BACKGROUND: Several mechanisms have been proposed for ventriculophasic sinus arrhythmia: phasic changes in baroreceptor mediated vagal input to the sinus node, mechanical effects and pressure changes caused by ventricular systole, and increased blood flow to the sinus node. We attempt to elucidate the role of SA nodal blood flow in the generation of ventriculophasic sinus arrhythmia by measuring phasic changes in PP intervals from the atrial remnants of patients who have received cardiac transplant. METHODS: A total of 16 atrial electrogram recordings were obtained from the recipient atrial remnant in 12 patients who had undergone heart transplantation at the University of Miami/Jackson Memorial Hospital. Concomitant recordings of the donor surface ECG were also obtained. Recipient atrial PP intervals that contained a QRS were measured. The QP intervals were also measured and plotted against the associated PP interval to assess the relationship between varying QP intervals and the associated PP interval. RESULTS: A linear relationship between the PP intervals and the associated QP intervals was seen in all patients. Despite widely varying QP intervals, there was little change in the PP intervals suggesting absence of ventriculophasic arrhythmia. Our linear graphs are in contrast to the typical curves seen in ventriculophasic arrhythmia that have been described by Lepeschkin. CONCLUSIONS: In our study, there appeared to be absence of ventriculophasic arrhythmia despite intact vagal innervation to the atrial remnant suggesting that the lack of pulsatile SA node blood flow may contribute to the absence of ventriculophasic arrhythmia. We conclude that the transplanted heart, when performed by the standard technique, may provide a model to study mechanisms of ventriculophasic arrhythmia.
BACKGROUND: Several mechanisms have been proposed for ventriculophasic sinus arrhythmia: phasic changes in baroreceptor mediated vagal input to the sinus node, mechanical effects and pressure changes caused by ventricular systole, and increased blood flow to the sinus node. We attempt to elucidate the role of SA nodal blood flow in the generation of ventriculophasic sinus arrhythmia by measuring phasic changes in PP intervals from the atrial remnants of patients who have received cardiac transplant. METHODS: A total of 16 atrial electrogram recordings were obtained from the recipient atrial remnant in 12 patients who had undergone heart transplantation at the University of Miami/Jackson Memorial Hospital. Concomitant recordings of the donor surface ECG were also obtained. Recipient atrial PP intervals that contained a QRS were measured. The QP intervals were also measured and plotted against the associated PP interval to assess the relationship between varying QP intervals and the associated PP interval. RESULTS: A linear relationship between the PP intervals and the associated QP intervals was seen in all patients. Despite widely varying QP intervals, there was little change in the PP intervals suggesting absence of ventriculophasic arrhythmia. Our linear graphs are in contrast to the typical curves seen in ventriculophasic arrhythmia that have been described by Lepeschkin. CONCLUSIONS: In our study, there appeared to be absence of ventriculophasic arrhythmia despite intact vagal innervation to the atrial remnant suggesting that the lack of pulsatile SA node blood flow may contribute to the absence of ventriculophasic arrhythmia. We conclude that the transplanted heart, when performed by the standard technique, may provide a model to study mechanisms of ventriculophasic arrhythmia.