Background and hypothesis: Previous research has failed to document tempora
l changes in epinephrine levels in patients with neurally mediated syncope
associated with exercise. The purpose of this study was to investigate the
role of circulatory catecholamines in exercise-induced neurally mediated sy
ncope, specifically focusing on epinephrine levels.
Methods: The present study deals with temporal changes of circulatory catec
holamine levels during head-up tilt tests (40 min, 80 degrees tilt) in 62 p
atients with syncope of unknown origin, 7 of whom had syncope associated wi
th exercise (exercise-induced group, 19 +/- 3 years). Data were compared wi
th 10 control subjects (control group, 45 +/- 23 years). Of the 55 patients
with syncope not associated with exercise, 32 tested positive for the head
-up tilt tests (positive group, 31 +/- 16 years) and 23 patients tested neg
ative (negative group, 46 +/- 19 years). Blood samples for circulatory cate
cholamine assay were obtained from the antecubital vein in the baseline sup
ine position 2 min after the tilt started, every 10 min during till, and at
the time of the onset of symptoms or the end of tilt. Levels of norepine-p
hrine and epinephrine were determined using the high-pressure liquid chroma
tography (HPLC) method (pg/ml).
Results: plasma norepinephrine levels among the four groups were similar at
the supine position and during had testing. In contrast, patients in the e
xorcise-induced group had significantly higher maximum epinephrine levels d
uring head-up tilt resting than the other three groups (288 +/- 191 vs. 148
+/- 117, 66 +/- 31, and 54 +/- 27 pg/ml, respectively, p < 0.05). Patients
in the positive group had higher maximum epinephrine levels than those in
the negative group (p< 0.05). Also, patients in the exercise-induced group
and those in the positive group had a significantly shorter tilt-testing ti
me than patients in the negative and control groups.
Conclusions: A marked increase of epinephrine was observed during head-up t
ilt testing in patients with neurally mediated syncope associated with exer
cise. The present findings further accelerate the identification of the rol
e of epinephrine in the mechanisms behind neurally mediated syncope associa
ted with exercise.