Expression of epicardial adipose tissue thermogenic genes in patients with reduced and preserved ejection fraction heart failure

Pérez‐Belmonte, Luis M.; Moreno-Santos, Inmaculada; Gómez‐Doblas, Juan José; García‐Pinilla, José Manuel; Morcillo‐Hidalgo, Luis; Garrido‐Sánchez, Lourdes; Santiago‐Fernández, Concepción; Crespo-Leiro, María G.; Carrasco-Chinchilla, Fernando; Sánchez‐Fernández, Pedro L.; Teresa–Galván, Eduardo de; Jiménez-Navarro, Manuel F.

doi:10.7150/ijms.19854

Cited by 31 publications

(21 citation statements)

References 9 publications

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“…Doesch et al [32] measured EAT volume in patients with dilated cardiomyopathy using MRI and found that it was associated with HF with reduced EF, but not with a preserved EF as in our study. Other studies are in line with that and show a correlation for EAT and reduced LV-EF [33,34]. We concur that the influence of EAT volume on LVDD in patients with AS might be of minor concern as shown by our preliminary data and that an increase in afterload and other changes associated with AS may play a more important role in causing LVDD and LV hypertrophy.…”

Section: Plos Onesupporting

confidence: 90%

Impact of epicardial adipose tissue volume upon left ventricular dysfunction in patients with mild-to-moderate aortic stenosis: A post-hoc analysis

et al. 2020

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Background Aortic stenosis (AS) may lead to diastolic dysfunction and later on heart failure (HF) with preserved left ventricular ejection fraction (HFpEF) via increased afterload and left-ventricular (LV) hypertrophy. Since epicardial adipose tissue (EAT) is a metabolically active fat depot that is adjacent to the myocardium and can influence cardiomyocytes and LV function via secretion of proinflammatory cytokines, we hypothesized that high amounts of EAT, as assessed by computed tomography (CT), may aggravate the development and severity of LV hypertrophy and diastolic dysfunction in the context of AS. Methods We studied 50 patients (mean age 71 ± 9 years; 9 women) in this preliminary study with mild or moderate AS and mild to severe LV diastolic dysfunction (LVDD), diagnosed by echocardiography, who underwent non-contrast cardiac CT and echocardiography. EAT parameters were measured on 2nd generation dual source CT. Conventional two-dimensional echocardiography and Tissue Doppler Imaging (TDI) was performed to assess LV function and to derive myocardial straining parameter. All patients had a preserved LV ejection fraction > 50%. Data was analysed using Pearson's correlation. Results Only weak correlation was found between EAT volume or density and E/é ratio as LVDD marker (r =-.113 p = .433 and r = .260, p = .068 respectively). Also, EAT volume or density were independent from Global Strain Parameters (r = 0.058 p = .688 and r =-0.207 p = .239). E/é ratio was strongly associated with LVDD (r = .761 p�0.0001) and Strain Parameters were moderately associated with LV Ejection Fraction (r =-.669 p�0.001 and r =-.454 P�0.005).

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Section: Plos Onesupporting

confidence: 90%

Impact of epicardial adipose tissue volume upon left ventricular dysfunction in patients with mild-to-moderate aortic stenosis: A post-hoc analysis

et al. 2020

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“…This way, it is suggested epicardial fat may affect the myocardium by directly releasing adipokines near the cardiomyocytes or via the vasa vasora where adipokines may interact with the myocardium downstream causing cardiac endothelial dysfunction and remodelling, possibly leading to HF with LVEF >40% and/or atrial fibrillation . For HFrEF, epicardial fat may yield different effects on the myocardium, as in these patients the pathophysiological mechanism resulting in HF differs from those with HF with LVEF >40% and epicardial fat seems to be reduced compared to controls instead of increased . On the other hand, epicardial fat may also negatively impact cardiac performance by a direct mechanical effect caused by increased pericardial restraint and enhanced ventricular interdependence, as recently shown in a haemodynamic exercise study in patients with HFpEF .…”

Section: Discussionmentioning

confidence: 50%

“…26,27 For HFrEF, epicardial fat may yield different effects on the myocardium, as in these patients the pathophysiological mechanism resulting in HF differs from those with HF with LVEF >40% and epicardial fat seems to be reduced compared to controls instead of increased. 11,28 On the other hand, epicardial fat may also negatively impact cardiac performance by a direct mechanical effect caused by increased pericardial restraint and enhanced ventricular interdependence, as recently shown in a haemodynamic exercise study in patients with HFpEF. 6 Unfortunately for the present study, dynamic exercise CMR was Table 3 Associations between epicardial fat, patient characteristics and cardiac magnetic resonance parameters HF patients (n = 64) Controls (n = 20) .…”

Section: Discussionmentioning

confidence: 93%

Epicardial fat in heart failure patients with mid‐range and preserved ejection fraction

