Background ''Inappropriate'' sinus tachycardia (IST) is an uncommon an
d poorly defined atrial tachycardia characterized by inappropriate tac
hycardia and exaggerated acceleration of heart rate with ''normal'' P
wave. The mechanism of this tachycardia is unknown. The purpose of the
present study was to determine the role of autonomic balance in the g
enesis of IST. Methods and Results Six female patients aged 23 to 38 y
ears with IST and 10 age- and sex-matched control subjects were assess
ed with the following autonomic function tests: (1) sympathovagal bala
nce to the sinus node assessed by calculating the LF/HF (low frequency
/high frequency) ratio using power spectral analysis both in the supin
e position and after 10 minutes of head-up tilt to 60 degrees, (2) car
diovagal reflex assessed by cold face test (CFT), (3) beta-adrenergic
sensitivity as determined by calculating isoproterenol dose-response c
urves and isoproterenol chronotropic dose 25 (CD25), and (4) intrinsic
heart rate (IHR) assessed after autonomic blockade with atropine 0.04
mg/kg and propranolol 0.2 mg/kg administered as an intravenous bolus.
No significant differences in the LF/HF ratio both in the supine posi
tion (2.8+/-0.3 versus 2.6+/-0.4) and during upright tilt (8.7+/-1.3 v
ersus 8.5+/-0.5) were observed between control subjects and IST patien
ts. Cardiovagal response to CFT was markedly depressed in all patients
(6.3% IST patients versus 24.2% control subjects, P<.001). beta-Adren
ergic hypersensitivity to isoproterenol was noted in all patients (mea
n CD25 0.29+/-0.10 mu g IST patients versus 1.27+/-0.4 mu g control su
bjects; P<.001), and high IHR was noted in all cases. The patients wer
e treated with high doses of beta-blockers with adequate short-term co
ntrol. Radiofrequency catheter ablation of the sinus node area was per
formed in one drug-refractory patient. Conclusions These findings sugg
est that the mechanism leading to IST is related to a primary sinus no
de abnormality characterized by a high IHR, depressed efferent cardiov
agal reflex, and beta-adrenergic hypersensitivity.