Key result
Cardiac syndrome X was associated with reduced parasympathetic tone and vagal impairment in 13 of 20 patients, rather than augmented sympathetic activity.
Why the study?
Is autonomic imbalance in cardiac syndrome X caused by parasympathetic dysfunction rather than sympathetic hyperactivity?
Case-Control (n=32)
Is autonomic imbalance in cardiac syndrome X caused by parasympathetic dysfunction rather than sympathetic hyperactivity?
In approximately two-thirds of patients with cardiac syndrome X, the pathophysiological mechanism may be related to reduced parasympathetic tone rather than augmented sympathetic activity.
Challenges sympathetic-focused views of cardiac syndrome X; leaves open vagal-targeted therapies pending prospective trials.
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.
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Giosué Gulli (2001) conducted a case-control in Cardiac syndrome X (n=32). Cardiac syndrome X vs. Age-matched controls was evaluated on Autonomic function assessed by spectral analysis of RR interval and finger arterial pressure. Cardiac syndrome X was associated with reduced parasympathetic tone and vagal impairment in 13 of 20 patients, rather than augmented sympathetic activity.
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