American Heart Congress - CVD

Biography

Biography: Arianna Pahlavan

Abstract

Acute cardiac arrhythmias are the main cause of death in industrialized countries; despite clinical importance, the mechanisms behind the onset and dynamics of cardiac arrhythmias are still poorly understood. The purpose of this work is twofold: (1) determine how smaller blood vessel radii affect the moving wave-front velocity, virtual electrode (VE) formation, and transmembrane potential induced by a shock (2) to elucidate a minimum radius correlative to shock strengths of interest. The model described here resolved tissue dynamics with a second-order solution to Poisson’s equation uniformly to boundaries. Through examining the role of small blood vessels, a minimum radius was identified at which a current will propagate, a range of 100-400µm. The velocity of the moving wave-front remained constant and no VEs form in the blood vessel region for all blood vessels below the size of the minimum radius. An alteration of fiber orientation, perpendicular to parallel, caused a twofold reduction in minimum radius. Blood vessels of radii 400µm do not affect the propagation of a 6V, 3V, 1.5V, .75V, and .33V induced shock strengths. Thus, 400µm blood vessels can be excluded in the first ever vascular mathematical model of the human heart at a feasible cost. An accurate anatomical model is needed to computationally verify the results of low energy antifibrillation pacing (LEAP) for the implication of painless defibrillation therapy in hospitals. The implementation of low energy automated defibrillators will save the US $1.1 trillion annually and universalize the CPR protocol for the minimization of anoxic encephalopathy. Future investigations may involve nanoparticles monitoring the cardiac ion channel currents and activating a painless electric shock where re-entry begins to occur, a potential solution to sudden cardiac arrhythmia death.