TY - JOUR
T1 - Effects of An Acute Increase in Atrial Pressure on Atrial Refractoriness in Humans
AU - CALKINS, HUGH
AU - EL‐ATASSI, RAFEL
AU - KALBFLEISCH, STEVEN
AU - LANGBERG, JONATHAN
AU - MORADY, FRED
PY - 1992/11
Y1 - 1992/11
N2 - Contraction‐excitation feedback has been studied extensively in mammalian ventricles. In contrast, little is known about contraction‐excitation feedback in mammalian atria. The objective of this study was to investigate the effect of acute alterations in atrial pressure, induced by varying the atrioventricular (AV) interval, on atrial refractoriness. Twenty patients without structural heart disease participated in the study. In each patient the atrial effective (ERP) and absolute refractory periods (ARP) were measured during AV pacing at a cycle length of 500 msec and an AV interval of 120 msec. Acute increases in atrial pressure were induced by pacing the atrium and ventricle simultaneously for the final two beats of the drive train. The ERP was defined as the longest extrastimulus coupling interval that failed to capture with an extrastimulus current strength of twice the stimulation threshold. The ARP was defined in a similar manner with an extrastimulus current strength of 10 mA. The ERP and ARP were determined using the incremental extrastimulus technique. A subset of patients had the pacing protocol performed during autonomic blockade. As the AV interval of the final two beats of the drive train was shortened from 120 msec to 0 msec, the peak right atrial pressure increased from 7 ± 3 mmHg to 15 ± 5 mmHg (P < 0.001). The increase in atrial pressure associated with simultaneous pacing of the atrium and ventricle resulted in shortening of the atrial ERP and ARP by 7.3 ± 5.2 and 6.2 ± 3.5 msec, respectively (P < 0.0011). Similar results were obtained during autonomic blockade. These findings confirm the presence of contraction‐excitation feedback in normal human atria.
AB - Contraction‐excitation feedback has been studied extensively in mammalian ventricles. In contrast, little is known about contraction‐excitation feedback in mammalian atria. The objective of this study was to investigate the effect of acute alterations in atrial pressure, induced by varying the atrioventricular (AV) interval, on atrial refractoriness. Twenty patients without structural heart disease participated in the study. In each patient the atrial effective (ERP) and absolute refractory periods (ARP) were measured during AV pacing at a cycle length of 500 msec and an AV interval of 120 msec. Acute increases in atrial pressure were induced by pacing the atrium and ventricle simultaneously for the final two beats of the drive train. The ERP was defined as the longest extrastimulus coupling interval that failed to capture with an extrastimulus current strength of twice the stimulation threshold. The ARP was defined in a similar manner with an extrastimulus current strength of 10 mA. The ERP and ARP were determined using the incremental extrastimulus technique. A subset of patients had the pacing protocol performed during autonomic blockade. As the AV interval of the final two beats of the drive train was shortened from 120 msec to 0 msec, the peak right atrial pressure increased from 7 ± 3 mmHg to 15 ± 5 mmHg (P < 0.001). The increase in atrial pressure associated with simultaneous pacing of the atrium and ventricle resulted in shortening of the atrial ERP and ARP by 7.3 ± 5.2 and 6.2 ± 3.5 msec, respectively (P < 0.0011). Similar results were obtained during autonomic blockade. These findings confirm the presence of contraction‐excitation feedback in normal human atria.
KW - atriovenfricular interval
KW - atrioventricular pacing
KW - contraction‐excitation feedback
KW - refractoriness
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U2 - 10.1111/j.1540-8159.1992.tb02954.x
DO - 10.1111/j.1540-8159.1992.tb02954.x
M3 - Article
C2 - 1279534
AN - SCOPUS:0026465474
SN - 0147-8389
VL - 15
SP - 1674
EP - 1680
JO - Pacing and Clinical Electrophysiology
JF - Pacing and Clinical Electrophysiology
IS - 11
ER -