The Effect of Calcium Channel Blockers on Ventricular Fibrillation
The most frequent cause of sudden cardiac death is unstable ventricular tachycardia or fibrillation. Fibrillation is characterized by the propagation and breakup of rotary electrical waves, which leads to a chaotic distribution of electrical activation of the tissue. This leads to uncoordinated contraction of the chambers of the heart, inhibiting the heart from pumping blood to the rest of the body. Successful electrical defibrillation has been limited to delivering high-energy shocks to the entire heart, causing rotary electrical activity to cease and normal sinus rhythm to resume. This has several adverse effects on the heart, including tissue damage and post-shock dysrhythmias. The high-energy shock also causes significant pain and anxiety to the patient. Thus, a combination of low-energy electrical stimulations with antiarrhythmic, ion channel-blocking drugs is of interest. This combination is examined in silica using the Fenton-Karma model. Calcium channel block was found to sustain fibrillation when compared to defibrillation rates without drug or electrical intervention. The number of phase singularities on the tissue was also found to decrease initially but increase at higher concentrations of calcium channel block. These findings provide some insight into possible mechanisms of the proarrhythmic effects of calcium channel blocking drugs, and will ultimately aid in progress toward a lower-energy defibrillator.
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