Renal Denervation for Chronic Heart Failure: Background and Pathophysiological Rationale

Figures

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  Fig. 1. Pathophysiological interaction between the brain, the kidney and other peripheral organs like heart, liver and vasculature after sympathetic activity is enhanced. Efferent signals generated in the sympathetic nervous system stimulate the heart and other organs producing maladaptive responses. In the kidney, sympathetic activation reduces renal blood flow, increases sodium retention and activates renin-angiotensin system. Efferents further enhance sympathetic outflow providing a vicious cycle in the stepwise increase of the sympathetic activation in the interaction between the heart and the brain. modified from reference 11. RAAS: renin angiotension aldosteron system.

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  Fig. 2. Summary of beta-adrenergic signal transduction in heart failure. Modified from reference.28) AR: adrenoreceptor, NA: noradrenaline, Gs: stimulatory G protein, AC: adenylyl cyclase, Gi: inhibitory G protein, mRNA: messenger ribonucleic acid, Gia: inhibitory guanine binding protein.

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  Fig. 3. Left atrial de-remodeling according to tertiles of left ventricular and left atrial volume index at baseline. Modified according to Schirmer et al.49) LAVI: left atrial volume index.

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  Fig. 4. Effect of renal denervation in a patient with dilated cardiomyopathy presenting with an electrical storm. Depicted are the numbers of VF episodes (left) and the systolic blood pressure values (right). It becomes clear that after one week of renal denervation no further charges of the ICD were detected. The blood pressure was particularly low in this patient, but remained stable over time. Modified according to Ukena et al.52) RDN: renal denervation, VF: ventricular fibrillation.