Anode-break excitation during end-diastolic stimulation is explained by half-cell double layer discharge.

The phenomenon of anodal-break excitation during end-diastolic stimulation of the heart was discovered many years ago by B. Hoffman. Yet, the existence and mechanistic explanation of this effect remain controversial. We sought to confirm its existence and to determine a possible role of half-cell potential. We used isolated Langendorff-perfused rabbit hearts (n = 6) which were stained with di-4-ANEPPS and perfused with 15-mM butanedione monoxime (BDM). Transmembrane potentials were optically recorded at the left ventricular epicardium with a high spatial and temporal resolution (200 microm/343 micros) near the tip of a 120-microm platinum-iridium Teflon-coated unipolar pacing electrode to detect virtual electrode polarization and to reconstruct an activation pattern. Hearts were paced at a cycle length of 300 ms by anodal square pulses with an amplitude of 0.1-10 mA and a duration of 5-60 ms. Data revealed that the anodal-break excitation does exists and is accompanied by an overshoot in the recordings of the pacing current. Addition of a diode in the stimulation circuit eliminated both the overshoot and the break excitation. The findings suggest that a half-cell surface potential at the pacing electrode metal-saline interface may influence the pacing currents during unipolar anodal cardiac stimulation providing "break"-like activation. We also confirmed that the threshold of "break"-like excitation is lower than make-excitation. We suggest that further exploration of this effect is needed in order to design improved multiphasic pacing waveforms.