Tachy-brady arrhythmias: The critical role of adenosine-induced sinoatrial conduction block in post-tachycardia pauses

BACKGROUND In patients with sinoatrial nodal (SAN) dysfunction, atria L pauses Lasting several seconds may follow rapid atrial pacing or paroxysmal tachycardia (tachy-brady arrhythmias). Clinical studies suggest that adenosine may pray an important rote in SAN dysfunction, but the mechanism remains unclear. OBJECTIVE To define the mechanism of SAN dysfunction induced by the combination of adenosine and tachycardia. METHODS We studied the mechanism of SAN dysfunction produced by a combination of adenosine and rapid atria L pacing in isolated coronary-perfused canine atria L preparations by using highresolution optical mapping (n = 9). Sinus cycle Length and sinoatrial conduction time (SACT) were measured during adenosine (1-100 mu M) and DPCPX (1 mu M; A1 receptor antagonist; n = 7) perfusion. Sinoatrial node recovery time was measured after 1 minute of slow pacing (3.3 Hz) or tachypacing (7-9 Hz). RESULTS Adenosine significantly increased sinus cycle Length (477 +/- 62 ms vs 778 +/- 114 ms; P < .01) and SACT during sinus rhythm (41 +/- 11 ms vs 86 +/- 16 ms; P < .01) in a dose-dependent manner. Adenosine dramatically affected SACT of the first SAN beat after tachypacing (41 +/- 5 ms vs 221 +/- 98 ms; P < .01). Moreover, at high concentrations of adenosine (10-100 mu M), termination of tachypacing or atria L flutter/fibrillation produced atrial pauses of 4.2 +/- 3.4 seconds (n = 5) owing to conduction bock between the SAN and the atria, despite a stable SAN intrinsic rate. Conduction bock was preferentially related to depressed excitability in SAN conduction pathways. Adenosine-induced changes were reversible on washout or DPCPX treatment. CONCLUSIONS These data directly demonstrate that adenosine contributes to post-tachycardia atria L pauses through SAN exit block rather than stowed pacemaker automaticity. Thus, these data suggest an important modulatory rote of adenosine in tachy-brady syndrome.