Woerden

Gorter

Westenbrink

et al. 2018

European J of Heart Fail

204

180

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Aims Adipose tissue and inflammation may play a role in the pathophysiology of patients with heart failure (HF) with mildly reduced or preserved ejection fraction. We therefore investigated epicardial fat in patients with HF with preserved (HFpEF) and mid‐range ejection fraction (HFmrEF), and related this to co‐morbidities, plasma biomarkers and cardiac structure. Methods and results A total of 64 HF patients with left ventricular ejection fraction >40% and 20 controls underwent routine cardiac magnetic resonance examination. Epicardial fat volume was quantified on short‐axis cine stacks covering the entire epicardium and was related to clinical correlates, biomarkers associated with inflammation and myocardial injury, and cardiac function and contractility on cardiac magnetic resonance. HF patients and controls were of comparable age, sex and body mass index. Total epicardial fat volume was significantly higher in HF patients compared to controls (107 mL/m 2 vs. 77 mL/m 2 , P <0.0001). HF patients with atrial fibrillation and/or type 2 diabetes mellitus had more epicardial fat than HF patients without these co‐morbidities (116 vs. 100 mL/m 2 , P =0.03, and 120 vs. 97 mL/m 2 , P =0.001, respectively). Creatine kinase‐MB, troponin T and glycated haemoglobin in patients with HF were positively correlated with epicardial fat volume (R =0.37, P =0.006; R =0.35, P =0.01; and R =0.42, P =0.002, respectively). Conclusion Heart failure patients had more epicardial fat compared to controls, despite similar body mass index. Epicardial fat volume was associated with the presence of atrial fibrillation and type 2 diabetes mellitus and with biomarkers related to myocardial injury. The clinical implications of these findings are unclear, but warrant further investigation.

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“…However, patients with HFrEF exhibit evidence of decreased epicardial fat, 54,55 which typically provides a nourishing function in these individuals. 56 By contrast, in patients with HFpEF, epicardial adipose volume is increased and is a source of inflammation and injury to the underlying ventricular muscle. 15,37,57 This inflammatory process appears to be the primary pathophysiological determinant of HFpEF, whereas cardiomyocyte loss and stretch are the principal drivers of HFrEF.…”

Section: Differential Effects Of Statins In Preserved Vs Reduced Ejementioning

confidence: 99%

“…However, in the large‐scale clinical trials of rosuvastain in chronic heart failure, patients with HFpEF were poorly represented, either because they were excluded from participation or were not recruited; these trials focused on patients with impaired systolic function. However, patients with HFrEF exhibit evidence of decreased epicardial fat, which typically provides a nourishing function in these individuals . By contrast, in patients with HFpEF, epicardial adipose volume is increased and is a source of inflammation and injury to the underlying ventricular muscle .…”

Section: Differential Effects Of Statins In Preserved Vs Reduced Ejementioning

confidence: 99%

Are the effects of drugs to prevent and to treat heart failure always concordant? The statin paradox and its implications for understanding the actions of antidiabetic medications

Packer

2018

European J of Heart Fail

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Most treatments for chronic heart failure are effective both in preventing its onset and reducing its progression. However, statins prevent the development of heart failure, but they do not decrease morbidity and mortality in those with established heart failure. This apparent discordance cannot be explained by an effect to prevent interval myocardial infarctions. Instead, it seems that the disease that statins were preventing in trials of patients with a metabolic disorder was different from the disease that they were treating in trials of chronic heart failure. The most common phenotype of heart failure in patients with obesity and diabetes is heart failure with a preserved ejection fraction (HFpEF). In this disorder, the anti-inflammatory effects of statins might ameliorate myocardial fibrosis and cardiac filling abnormalities, but these actions may have little relevance to patients with heart failure and a reduced ejection fraction (HFrEF), whose primary derangement is cardiomyocyte loss and stretch. These distinctions may explain why statins were ineffective in trials that focused on HFrEF, but have been reported to produce favourable effects in observational studies of HFpEF. Similarly, selective cytokine antagonists were ineffective in HFrEF, but have been associated with benefits in HFpEF. These observations may have important implications for our understanding of the effects of antihyperglycaemic medications. Glucagon-like peptide-1 receptor agonists have had neutral effects on heart failure events in people at risk for HFpEF, but have exerted deleterious actions in HFrEF. Similarly, sodium-glucose co-transporter 2 inhibitors, which exert anti-inflammatory effects and reduce heart failure events in patients who are prone to HFpEF, may not be effective in HFrEF. The distinctions between HFrEF and HFpEF may explain why the effects of drugs on heart failure events in diabetes trials may not be relevant to their use in patients with systolic dysfunction.

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Expression of epicardial adipose tissue thermogenic genes in patients with reduced and preserved ejection fraction heart failure

Cited by 31 publications

References 9 publications

Impact of epicardial adipose tissue volume upon left ventricular dysfunction in patients with mild-to-moderate aortic stenosis: A post-hoc analysis

Impact of epicardial adipose tissue volume upon left ventricular dysfunction in patients with mild-to-moderate aortic stenosis: A post-hoc analysis

Epicardial fat in heart failure patients with mid‐range and preserved ejection fraction

Are the effects of drugs to prevent and to treat heart failure always concordant? The statin paradox and its implications for understanding the actions of antidiabetic medications

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