Renal function and cardiac adrenergic impairment in patients affected by heart failure

123I-MIBG imaging in heart failure: impact of comorbidities on cardiac sympathetic innervation

“…Of note, patients with highly impaired renal function were not included in that study [38]. More recently, Marsico et al showed that, in a population of 263 patient with mild-to-severe HF, 123 I-MIBG uptake was significantly reduced in HF patients with severely impaired renal function compared to HF subjects with preserved renal function [39]. Furthermore, the combination of chronic kidney dysfunction and impaired cardiac sympathetic nervous activity, assessed by 123 I-MIBG scintigraphy, has been shown to have a high prognostic value in the prediction of lethal arrhythmic events in HF patients [40].…”

An Overview of the Role of Calcium/Calmodulin-Dependent Protein Kinase in Cardiorenal Syndrome

“…Many inflammatory cytokines are enhanced in experimental models of renal ischemia (TNF-a, IL-1, and IL-6) and also markers, including the factor nuclear kappa B (NF-kB), which is very important for cell signaling during inflammatory processes (Trentin-Sonoda et al, 2015). Given that, some studies present the participation of inflammation as a cause of CKD progression in CHF patients (House et al, 2019;Marsico et al, 2019). During cardiac ischemia, myocytes release inflammatory cytokines (Colombo et al, 2012), and they can reach renal tissue, inducing local inflammation, apoptosis, or oxidative stress (Ronco and Di Lullo, 2014).…”

123I-MIBG cardiac sympathetic imaging provides further insight into cardiorenal interactions in systolic heart failure patients

“…Such downregulation of myocardial b1-receptors also results in a decrease in myocardial 123 I-MIBG uptake reflecting impaired cardiac sympathetic activity. 14,15 The study conducted by Marsico et al 7 adds further important information that a worsening of kidney function may not only be seen as a consequence of heart failure-related low cardiac output leading to low arterial blood pressures and relative hypoperfusion of the kidneys 13 but also as a source causing a further impairment of cardiac sympathetic activity associated with a further worsening of cardiac function. The exact kidney-related mechanism mediating a further decrease of cardiac sympathetic activity remain uncertain but it may offer a new and critical target of systolic heart failure therapy as current observations suggest.…”

“…1,2 Given the reported variability in myocardial response to medical RAS blockade, apart from suboptimal medical RAS blockade in the myocardium, differences in myocardial contractile responsiveness to sympathetic activation and its interaction with decreased renal function may, at least in part, account for observed variability in treatment responses in heart failure patients. 5,6 In this issue of the Journal of Nuclear Cardiology, Marsico et al 7 report of novel and important findings in that patients with renal dysfunction and systolic heart failure have a worse impairment of cardiac sympathetic activity than in those systolic heart failure patients with preserved renal function. The study consisted of 263 patients with mild-to-severe heart failure (NYHA II-III) of ischemic and non-ischemic origin (27% vs. 73%) undergoing 123 I-meta-iodobenzylguanidine ( 123 I-MIBG) myocardial scintigraphy assessing cardiac sympathetic activation.…”

“…The exact kidney-related mechanism mediating a further decrease of cardiac sympathetic activity remain uncertain but it may offer a new and critical target of systolic heart failure therapy as current observations suggest. 7 This appears of utmost importance, as the manifestation of a cardiorenal syndrome commonly leads to a further worsening of clinical outcome in systolic heart failure patients.…”