2016
DOI: 10.1161/circresaha.116.308621
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Cardiac Sympathetic Denervation in the Failing Heart

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Cited by 12 publications
(9 citation statements)
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“…EAT can also be involved in the pathogenesis of heart failure through neurohormonal mechanisms via the intrinsic adrenergic and cholinergic nerves, which interact with the extrinsic cardiac sympathetic and parasympathetic nervous systems 113 115 . EAT is, therefore, an important source of catecholamines, both noradrenaline and adrenaline 116 .…”
Section: Role Of Eat In Cardiovascular Diseasementioning
confidence: 99%
“…EAT can also be involved in the pathogenesis of heart failure through neurohormonal mechanisms via the intrinsic adrenergic and cholinergic nerves, which interact with the extrinsic cardiac sympathetic and parasympathetic nervous systems 113 115 . EAT is, therefore, an important source of catecholamines, both noradrenaline and adrenaline 116 .…”
Section: Role Of Eat In Cardiovascular Diseasementioning
confidence: 99%
“…These EAT nerves represent a significant source of norepinephrine and epinephrine. White (30) reported that an increase in EAT volume correlates with a hyperactive adrenergic signaling resulting from an increased catecholamine biosynthesis. EAT thickness is also associated with higher levels of inflammatory cytokines, and a higher inflammatory state can subsequently lead to a higher structural and electrical remodeling of the heart and finally a higher incidence of arrhythmia.…”
Section: Discussionmentioning
confidence: 99%
“…Finally, an Italian study in systolic heart failure patients identified a highly significant correlation between EAT thickness and the extent of cardiac sympathetic denervation [ 65 ]. Specifically, EAT thickness was reported to be useful as an independent predictor of SNS dysfunction, since left ventricular mass, EAT thickness, and cardiac sympathetic denervation were found to correlate well with one another in systolic heart failure patients [ 66 ].…”
Section: Autonomic Dysregulation and Eat: Implications For Human Afib...mentioning
confidence: 99%
“…Although the reported elevations in expression of these enzymes were astonishingly huge (~8-fold for the mRNAs and ~15-fold (!) for the proteins), raising concerns about the accuracy of the reported values, this study clearly identified human EAT as a significant source of both NE and Epi, at least in the context of systolic heart failure, which might contribute to the well-documented SNS hyperactivity that accompanies and aggravates human heart failure [ 65 , 66 ]. The increased catecholamine biosynthetic activity of EAT in systolic heart failure, which is obviously the result of a thickened EAT (higher volume EAT contains more adipocytes synthesizing more catecholamines), adds to the total catecholamine accumulation in the failing heart’s EAT [ 65 ].…”
Section: Autonomic Dysregulation and Eat: Implications For Human Afib...mentioning
confidence: 99%