Premium
Effects of An Acute Increase in Atrial Pressure on Atrial Refractoriness in Humans
Author(s) -
CALKINS HUGH,
ELATASSI RAFEL,
KALBFLEISCH STEVEN,
LANGBERG JONATHAN,
MORADY FRED
Publication year - 1992
Publication title -
pacing and clinical electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.686
H-Index - 101
eISSN - 1540-8159
pISSN - 0147-8389
DOI - 10.1111/j.1540-8159.1992.tb02954.x
Subject(s) - medicine , refractory period , cardiology , ventricle , atrium (architecture) , effective refractory period , anesthesia , blood pressure , atrial fibrillation
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.