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.