Optimal Programming of the Atrioventricular Delay Using the Phonocardiogram

Purpose: To predict the optimal atrioventricular (AV) delay using the phonocardiogram (PCG).
Methods: We studied 12 recipients of cardiac resynchronization therapy (CRT) system and eight recipients of dual-chamber pacemakers implanted for AV block with normal left ventricular (LV) function. The amplitude of the first heart sound (S1) was recorded by PCG and the LV outflow tract (OT) time-velocity integral (TVI) was measured by pulsed Doppler echocardiography. The AV delay was prolonged in 20-ms increments, from 60 ms to 240 ms. Ishikawa's method was used for the echocardiographic optimization of the AV delay. The relation between S1 amplitude and the AV delay was analyzed.
Results: The correlation between the amplitude of S1 and the length of AV delay showed an S-shaped curve. The AV delay at the inflection point of each patient's S-shaped curve (161.2 ± 19.5 ms) was positively correlated with the optimal AV delay determined by echocardiography (148.3 ± 16.9 ms, r = 0.83, P < 0.001). In addition, there was a positive correlation between the AV delay at the maximal TVI of LVOT (150.8 ± 22.7 ms) and the AV delay at the inflection point of the S-shaped curve (159.5 ± 24.9 ms, r = 0.87, P < 0.001). In two CRT system recipients, an optimal AV delay could not be found by echocardiography; however, an optimal AV delay could be determined by PCG.
Conclusions: A high correlation was observed between the optimal AV delay determined by phonocardiography versus echocardiography.     

Electroporation in a Model of Cardiac Defibrillation

INTRODUCTION: It is known that high-strength shock disrupts the lipid matrix of the myocardial cell membrane and forms reversible aqueous pores across the membrane. This process is known as "electroporation." However, it remains unclear whether electroporation contributes to the mechanism of ventricular defibrillation. The aim of this computer simulation study was to examine the possible role of electroporation in the success of defibrillation shock. METHODS AND RESULTS: Using a modified Luo-Rudy-1 model, we simulated two-dimensional myocardial tissue with a homogeneous bidomain nature and unequal anisotropy ratios. Spiral waves were induced by the S1-S2 method. Next, monophasic defibrillation shocks were delivered externally via two line electrodes. For nonelectroporating tissue, termination of ongoing fibrillation succeeded; however, new spiral waves were initiated, even with high-strength shock (24 V/cm). For electroporating tissue, high-strength shock (24 V/cm) was sufficient to extinguish ongoing fibrillation and did not initiate any new spiral waves. Weak shock (16 to 20 V/cm) also extinguished ongoing fibrillation; however, in contrast to the high-strength shock, new spiral waves were initiated. Success in defibrillation depended on the occurrence of electroporation-mediated anodal-break excitation from the physical anode and the virtual anode. Some excitation wavefronts following electrical shock used a deexcited area with recovered excitability as a pass-through point; therefore, electroporation-mediated anodal-break excitation is necessary to block out the pass-through point, resulting in successful defibrillation. CONCLUSION: The electroporation-mediated anodal-break excitation mechanism may play an important role in electrical defibrillation.