation, metabolic abnormalities, telomere length shortening, and epigenetic changes associated with aging and obesity may not only reduce normal immune function, but also induce inflammatory tendencies, a process referred to as immunosenescence. Since the disruption of biological homeostasis by T cell immunosenescence is closely related to the development and progression of CVD via inflammation, senescent T cells are attracting attention as a new therapeutic target. In this review, we discuss the relationship between CVD and T cell immunosenescence associated with aging and obesity.

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Pericardial Fat and the Risk of Heart Failure

Cited by 85 publications

References 40 publications

Epicardial Adipose Tissue and Outcome in Heart Failure With Mid-Range and Preserved Ejection Fraction

Epicardial Adipose Tissue and Outcome in Heart Failure With Mid-Range and Preserved Ejection Fraction

Diabetes Mellitus and Heart Failure With Preserved Ejection Fraction: Role of Obesity

T Cell Immunosenescence in Aging, Obesity, and Cardiovascular Disease

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