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Sympathetic Activation in Hypertensive Chronic Kidney Disease - A Stimulus for Cardiac Arrhythmias and Sudden Cardiac
Márcio Galindo Kiuchi1, Jan K Ho1, Janis Marc Nolde1
1Dobney Hypertension Centre, School of Medicine - Royal Perth Hospital Unit/Medical Research Foundation, The University of Western Australia, Perth, WA, Australia.
Insights
Chronic kidney disease (CKD) is linked to cardiovascular events and sudden cardiac death (SCD). Targeting sympathetic overactivity may reduce arrhythmias in CKD patients.
Area of Science:
- Nephrology
- Cardiology
- Neuroscience
Background:
- Chronic kidney disease (CKD) strongly correlates with cardiovascular (CV) events, including death and heart failure.
- Recent studies link CKD to malignant ventricular arrhythmias and sudden cardiac death (SCD).
- Cardiac structural and electrophysiological changes are common in CKD patients, increasing arrhythmia risk.
Purpose of the Study:
- To review the role of sympathetic neural cycle feedback in CKD.
- To explore how this cycle aggravates risk factors for SCD in CKD.
- To discuss therapeutic targeting of the sympathetic nervous system for arrhythmias in CKD.
Main Methods:
- Literature review of studies on CKD, CV events, and the sympathetic nervous system.
- Analysis of the feedback loop of the sympathetic neural cycle in kidney failure.
- Discussion of pharmacological and device-based interventions.
Main Results:
- Sympathetic overactivity is associated with increased CV risk in CKD patients.
- Sympathetic hyperactivity is present from early CKD stages and worsens with renal failure.
- Kidney failure facilitates sympathetic neural activity, perpetuating disease and increasing SCD risk.
Conclusions:
- Targeting the overactive sympathetic nervous system is a potential key intervention.
- Therapeutic strategies may reduce cardiac arrhythmias and SCD in high-risk CKD patients.
- Understanding the sympathetic neural cycle is crucial for managing CV complications in CKD.
Abstract:
Studies have revealed a robust and independent correlation between chronic kidney disease (CKD) and cardiovascular (CV) events, including death, heart failure, and myocardial infarction. Recent clinical trials extend this range of adverse CV events, including malignant ventricular arrhythmias and sudden cardiac death (SCD). Moreover, other studies point out that cardiac structural and electrophysiological changes are a common occurrence in this population. These processes are likely contributors to the heightened hazard of arrhythmias in CKD population and may be useful indicators to detect patients who are at a higher SCD risk. Sympathetic overactivity is associated with increased CV risk, specifically in the population with CKD, and it is a central feature of the hypertensive state, occurring early in its clinical course. Sympathetic hyperactivity is already evident at the earliest clinical stage of CKD and is directly related to the progression of renal failure, being most pronounced in those with end-stage renal disease. Sympathetic efferent and afferent neural activity in kidney failure is a crucial facilitator for the perpetuation and evolvement of the disease. Here, we will revisit the role of the feedback loop of the sympathetic neural cycle in the context of CKD and how it may aggravate several of the risk factors responsible for causing SCD. Targeting the overactive sympathetic nervous system therapeutically, either pharmacologically or with newly available device-based approaches, may prove to be a pivotal intervention to curb the substantial burden of cardiac arrhythmias and SCD in the high-risk population of patients with CKD.
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