Abstract

Tilt was used physiologically, 1930s–1970s, becoming a clinical diagnostic test for syncope in 1980s. Tilt has been criticized recently for failing to discriminate between reflex and more sinister syncope. Studies on possible benefit of pacing for older reflex syncope patients (2012–2014) yielded unexpected results. Patients with electrocardiogram implantable loop recorder (ILR) documented asystole and negative tilt, despite history strongly suggestive of reflex syncope, did well with pacing having syncope recurrence similar to that in paced His-Purkinje disease, while those with identical ILR findings and positive tilt did little better than those without pacing. These findings prompted explanation. The hypothesis hinged on tilt revealing a hypotensive/vasodepressor tendency rather than defining vasovagal syncope. Support was drawn from literature demonstrating good test sensitivity and specificity but no clinical value in arrhythmic, unexplained, or structural cardiovascular disease syncope. Further, in carotid sinus syndrome, another reflex syncope, the same pattern of disappointing pacing results was seen when tilt was positive but lack of syncope when tilt was negative. Thus, rethinking tilt testing is required to portray it in reflex, arrhythmic, unexplained, and cardiovascular syncope as having value in demonstrating risk of recurrence rather than being diagnostic. Its value in diagnosis of orthostatic hypotension (immediate/delayed), psychogenic pseudosyncope, and postural orthostatic tachycardia remains important and unchanged. The hypothesis has additional implications for management of hypertensive patients with syncope where medication may exacerbate symptoms requiring reduction/discontinuation. Tilt testing has greater value now than that claimed at its 1986 introduction.

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