Abstract 4598: The Individual Effect of Components of Defibrillation Waveform on the Contractile Function and Intracellular Calcium Dynamics of Cardiomyocytes
Although electrical shock is the unique treatment for fatal arrhythmia, it causes myocardial dysfunction which is closely related to the energy delivered. The individual contribution of defibrillation waveform components to post-shock contractile impairment is not yet established. Peak current may play a more important role than energy on post-shock myocardial dysfunction. Prolongation of the duration of electrical shock may reduce contractile impairment. 324 cardiomyocytes isolated from adult male rats were assigned into 11 groups and received different waveforms (triangular and square), peak currents (derived from peak voltage of 25 V, 35.4 V, 50 V, 70.7 V and 100V) and durations (10 and 20 ms) shocks (Figure⇓). A single shock was given to each cardiomyocyte. The length shortening and Ca2+ transients were recorded optically with fura-2 loading. Increase of peak current and corresponding energy caused more cells to have irregular beating (p<0.001) and reduced length shortening (p<0.001). This was associated with increased Ca2+ abnormality (p<0.05). Increasing peak current independent of energy significantly impaired post-shock contractile function (p<0.05), whereas change of energy alone did not. Prolongation of duration independent of energy and peak current reduced post-shock contractile impairment (p<0.05). Increasing delivered energy by increasing peak current causes more contractile impairment and associated Ca2+ abnormality. Peak current may play a more determinative role on post-shock contractile dysfunction than energy. Prolonging the duration reduced contractile impairment.