Abstract:EAT can be effective on blood pressure by several mechanisms. In this study, for the first time in the literature, the association of EAT with RHT is reported.
“…Some previous studies conducted by other authors confirm the increase in size of EAT depots among the patients with EH [18,19,31,32,33,34,35]. The difference between our study and the majority of previous studies is that along with EAT thickness measurements we have also measured EAT volume.…”
Background and Objectives: Epicardial adipose tissue (EAT) is shown to be an important factor in the development of coronary artery disease, but numerous pathophysiological mechanisms of its action are still only partially understood. There is a lack of studies on its association with different grades of essential hypertension (EH). Therefore, we aimed to evaluate the association between size of EAT depots and the risk of EH taking into account its grade. Materials and Methods: Non-obese adult patients with various cardiovascular diseases were investigated: 157 of them had essential hypertension and 101 did not. Hypertensive patients were assigned to three groups according to the grade of hypertension. EAT volume and thickness on ventricular free walls (6 locations) and grooves (5 locations) were measured using cardiac magnetic resonance imaging and compared between groups. A regression model for the prediction of EH was constructed. Results: In general, thickness (in all locations) and volume of EAT depots was greater among hypertensive patients than in normotensive (NORM) group. Mean EAT thickness in all 11 locations and EAT volume were lower in NORM than in grade 1 hypertension group; similarly, EAT volume was lower in grade 1 than in grade 2 hypertension group. EAT accumulation did not differ between grade 2 and severe hypertension groups. EAT volume, dyslipidaemia status, body mass index, and age were independent predictors for EH in regression model. Conclusions: EAT accumulation is larger among hypertensive than normotensive individuals. Measurement of EAT depots could be beneficial for identification of hypertensive patients and prediction of hypertension severity.
“…Some previous studies conducted by other authors confirm the increase in size of EAT depots among the patients with EH [18,19,31,32,33,34,35]. The difference between our study and the majority of previous studies is that along with EAT thickness measurements we have also measured EAT volume.…”
Background and Objectives: Epicardial adipose tissue (EAT) is shown to be an important factor in the development of coronary artery disease, but numerous pathophysiological mechanisms of its action are still only partially understood. There is a lack of studies on its association with different grades of essential hypertension (EH). Therefore, we aimed to evaluate the association between size of EAT depots and the risk of EH taking into account its grade. Materials and Methods: Non-obese adult patients with various cardiovascular diseases were investigated: 157 of them had essential hypertension and 101 did not. Hypertensive patients were assigned to three groups according to the grade of hypertension. EAT volume and thickness on ventricular free walls (6 locations) and grooves (5 locations) were measured using cardiac magnetic resonance imaging and compared between groups. A regression model for the prediction of EH was constructed. Results: In general, thickness (in all locations) and volume of EAT depots was greater among hypertensive patients than in normotensive (NORM) group. Mean EAT thickness in all 11 locations and EAT volume were lower in NORM than in grade 1 hypertension group; similarly, EAT volume was lower in grade 1 than in grade 2 hypertension group. EAT accumulation did not differ between grade 2 and severe hypertension groups. EAT volume, dyslipidaemia status, body mass index, and age were independent predictors for EH in regression model. Conclusions: EAT accumulation is larger among hypertensive than normotensive individuals. Measurement of EAT depots could be beneficial for identification of hypertensive patients and prediction of hypertension severity.
“…Many studies agree that the amount of EAT is higher in hypertensive adult patients [ 16 , 26 , 27 , 28 , 29 ]. There are fewer studies which propose this link in children and adolescents [ 19 ].…”
Background and purpose: Epicardial adipose tissue (EAT) is a metabolically active tissue located on the surface of the myocardium, which might have a potential impact on cardiac function and morphology. The aim of this study was to evaluate whether EAT is associated with essential arterial hypertension (AH) in children and adolescents. Methods: Prospective cardiovascular magnetic resonance (CMR) study and clinical evaluation were performed on 72 children, 36 of whom were diagnosed with essential AH, and the other 36 were healthy controls. The two groups were compared in volume and thickness of EAT, end-diastolic volume, end-systolic volume, stroke volume, left ventricular (LV) ejection fraction, average heart mass, average LV myocardial thickness, peak filling rate, peak filling time and clinical parameters. Results: Hypertensive patients have a higher volume (16.5 ± 1.9 cm3 and 10.9 ± 1.5 cm3 (t = −13.815, p < 0.001)) and thickness (0.8 ± 0.3 cm and 0.4 ± 0.1 cm, (U = 65.5, p < 0.001)) of EAT compared to their healthy peers. The volume of EAT might be a potential predictor of AH in children. Conclusions: Our study indicates that the volume of EAT is closely associated with hypertension in children and adolescents.
“…A larger EAT depot could have important health consequences. For example, the thickness of human EAT is correlated at only 8 years of age with increased risk of higher corrected-BMI and metabolic syndrome (Barbaro et al, 2016), and the volume and density of EAT is associated with cardiovascular disease including hypertension (Börekçi et al, 2015), resistant hypertension (Erdogan et al, 2016), myocardial ischemia (Hell et al, 2016) and coronary artery calcification (Gauss et al, 2015).…”
In utero
treatment with glucocorticoids have been suggested to reprogram postnatal cardiovascular function and stress responsiveness. However, little is known about the effects of prenatal exposure to the natural corticosteroid, cortisol, on postnatal cardiovascular system or metabolism. We have demonstrated an increased incidence of stillbirth in sheep pregnancies in which there is mild maternal hypercortisolemia caused by infusion of 1 mg/kg/d cortisol. In order to model corticosteroid effects in the neonate, we created a second model in which cortisol was infused for 12 h per day for a daily infusion of 0.5 mg/kg/d. In this model we had previously found that neonatal plasma glucose was increased and plasma insulin was decreased compared to those in the control group, and that neonatal ponderal index and kidney weight were reduced and left ventricular wall thickness was increased in the 2 week old lamb. In this study, we have used transcriptomic modeling to better understand the programming effect of this maternal hypercortisolemia in these hearts. This is a time when both terminal differentiation and a shift in the metabolism of the heart from carbohydrates to lipid oxidation are thought to be complete. The transcriptomic model indicates suppression of genes in pathways for fatty acid and ketone production and upregulation of genes in pathways for angiogenesis in the epicardial adipose fat (EAT). The transcriptomic model indicates that RNA related pathways are overrepresented by downregulated genes, but ubiquitin-mediated proteolysis and protein targeting to the mitochondria are overrepresented by upregulated genes in the intraventricular septum (IVS) and left ventricle (LV). In IVS the AMPK pathway and adipocytokine signaling pathways were also modeled based on overrepresentation by downregulated genes. Peroxisomal activity is modeled as increased in EAT, but decreased in LV and IVS. Our results suggest that pathways for lipids as well as cell proliferation and cardiac remodeling have altered activity postnatally after the
in utero
cortisol exposure. Together, this model is consistent with the observed increase in cardiac wall thickness at necropsy and altered glucose metabolism observed
in vivo
, and predicts that
in utero
exposure to excess maternal cortisol will cause postnatal cardiac hypertrophy and altered responses to oxidative stress.
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