912-43 Sick Sinus Syndrome. A Cardiac or a Neurocardiogenic Disorder?

Abstract

The commonly proposed mechanism of syncope in patients (pts) with sick sinus syndrome (SSS) is a long sinus pause without an effective escape rhythm. Nevertheless, the probability of a coexistent neurally mediated syncope (NMS) component has not been adequatelly investigated in these pts. We studied 3 groups: Gl: 12 syncopal pts (age: 58 ± 12 years, M/F: 9/3) with SSS (unexplained sinus bradycardia with inadequate chronotropic response to exercise or atropine, long sinus node recovery or sinoatrial conduction times and low intrinsic heart rate), G2; 52 pts (37 ± 17 years, M/F; 18/12) with syncope of unknown etiology and G3: 20 healthy controls (HC) (34 ± 9 years, M/F: 16/4). The same tilt table test (TTT) protocol was used (20 min in 80° upright followed by three 10 min stages in the same position under graded isoproterenol intravenous infusion at 1 – 3μg/min). TTT was considered positive (pos) if induced pre or syncope due to hypotension with or without bradycardia. A pos TTT was observed in 7 Gl pts (58.3%) and 30 G2 pts (57.7%) (p: NS). In contrast, only 4 of the G3 HC (20%) developed syncope (p < 0.005). The mean pos TTT duration was similar in both pts with SSS and pts with NMS (57 ± 18 vs 55 ± 17 min, p: NS). The mean posm duration was longer in the 4 HC with an induced vagotonic reaction when compared to the 30 NMS pts of G2168 ± 10 vs 55 ± 17 min, p < 0.05). We conclude that syncopal SSS pts commonly demonstrate a pos TTT. This might explain the occasional failure to avoid recurrence of syncope in SSS pts treated with cardiac pacing.