Key result
Tilt-table testing induced a neurally mediated syncope reaction in 48% of syncopal patients with sick sinus syndrome, significantly higher than the 20% observed in healthy controls (P<0.005).
Why the study?
Do syncopal patients with sick sinus syndrome exhibit a neurally mediated syncope reaction during tilt-table testing compared to patients with syncope of unknown etiology and healthy controls?
Observational (n=90)
Do syncopal patients with sick sinus syndrome exhibit a neurally mediated syncope reaction during tilt-table testing compared to patients with syncope of unknown etiology and healthy controls?
Absolute Event Rate: 48% vs 20%
p-value: p=< 0.005
Syncopal patients with sick sinus syndrome frequently exhibit a neurally mediated syncope reaction during tilt-table testing, suggesting a potential role for concurrent beta-blocker therapy to prevent recurrent syncope.
May indicate overlapping vasovagal mechanisms in sick sinus syndrome syncope; hypothesis-generating and should not yet change practice.
Background A possible role of a neurally mediated component in the syncope mechanism of patients with sick sinus syndrome has not been adequately evaluated. Methods We examined and compared three groups: group 1, 25 syncopal patients (age 55 ± 15, M/F 18/7, syncope attacks per patient 6 ± 7) with sick sinus syndrome (persistent unexplained bradycardia with a long sinus pause and/or a long sinus node recovery time, a long sinoatrial conduction time, a low intrinsic heart rate, and/or an incompetent chronotropic response to atropine); group 2: 45 patients (age 43 ± 18, M/F 28/17, syncope attacks per patient 6 ± 7) with syncope of unknown etiology; group 3:20 healthy controls (age 34 ± 9, M/F 16/4). The tilt‐table test protocol used consisted of an initial 20‐minute period at 80° tilt followed by three 10‐minute periods in the same position under graded isoproterenol intravenous infusion at 1–3 μ;g/min. The test was considered positive if presyncope or syncope due to hypotension and/or bradycardia was induced. Results A similar proportion of group 1 and group 2 patients developed a positive test (12 or 48% and 25 or 56%, respectively, P:NS) with a similar positive tilt‐table test duration in both groups (41 ± 22 vs 43 ± 17 minutes, P:NS). In contrast, only four of the group 3 healthy controls (20%) developed a positive test with a much longer test duration (P < 0.005). Conclusions Syncopal patients with sick sinus syndrome commonly exhibit a neurally mediated syncope reaction during a tilt‐table test. This might explain the occasional failure to prevent recurrent syncope in sick sinus syndrome patients treated with cardiac pacing. Concurrent β‐blocker therapy may be indicated for such patients.
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Gatzoulis et al. (1999) conducted an observational in Syncope with sick sinus syndrome (n=90). Tilt-table testing vs. Healthy controls and syncope of unknown etiology was evaluated on Positive tilt-table test (presyncope or syncope due to hypotension and/or bradycardia) (p=< 0.005). Tilt-table testing induced a neurally mediated syncope reaction in 48% of syncopal patients with sick sinus syndrome, significantly higher than the 20% observed in healthy controls (P<0.005).
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