Abstract
Damage from myocardial infarction (MI) and subsequent heart failure are serious public health concerns. Current clinical treatments and therapies to treat MI damage largely do not address the regeneration of cardiomyocytes. In a previous study, we established that it is possible to promote regeneration of cardiac muscle with vascular endothelial growth factor B gene delivery directly to the ischemic myocardium. In the current study we aim to optimize cardioporation parameters to increase expression efficiency by varying electrode configuration, applied voltage, pulse length, and plasmid vector size. By using a surface monopolar electrode, optimized pulsing conditions and reducing vector size, we were able to prevent ventricular fibrillation, increase survival, reduce tissue damage, and significantly increase gene expression levels.
Highlights
An estimated of 92.1 million adults have at least one type of cardiovascular disease (CVD) in the United States
The first leading cause of death remained the same in the recent years (2015–2016) as heart disease and 17.6 million deaths were attributed to CVD globally [2], until Covid-19
One challenge that we discovered in our previous work, is that while cardiomyogenesis post ischemia can be induced in detectable quantities, these quantities are still very low, and not clinically useful
Summary
An estimated of 92.1 million adults have at least one type of cardiovascular disease (CVD) in the United States. The first leading cause of death remained the same in the recent years (2015–2016) as heart disease and 17.6 million deaths were attributed to CVD globally [2], until Covid-19. Myocardial infarction (MI) occurs in about 790,000 people in the United States every year. The heart has insufficient regenerative capacity; cardiomyocytes do not return. Cardiac fibroblast proliferation, infiltration and creation of collagenous, non-contractile scar tissue replaces cardiomyocytes, resulting in a thin myocardial wall unable to pump enough blood to meet the demand and leading to lower quality of life and heart failure [3]. Current clinical therapies do not regenerate cardiac myocardium [4,5], cardiomyocyte proliferation is possible [6]
Sign-in/Register to view highlights & summary 
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call