ORIGINAL ARTICLE Heart Vessels (2004) 19:221–224 © Springer-Verlag 2004 DOI 10.1007/s00380-004-0772-x Michael Efremidis · Antonios Sideris Gerasimos Filippatos · Dimitrios Manolatos Sotiris Xydonas · Dimitrios Ikonomou Dimitrios Evangelou · Ilias Sioras · Michael Argyriou Fotis Kardaras Effect of atrial pressure increase on sinus node automaticity Received: June 19, 2003 / Accepted: February 28, 2004 Abstract There is evidence suggesting that atrial electro- physiological properties may be changed by an acute in- crease in atrial pressure. The aim of the present study was to investigate the effect of alteration, in atrial pressure on sinus node recovery time. Twelve patients (8 men and 4 women, mean age 61.3  14.1 years) were included in this study. None of the patients had organic heart disease. Sinus node recovery time (SNRT) was measured following atrial pacing and atrioventricular (AV) pacing at sequential cycle lengths of 600, 545, 500, 461, 428, and 400 ms with two different AV intervals (150, 0 ms). Peak and minimal atrial pressure increased significantly from 8.5  2.8 to 20.1  2.9 mmHg (11.56  3.8 to 27.3  3.9 cmH 2 O) (P = 0.001) and from 2.06  1.69 to 5.33  2.9 mmHg (2.8  2.29 to 7.2  3.9 cmH 2 O), respectively (P = 0.002) during AV interval modification. Sinus node recovery time did not change de- spite the increase in atrial pressure. Autonomic blockade had no effect on SNRT. This study demonstrates that atrial pressure increase does not significantly affect sinus node automaticity expressed by SNRT. Key words Sinus automaticity · Contraction–excitation feedback · Mechanoelectrical feedback · Atrial pressure increase Introduction The occurrence of electrophysiological changes in response to mechanical perturbations or changes in hemodynamic M. Efremidis · A. Sideris · G. Filippatos 1 (*) · D. Manolatos · S. Xydonas · D. Ikonomou · D. Evangelou · I. Sioras · M. Argyriou · F. Kardaras Second Department of Cardiology, “Evangelismos” General Hospital, Athens, Greece Correspondence address: 1 28 Doukissis Plakentias Street, 115 23 Ambelokipi, Athens, Greece Tel. +30-210-804-8427; Fax +30-210-810-4367 e-mail: geros@otenet.gr loading has been termed mechanoelectrical feedback. 1 Calkins et al. studied the effect of the atrioventricular rela- tionship on atrial refractoriness in humans. 2 The effective (ERP) and absolute refractory periods (ARP) were mea- sured during atrioventricular (AV) pacing with varying AV intervals. The increase in atrial pressure associated with simultaneous pacing of the atrium and ventricle resulted in shortening of the atrial ERP and ARP. Efremidis et al. showed that atrial pressure increase did not significantly change the ERP, the dispersion of ERP, or the functional refractory period in patients with a history of lone atrial fibrillation. 3 In contrast, Klein et al. demonstrated in human atrium that a very short or very long AV interval causes an increase in right atrial pressure and right atrial refractori- ness. 4 Although the mechanoelectrical feedback has been well studied in ventricular and atrial myocardium, its effect on sinus node electrophysiological parameters has not been fully investigated. The aim of the present study was to ex- amine whether an increase in atrial pressure during atrio- ventricular interval modification might affect the sinus node recovery time. Patients and methods Twelve patients (8 men and 4 women, mean age 61.3  14.1 years) were included in this study. Informed consent was obtained and the protocol was approved by the hospital’s ethical committee. The electrophysiological study was performed to investigate episodes of syncope. None of the patients in this study had structural heart disease, atrial tachyarrhythmias, hypertension, or thyroid disease. The electrophysiological study was performed with the patient in a lightly sedated, postabsorptive state. Two 6-F quadripolar catheter electrodes, with an interelectrode dis- tance of 5 mm, were inserted percutaneously through the femoral vein. The first one was positioned at the high lateral wall near the junction of the superior vena cava and the right atrium, and the second one at the right ventricular apex. A pressure-recording catheter was inserted into the