Epicardial Adipose Tissue and Myocardial Fibrosis in Aortic Stenosis Relationship With Symptoms and Outcomes

Davin, Laurent; Nchimi, Alain; Ilardi, Federica; Marchetta, Stella; Gach, Olivier; Maréchal, Patrick; Cimino, Sara; Bruyère, Pierre-Julien; Georgiopoulos, A; Dibato, John Epoh; D’Amico, G.; Galderisi, Maurizio; Parisi, Valentina; Oury, Cécile; Lancellotti, Patrizio

doi:10.1016/j.jcmg.2018.06.025

Cited by 23 publications

(14 citation statements)

References 4 publications

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“…These cells secrete proinflammatory cytokines, such as interleukin 1β (IL-1β), tumor necrosis factor (TNF-a), IL-6, IL-8, insulin-like growth factor 1, transforming growth factor β (TGF-β), thus promoting the differentiation of resident valvular interstitial cells to an osteoblast-like phenotype, leading to bone deposition and calcification. The increase of EAT thickness and its pro-inflammatory status, through the secretion of pro-inflammatory cytokines may promote these inflammatory and atherogenic phenomena occurring in the aortic valve; moreover, EAT pro-inflammatory activation may drive LV hypertrophy and fibrosis promoting adverse remodeling and evolves towards diastolic dysfunction, finally leading to heart failure [38]. A close correlation between an increase in EAT and increase in LV mass has been described in literature and supports the role of EAT in promoting myocardial hypertrophy [39].…”

Section: Eat and Asmentioning

confidence: 99%

The role of inflammation and metabolic risk factors in the pathogenesis of calcific aortic valve stenosis

et al. 2020

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Given the epidemiologic increase of aged population in the world, aortic stenosis (AS) represents now the most common valvular heart disease in industrialized countries. It is a very challenging disease, representing an important cause of morbidity, hospitalization and death in the elderly population. It is widely recognized that AS is the result of a very complex active process, driven by inflammation and involving multifactorial pathological mechanisms promoting valvular calcification and valvular bone deposition. Several evidence suggest that epicardial adipose tissue (EAT), the visceral fat depot of the heart, represents a direct source of cytokines and could mediate the deleterious effects of systemic inflammation on the myocardium. Importantly, obesity and metabolic disorders are associated with chronic systemic inflammation leading to a significant increase of EAT amount and to a pro-inflammatory phenotypic shift of this fat depot. It has been hypothesized that the EAT inflammatory state can influence the structure and function of the heart, thus contributing to the pathogenesis of several cardiac diseases, including calcific AS. The current review will discuss the recently discovered mechanisms involved in the pathogenesis of AS, with particular attention to the role of inflammation, metabolic risk factors and pro-fibrotic and pro-osteogenic signal pathways promoting the onset and progression of the disease. Moreover, it will be explored the potential role of EAT in the AS pathophysiology.

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Section: Eat and Asmentioning

confidence: 99%

The role of inflammation and metabolic risk factors in the pathogenesis of calcific aortic valve stenosis

et al. 2020

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“…In patients with aortic stenosis (AS), left ventricular hypertrophy (LVH) is considered to be an adaptive response to the increased afterload [1,2]. LVH reduces systolic wall stress and helps to preserve LV ejection fraction (LVEF), but it may lead to some long term adverse consequences such as myocardial fibrosis, diastolic filling impairment and finally LV dysfunction [3]. Different types of LVH have been previously described.…”

Section: Introductionmentioning

confidence: 99%

Myocardial contractility recovery following acute pressure unloading after transcatheter aortic valve intervention (TAVI) in patients with severe aortic stenosis and different left ventricular geometry: a multilayer longitudinal strain echocardiographicanalysis

Cimino

Monosilio

Luongo

et al. 2020

Int J Cardiovasc Imaging

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Aim of the present study was to describe the left ventricular longitudinal strain (LS) in all myocardial layers in patients with severe aortic stenosis (AS), preserved left ventricular ejection fraction (LVEF) in different LV geometry and to compare LS analysis before and early after acute LV unloading provided by transcatheter aortic valve implantation (TAVI). 68 patients were enrolled. LS was measured from the endocardial layer (Endo-LS), epicardial layer (Epi-LS) and full thickness of myocardium (Transmural-LS) before and after TAVI. Patients were divided in two groups accordingly with relative wall thickness (RWT): concentric LV hypertrophy (cLVH) vs eccentric LV hypertrophy (eLVH). Less impaired values of LS at baseline were observed, in all layers, in patients with cLVHas compared to patients with eLVH (Endo-LS was − 13.2 ± 2 vs − 11.1±3 %, p = 0.041; Epi-LS was − 11.8 ± 1.8 vs − 9.9 ± 3 %, p = 0.043; Transmural-LS was − 12.3 ± 1.8 vs − 10.49 ± 3.3 %, p = 0.02, respectively). A significant improvement in endocardial LS (Endo-LS) after TAVI was detected only in cLVH(− 13 ± 2 vs − 14 ± 2, p = 0.011). Our findings documented that concentric LVH had better basal strain function and showed a better myocardial recovery after TAVI compared to eLVH.

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“…Third, our study group is composed of both CABG and VR patients. Although the mechanisms driving the two pathologies are different, many studies demonstrated the involvement of EAT amount and secretome in the progression of both diseases [14,[49][50][51][52]. Fourth, since our study is cross-sectional, our findings cannot imply causality.…”

Section: Mediators Of Inflammationmentioning

confidence: 71%

PCSK9 Expression in Epicardial Adipose Tissue: Molecular Association with Local Tissue Inflammation

Dozio

Ruscica

Vianello

et al. 2020

Mediators of Inflammation

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Epicardial adipose tissue (EAT) has the unique property to release mediators that nourish the heart in healthy conditions, an effect that becomes detrimental when volume expands and proinflammatory cytokines start to be produced. Proprotein convertase subtilisin/kexin type 9 (PCSK9), a proinflammatory mediator involved in atherosclerosis, is also produced by visceral fat. Due to the correlation of inflammation with PCSK9 and EAT enlargement, we evaluated whether PCSK9 was expressed in EAT and associated with EAT inflammation and volume. EAT samples were isolated during surgery. EAT thickness was measured by echocardiography. A microarray was used to explore EAT transcriptoma. The PCSK9 protein levels were measured by Western Blot in EAT and ELISA in plasma. PCSK9 was expressed at both the gene and protein levels in EAT. We found a positive association with EAT thickness and local proinflammatory mediators, in particular, chemokines for monocytes and lymphocytes. No association was found with the circulating PCSK9 level. The expression of PCSK9 in EAT argues that PCSK9 is part of the EAT secretome and EAT inflammation is associated with local PCSK9 expression, regardless of circulating PCSK9 levels. Whether reducing EAT inflammation or PCSK9 local levels may have beneficial effects on EAT metabolism and cardiovascular risk needs further investigations.

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Epicardial Adipose Tissue and Myocardial Fibrosis in Aortic Stenosis Relationship With Symptoms and Outcomes

Cited by 23 publications

References 4 publications

The role of inflammation and metabolic risk factors in the pathogenesis of calcific aortic valve stenosis

The role of inflammation and metabolic risk factors in the pathogenesis of calcific aortic valve stenosis

Myocardial contractility recovery following acute pressure unloading after transcatheter aortic valve intervention (TAVI) in patients with severe aortic stenosis and different left ventricular geometry: a multilayer longitudinal strain echocardiographicanalysis

PCSK9 Expression in Epicardial Adipose Tissue: Molecular Association with Local Tissue Inflammation

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