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Updated: Nov 29, 2025
High-Resolution Endocardial and Epicardial Optical Mapping in a Sheep Model of Stretch-Induced Atrial Fibrillation
Published on: July 29, 2011
Acute pathophysiological myocardial changes following intra-cardiac electrical shocks using a proteomic approach in a
Alexandre Bodin1,2, Valérie Labas3,4, Arnaud Bisson5
1Service de Cardiologie, Centre Hospitalier Universitaire Trousseau Et EA7505, Faculté de Médecine, Université François Rabelais, Tours, France. alexandre.bodin@etu.univ-tours.fr.
Insights
Implantable cardioverter-defibrillator (ICD) shocks, while life-saving, can cause myocardial injury. Proteomic analysis revealed significant protein changes, including damage and inflammation, even far from the shock site.
Area of Science:
- Cardiology
- Proteomics
- Biomarkers
Background:
- Implantable cardioverter-defibrillators (ICDs) treat ventricular arrhythmias and reduce mortality.
- Paradoxically, ICD shocks are linked to increased mortality.
- Myocardial protein-level changes post-shock require investigation.
Purpose of the Study:
- To identify myocardial protein changes immediately after ICD electrical shocks.
- To investigate potential mechanisms of shock-induced myocardial injury.
- To identify novel biomarkers of myocardial response to ICD shocks.
Main Methods:
- Surgical implantation of ICDs in a sheep model (N=10).
- Delivery of 5 consecutive 41 J shocks to the shock group (N=5).
- Proteomic analysis of myocardial tissue (near and far from the lead coil) using mass spectrometry.
Main Results:
- Significant proteome modification after electrical shock.
- Identified mechanisms include protein/DNA/membrane damage, regulated cell death, metabolic remodeling, oxidative stress, calcium dysregulation, inflammation, and fibrosis.
- N-term acetylated troponin C decreased significantly in the remote myocardium (AUC: 0.93).
Conclusions:
- Acute, shock-induced myocardial tissue injury occurs.
- This injury involves multiple cellular mechanisms.
- N-term acetylated troponin C may serve as a biomarker for remote myocardial injury after ICD shocks.
Abstract:
Implantable cardioverter-defibrillators (ICD) are meant to fight life-threatening ventricular arrhythmias and reduce overall mortality. Ironically, life-saving shocks themselves have been shown to be independently associated with an increased mortality. We sought to identify myocardial changes at the protein level immediately after ICD electrical shocks using a proteomic approach. ICD were surgically implanted in 10 individuals of a healthy male sheep model: a control group (N = 5) without any shock delivery and a shock group (N = 5) with the delivery of 5 consecutive shocks at 41 J. Myocardial tissue samples were collected at the right-ventricle apex near to the lead coil and at the right ventricle basal free wall region. Global quantitative proteomics experiments on myocardial tissue samples were performed using mass spectrometry techniques. Proteome was significantly modified after electrical shock and several mechanisms were associated: protein, DNA and membrane damages due to extreme physical conditions induced by ICD-shock but also due to regulated cell death; metabolic remodeling; oxidative stress; calcium dysregulation; inflammation and fibrosis. These proteome modifications were seen in myocardium both "near" and "far" from electrical shock region. N-term acetylated troponin C was an interesting tissular biomarker, significantly decreased after electrical shock in the "far" region (AUC: 0.93). Our data support an acute shock-induced myocardial tissue injury which might be involved in acute paradoxical deleterious effects such as heart failure and ventricular arrhythmias.
