Left ventricular myocardial damage associated with defibrillation in a porcine model of sudden cardiac arrest
: a genomic, light microscopic and ultrastructural investigation

  • Fiona Rogan

Student thesis: Doctoral Thesis


 Transthoracic defibrillation is performed to correct life-threatening cardiac arrhythmias of the heart, such as ventricular fibrillation (VF) and ventricular tachycardia (VT). These arrhythmias are due to the chaotic electrical excitation
of the heart chambers and loss of coordinated contraction of myocytes that may induce cardiac arrest. While it is accepted that resuscitation is required for reversing VF and restoring life, essential research indicates that these techniques may result in myocardial damage. However, there is limited information regarding the potentially damaging effects of this treatment on the tissues of the heart at structural and genetic levels.

This study investigates the extent of myocardial injury associated with the repeated use of increasing energies (200J & 360J) of defibrillation in an adult porcine model of cardiac arrest using genomic, histological and ultrastructural analysis techniques.

The current paradox is that cardiac defibrillation depends on the successful selection of energy to generate sufficient current flow through the heart (transmyocardial current) to achieve defibrillation, while at the same time causing minimal injury to the heart.

In this research study the timeframe following the cessation of repeated defibrillation protocols was finalised at 6 hours (due to animal license). The animals demonstrate the biological effects that repeated defibrillation has upon the cardiac tissues at a structural and genomic level. This study suggests there is a cardioprotective measure taken by the cardiomyocytes due to electrical overstimulation, resulting in changes of the cardiac tissue.

The results presented in this thesis show that repeated defibrillation at increasing energies produces immediate minor changes to the functional myocardium that is stunned yet still viable, at a genomic, microscopic and ultrastructural level. As the paradox suggests the success of defibrillation would be increased by the exact prognosis of prolonged defibrillation mechanism downstream and the impact upon cardiac function.
Date of AwardMar 2021
Original languageEnglish
SponsorsDepartment for the Economy, HeartSine Technologies, Ltd. & Stryker Corporation
SupervisorJim McLaughlin (Supervisor), Brian Meenan (Supervisor) & George Burke (Supervisor)

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