Abstract

Implantable cardiac defibrillators (ICDs) are recommended to prevent the risk of sudden cardiac death. However, shocks are associated with an increased mortality with a dose response effect, and a strategy of reducing electrical therapy burden improves the prognosis of implanted patients. We review the mechanisms of defibrillation and its consequences, including cell damage, metabolic remodeling, calcium metabolism anomalies, and inflammatory and pro-fibrotic remodeling. Electrical shocks do save lives, but also promote myocardial stunning, heart failure, and pro-arrhythmic effects as seen in electrical storms. Limiting unnecessary implantations and therapies and proposing new methods of defibrillation in the future are recommended.

Highlights

  • We review the mechanisms of defibrillation and the potential consequences of Implantable cardiac defibrillators (ICDs)

  • ICDs are sometimes useless, and indications for implantation in the future will probably have to be based on a new stratification of rhythmic risk, on the analysis of the ventricular fibrotic substrate, the truly arrhythmogenic substrate

  • RAD23 was more abundant after electrical shock and plays a role in the nucleotide excision/repair pathway, especially in the recognition of thermic DNA damages [76]

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Summary

Introduction

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Implantable cardiac defibrillators (ICDs) are recommended to prevent the risk of sudden cardiac death. More than 300,000 ICDs worldwide are implanted each year. Shocks are associated with an increased mortality with a dose response effect, and a strategy of reducing electrical therapy burden improves the prognosis of implanted patients. We review the mechanisms of defibrillation and the potential consequences of ICD shocks, including cell damage, metabolic remodeling, calcium metabolism dysregulation, inflammation, and fibrosis

Technology
Indications
Primary Prevention
Less Is More
Sudden Death
Electrical Storm
Acute Heart Failure
Adrenergic Storm
Mechanisms of Defibrillation
Electroporation
Cellular Destruction
Myocardial Dysfunction
Main Principles
Shock-Related Myocardial Injury in Proteomics
Conclusions
Metabolic Remodeling and Oxidative Stress
Calcium Regulation
Inflammation and Fibrosis
Findings
Outlook
Full Text
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