New Approaches in the Management of Sudden Cardiac Death in Patients with Heart Failure—Targeting the Sympathetic Nervous System
Cardiovascular diseases (CVDs) have been considered the most predominant cause of death and one of the most critical public health issues worldwide. In the past two decades, cardiovascular (CV) mortality has declined in high-income countries owing to preventive measures that resulted in the reduced...
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MDPI AG
2019-05-01
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Series: | International Journal of Molecular Sciences |
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Online Access: | https://www.mdpi.com/1422-0067/20/10/2430 |
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record_format |
Article |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Márcio Galindo Kiuchi Janis Marc Nolde Humberto Villacorta Revathy Carnagarin Justine Joy Su-Yin Chan Leslie Marisol Lugo-Gavidia Jan K. Ho Vance B. Matthews Girish Dwivedi Markus P. Schlaich |
spellingShingle |
Márcio Galindo Kiuchi Janis Marc Nolde Humberto Villacorta Revathy Carnagarin Justine Joy Su-Yin Chan Leslie Marisol Lugo-Gavidia Jan K. Ho Vance B. Matthews Girish Dwivedi Markus P. Schlaich New Approaches in the Management of Sudden Cardiac Death in Patients with Heart Failure—Targeting the Sympathetic Nervous System International Journal of Molecular Sciences heart failure positron emission tomography renal denervation sudden cardiac death sympathetic nervous system ventricular arrhythmias hypertension |
author_facet |
Márcio Galindo Kiuchi Janis Marc Nolde Humberto Villacorta Revathy Carnagarin Justine Joy Su-Yin Chan Leslie Marisol Lugo-Gavidia Jan K. Ho Vance B. Matthews Girish Dwivedi Markus P. Schlaich |
author_sort |
Márcio Galindo Kiuchi |
title |
New Approaches in the Management of Sudden Cardiac Death in Patients with Heart Failure—Targeting the Sympathetic Nervous System |
title_short |
New Approaches in the Management of Sudden Cardiac Death in Patients with Heart Failure—Targeting the Sympathetic Nervous System |
title_full |
New Approaches in the Management of Sudden Cardiac Death in Patients with Heart Failure—Targeting the Sympathetic Nervous System |
title_fullStr |
New Approaches in the Management of Sudden Cardiac Death in Patients with Heart Failure—Targeting the Sympathetic Nervous System |
title_full_unstemmed |
New Approaches in the Management of Sudden Cardiac Death in Patients with Heart Failure—Targeting the Sympathetic Nervous System |
title_sort |
new approaches in the management of sudden cardiac death in patients with heart failure—targeting the sympathetic nervous system |
publisher |
MDPI AG |
series |
International Journal of Molecular Sciences |
issn |
1422-0067 |
publishDate |
2019-05-01 |
description |
Cardiovascular diseases (CVDs) have been considered the most predominant cause of death and one of the most critical public health issues worldwide. In the past two decades, cardiovascular (CV) mortality has declined in high-income countries owing to preventive measures that resulted in the reduced burden of coronary artery disease (CAD) and heart failure (HF). In spite of these promising results, CVDs are responsible for ~17 million deaths per year globally with ~25% of these attributable to sudden cardiac death (SCD). Pre-clinical data demonstrated that renal denervation (RDN) decreases sympathetic activation as evaluated by decreased renal catecholamine concentrations. RDN is successful in reducing ventricular arrhythmias (VAs) triggering and its outcome was not found inferior to metoprolol in rat myocardial infarction model. Registry clinical data also suggest an advantageous effect of RDN to prevent VAs in HF patients and electrical storm. An in-depth investigation of how RDN, a minimally invasive and safe method, reduces the burden of HF is urgently needed. Myocardial systolic dysfunction is correlated to neuro-hormonal overactivity as a compensatory mechanism to keep cardiac output in the face of declining cardiac function. Sympathetic nervous system (SNS) overactivity is supported by a rise in plasma noradrenaline (NA) and adrenaline levels, raised central sympathetic outflow, and increased organ-specific spillover of NA into plasma. Cardiac NA spillover in untreated HF individuals can reach ~50-fold higher levels compared to those of healthy individuals under maximal exercise conditions. Increased sympathetic outflow to the renal vascular bed can contribute to the anomalies of renal function commonly associated with HF and feed into a vicious cycle of elevated BP, the progression of renal disease and worsening HF. Increased sympathetic activity, amongst other factors, contribute to the progress of cardiac arrhythmias, which can lead to SCD due to sustained ventricular tachycardia. Targeted therapies to avoid these detrimental consequences comprise antiarrhythmic drugs, surgical resection, endocardial catheter ablation and use of the implantable electronic cardiac devices. Analogous NA agents have been reported for single photon-emission-computed-tomography (SPECT) scans usage, specially the <sup>123</sup>I-metaiodobenzylguanidine (<sup>123</sup>I-MIBG). Currently, HF prognosis assessment has been improved by this tool. Nevertheless, this radiotracer is costly, which makes the use of this diagnostic method limited. Comparatively, positron-emission-tomography (PET) overshadows SPECT imaging, because of its increased spatial definition and broader reckonable methodologies. Numerous ANS radiotracers have been created for cardiac PET imaging. However, so far, [<sup>11</sup>C]-meta-hydroxyephedrine (HED) has been the most significant PET radiotracer used in the clinical scenario. Growing data has shown the usefulness of [<sup>11</sup>C]-HED in important clinical situations, such as predicting lethal arrhythmias, SCD, and all-cause of mortality in reduced ejection fraction HF patients. In this article, we discussed the role and relevance of novel tools targeting the SNS, such as the [<sup>11</sup>C]-HED PET cardiac imaging and RDN to manage patients under of SCD risk. |
topic |
heart failure positron emission tomography renal denervation sudden cardiac death sympathetic nervous system ventricular arrhythmias hypertension |
url |
https://www.mdpi.com/1422-0067/20/10/2430 |
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doaj-0f6879d3014542b0bf8a15d774ded33b2020-11-25T00:35:56ZengMDPI AGInternational Journal of Molecular Sciences1422-00672019-05-012010243010.3390/ijms20102430ijms20102430New Approaches in the Management of Sudden Cardiac Death in Patients with Heart Failure—Targeting the Sympathetic Nervous SystemMárcio Galindo Kiuchi0Janis Marc Nolde1Humberto Villacorta2Revathy Carnagarin3Justine Joy Su-Yin Chan4Leslie Marisol Lugo-Gavidia5Jan K. Ho6Vance B. Matthews7Girish Dwivedi8Markus P. Schlaich9Dobney Hypertension Cenre, School of Medicine—Royal Perth Hospital Unit, Faculty of Medicine, Dentistry & Health Sciences, The University of Western Australia Level 3, MRF Building, Rear 50 Murray St, Perth 6000, MDBP: M570, AustraliaDobney Hypertension Cenre, School of Medicine—Royal Perth Hospital Unit, Faculty of Medicine, Dentistry & Health Sciences, The University of Western Australia Level 3, MRF Building, Rear 50 Murray St, Perth 6000, MDBP: M570, AustraliaCardiology Division, Department of Medicine, Universidade Federal Fluminense, Niterói, Rio de Janeiro 24033-900, BrazilDobney Hypertension Cenre, School of Medicine—Royal Perth Hospital Unit, Faculty of Medicine, Dentistry & Health Sciences, The University of Western Australia Level 3, MRF Building, Rear 50 Murray St, Perth 6000, MDBP: M570, AustraliaDobney Hypertension Cenre, School of Medicine—Royal Perth Hospital Unit, Faculty of Medicine, Dentistry & Health Sciences, The University of Western Australia Level 3, MRF Building, Rear 50 Murray St, Perth 6000, MDBP: M570, AustraliaDobney Hypertension Cenre, School of Medicine—Royal Perth Hospital Unit, Faculty of Medicine, Dentistry & Health Sciences, The University of Western Australia Level 3, MRF Building, Rear 50 Murray St, Perth 6000, MDBP: M570, AustraliaDobney Hypertension Cenre, School of Medicine—Royal Perth Hospital Unit, Faculty of Medicine, Dentistry & Health Sciences, The University of Western Australia