EFFECT OF ATRIOVENTRICULAR INTERVAL DURING PACING OR RECIPROCATING TACHYCARDIA ON ATRIAL SIZE, PRESSURE, AND REFRACTORY PERIOD - CONTRACTION-EXCITATION FEEDBACK IN HUMAN ATRIUM

To determine whether a contraction-excitation feedback mechanism exists in human atrium, we investigated the effects of varying the atrioventricular (AV) interval from 0 to 360 msec during AV pacing at a cycle length of 400 msec on atrial pressure, size, and refractoriness in 10 patients (group 1, without supraventricular tachycardia). The same parameters were determined in another 10 patients (group 2, with different spontaneous AV relations) during AV reciprocating tachycardia or AV nodal reciprocating tachycardia and during high right atrial (RA) pacing at the tachycardia cycle length. In group 1 patients, peak and mean RA pressure, RA effective refractory period (RA-ERP), and left atrial (LA) size all decreased to minimal values at an AV interval of 120 msec and remained low as the AV interval was increased and approached 400 msec. The increase in each of the variables from its lowest to greatest value was as follows: Mean systemic blood pressure, 20.9±3.1 mm Hg; LA size, 0.55±0.05 cm; RA peak pressure, 10.4±1.8 mm Hg; RA mean pressure, 3.5±0.6 mm Hg; and RA-ERP, 22.5±3.0 msec, p<0.001 for each. The weighted mean correlation coefficient with RA-ERP was significant for RA peak pressure and LA size (p<0.001 for each). These same relations were investigated in five patients with the Wolff-Parkinson-White syndrome and AV reciprocating tachycardia and five patients with AV nodal reciprocating tachycardia (group 2). In the patients with Wolff-Parkinson-White syndrome, the increase in each variable measured during tachycardia versus that measured during RA pacing (at the tachycardia rate) was as follows: LA size, 0.45±0.28 cm (p<0.05); RA peak pressure, 4.5±2.0 mm Hg (p<0.01); RA mean pressure, 1.7±1.2 mm Hg (p<0.05); and RA-ERP, 30.0±23.2 msec (p<0.05). The mean blood pressure did not change. In the patients with AV nodal reciprocating tachycardia, similar increases occurred during tachycardia (compared with atrial pacing at the same rate) as follows: LA size, 0.59±0.20 cm (p=0.03); RA peak pressure, 8.0±5.2 mm Hg (p=0.03); RA mean pressure, 3.6±1.1 mm Hg (p=0.03); and RA-ERP, 57±56 msec (p=0.03). Again, the mean blood pressure did not change. We conclude that 1) a very short or very long AV interval causes an increase in RA pressure, LA size, and RA refractoriness, and 2) during reciprocating tachycardia, LA size, RA pressure, and RA-ERP are all greater than during atrial pacing at the same cycle length, probably due to the AV relations characteristic of these arrhythmias. Thus, a contraction-excitation feedback mechanism exists in the human atrium and might be partly responsible for some arrhythmias in man.