Introduction
Tilt-testing (TT) is a surrogate of orthostatic stress, and one of the
strongest stressors for precipitation of orthostatic reflex syncope. So
far, it is not known why TT is positive in some patients and negative in
others who have reflex syncope with similar clinical features and
demographic characteristics\sout. Low sensitivity of TT is claimed to
be the explanation for these differences in responses. We have sought an
alternative explanation in hemodynamic differences.
TT has been shown to be able to induce reflex syncope in 66% of
patients presenting a history compatible with reflex
syncope1, but the clinical features and the outcome of
patients with positive tilt response are similar to those of patients
with negative response 2. Patients with negative and
positive tests have similar symptoms and symptom
burdens3, similar clinical outcomes in the 3 years
following their TTs4, and have links between symptoms
and outcomes.4-6 Many studies have tried to find
variables associated with positive TT with uncertain or contrasting
results.7-13 In general, these studies being small and
with other limitations have been unable to give a definite answer, and
the applied methodology was inconsistent as, also, was selection of
patients and controls. Owing to the inability to identify variables able
to explain a positive TT, some authors have suggested that a significant
number of patients with a clinical history compatible with reflex
syncope may have falsely negative tilt table test
results.3,14
Recent studies15,16 have emphasized the primary role
of hemodynamic changes in the mechanism of impending reflex syncope
during TT. In brief, a decrease in stroke volume precedes and may even
trigger reflex bradycardia and vasodilation, leading to ultimate
circulatory collapse. Thus, important hemodynamic changes appear to play
a major part in the onset of the vasovagal
reflex.16,17 We, thus, conceived that resting
cardiovascular physiology may substantially differ in patients with
positive and negative TT prompting us to hypothesize that hypotensive
susceptibility revealed by TT is favored by a specific baseline
hemodynamic pattern. To test this hypothesis, we analyzed a large
multi-center population of consecutive patients who underwent TT for
suspected reflex syncope.