Level 3, MRF Building, Rear 50 Murray St, Perth 6000, MDBP: M570, AustraliaDobney Hypertension Cenre, School of Medicine—Royal Perth Hospital Unit, Faculty of Medicine, Dentistry & Health Sciences, The University of Western Australia Level 3, MRF Building, Rear 50 Murray St, Perth 6000, MDBP: M570, AustraliaHarry Perkins Institute of Medical Research and Fiona Stanley Hospital, The University of Western Australia, Perth 6150, AustraliaDobney Hypertension Cenre, School of Medicine—Royal Perth Hospital Unit, Faculty of Medicine, Dentistry & Health Sciences, The University of Western Australia Level 3, MRF Building, Rear 50 Murray St, Perth 6000, MDBP: M570, AustraliaCardiovascular diseases (CVDs) have been considered the most predominant cause of death and one of the most critical public health issues worldwide. In the past two decades, cardiovascular (CV) mortality has declined in high-income countries owing to preventive measures that resulted in the reduced burden of coronary artery disease (CAD) and heart failure (HF). In spite of these promising results, CVDs are responsible for ~17 million deaths per year globally with ~25% of these attributable to sudden cardiac death (SCD). Pre-clinical data demonstrated that renal denervation (RDN) decreases sympathetic activation as evaluated by decreased renal catecholamine concentrations. RDN is successful in reducing ventricular arrhythmias (VAs) triggering and its outcome was not found inferior to metoprolol in rat myocardial infarction model. Registry clinical data also suggest an advantageous effect of RDN to prevent VAs in HF patients and electrical storm. An in-depth investigation of how RDN, a minimally invasive and safe method, reduces the burden of HF is urgently needed. Myocardial systolic dysfunction is correlated to neuro-hormonal overactivity as a compensatory mechanism to keep cardiac output in the face of declining cardiac function. Sympathetic nervous system (SNS) overactivity is supported by a rise in plasma noradrenaline (NA) and adrenaline levels, raised central sympathetic outflow, and increased organ-specific spillover of NA into plasma. Cardiac NA spillover in untreated HF individuals can reach ~50-fold higher levels compared to those of healthy individuals under maximal exercise conditions. Increased sympathetic outflow to the renal vascular bed can contribute to the anomalies of renal function commonly associated with HF and feed into a vicious cycle of elevated BP, the progression of renal disease and worsening HF. Increased sympathetic activity, amongst other factors, contribute to the progress of cardiac arrhythmias, which can lead to SCD due to sustained ventricular tachycardia. Targeted therapies to avoid these detrimental consequences comprise antiarrhythmic drugs, surgical resection, endocardial catheter ablation and use of the implantable electronic cardiac devices. Analogous NA agents have been reported for single photon-emission-computed-tomography (SPECT) scans usage, specially the <sup>123</sup>I-metaiodobenzylguanidine (<sup>123</sup>I-MIBG). Currently, HF prognosis assessment has been improved by this tool. Nevertheless, this radiotracer is costly, which makes the use of this diagnostic method limited. Comparatively, positron-emission-tomography (PET) overshadows SPECT imaging, because of its increased spatial definition and broader reckonable methodologies. Numerous ANS radiotracers have been created for cardiac PET imaging. However, so far, [<sup>11</sup>C]-meta-hydroxyephedrine (HED) has been the most significant PET radiotracer used in the clinical scenario. Growing data has shown the usefulness of [<sup>11</sup>C]-HED in important clinical situations, such as predicting lethal arrhythmias, SCD, and all-cause of mortality in reduced ejection fraction HF patients. In this article, we discussed the role and relevance of novel tools targeting the SNS, such as the [<sup>11</sup>C]-HED PET cardiac imaging and RDN to manage patients under of SCD risk.https://www.mdpi.com/1422-0067/20/10/2430heart failurepositron emission tomographyrenal denervationsudden cardiac deathsympathetic nervous systemventricular arrhythmiashypertension |