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- W2490185523 abstract "Sympathetic nervous system (SNS) activation has long been known to be a cardinal feature in the pathophysiology of cardiac remodeling and systolic heart failure (SHF). It was reported to have implications for both disease progression and survival. SNS activation is assumed to be secondary to the decrease of sympathoinhibitory reflexes usually drove by the stimulation of afferent mechanoreceptors and by the increase of efferent sympatho-excitatory mechanisms associated with alteration in autonomic regulation. Activation of cardiac and peripheral sympathetic nervous systems has been linked to the rate of disease progression and sudden death. The main retrospective and prospective studies have shown that cardiac neuronal uptake based on Heart-Mediastinum Ratio (HMR) by I-Metaiodobenzylguanidine (MIBG) imaging was a prognostic indicator of severe heart failure and/or ventricular arrhythmia if HMR was less than 1.6 in patients with a left ventricular ejection fraction less than 35%. These findings have been the rationale for the use of betaadrenergic blocking agents in the management of patients with SHF. Several observations have suggested that ventricular systolic dysfunction per se was not the principal stimulus to sympathetic activation. If the decrease of sympatho-inhibitory reflexes is directly linked to the ventricular systolic dysfunction though the decrease of the cardiac output, mechanisms underlying the autonomic dysregulation seem more generalized. Among the parameters acting on nonbaroreflex-mediated sympathoexcitation, sleep-disordered breathing is one of the main actors." @default.
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- W2490185523 date "2016-07-25" @default.
- W2490185523 modified "2023-09-23" @default.
- W2490185523 title "Sympathetic nervous system, systolic heart failure, and central sleep apnea: Are we about to find the missing link?" @default.
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- W2490185523 doi "https://doi.org/10.1007/s12350-016-0584-2" @default.
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