© 2001 by European Society of Cardiology
Copyright © 2001, European Society of Cardiology
Evidence of parasympathetic impairment in some patients with cardiac syndrome X
aDepartment of Neurological Science and Vision, Section of Human Physiology, University of Verona, Strada Le Grazie 8, 37134 Verona, Italy
bDepartment of Biomedical and Surgical Science, Section of Cardiology, University of Verona, Verona, Italy
cUnit of Internal Medicine, Civic Hospital, San Bonifacio (Verona), Italy
dDivision of Cardiology, University ‘Piemonte Orientale’, Novara, Italy
* Corresponding author. Tel.: +39-45-802-7145; fax: +39-45-580-881 antonio.cevese{at}univr.it
Objectives: Cardiac syndrome X (SX) is a clinical condition characterised by angina, positive exercise stress test and negative coronary angiography; it has often been attributed to sympathetic hyperactivity. Here we tested the hypothesis that a parasympathetic, rather than a sympathetic, dysfunction could be the cause of the autonomic imbalance observed in SX. Methods: In 20 subjects with diagnosed SX and in 12 age-matched controls, we studied autonomic function by performing spectral analysis of RR interval and finger arterial pressure (SAP), in supine position and during head-up tilting. We also carried out a set of tests of parasympathetic function. Results: The group of SX patients did not differ significantly from control subjects in any of the variables tested. In a subgroup of 13 SX, however, tilting increased the low-frequency power of SAP, but did not induce the expected increase in low-frequency and decrease in high-frequency power of RR. These patients, in supine position, had significantly lower sinus arrhythmia and a higher ratio of low to high frequency of RR, in comparison with control subjects. We interpreted these differences as signs of reduced parasympathetic, but essentially normal sympathetic, activity. The parasympathetic tests confirmed vagal impairment in the same SX subjects. On the other hand, all the tests indicated normal parasympathetic functions in the control subjects and in those SX patients who displayed the expected spectral changes in tilting. Conclusions: In about two thirds of the patients with SX, the pathophysiological mechanism causing the symptoms could be related to the reduced parasympathetic tone, rather than to an augmented sympathetic activity.
KEYWORDS Autonomic nervous system; Coronary disease; Heart rate (variability); Microcirculation
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