Noninvasive investigation of autonomic activity after carotid stenting or carotid endarterectomy

Objective: Carotid artery stenting (CAS) has been introduced as an alternative to carotid endarterectomy (CEA) for the treatment of carotid artery stenosis. Both techniques seem to be associated with postoperative hemodynamic lability. Both may induce baroreceptor dysfunction, possibly leading to transient impairment of cardiovascular autonomic activity and resulting in hemodynamic instability. This instability might contribute to postoperative morbidity. To elucidate these phenomena, we studied the cardiac baroreflex and autonomic cardiovascular control after CAS and CEA. Method: In 20 patients scheduled for CAS (n = 10) or CEA (n = 10), intra-arterial pressures and electrocardiograms were recorded during 10 minutes before and 8 and 24 hours after the procedure. Spontaneous cardiac baroreflex sensitivity was assessed using the sequence method and cross-spectral analysis. In addition, cardiovascular autonomic activity was investigated using spectral analysis of heart rate variability and systolic arterial pressure variability. Results: After CAS, we demonstrated an increase of the spontaneous baroreflex sensitivity median (interquartile range) from 5.6 (5.1 to 6.2) ms/mm Hg before the procedure to 8.8 (6.8 to 10.5) ms/mm Hg and 7.7 (3.9 to 8.6) ms/mm Hg (P < .001), 8 and 24 hours after the procedure. This was consistent with the increase of the high frequency component of heart rate variability reflecting cardiac parasympathetic activity and a decrease of the low frequency of systolic arterial pressure variability reflecting sympathetic vascular activity. The postoperative period was also associated with decreased systolic arterial pressure from 173 (162 to 190) mm Hg at baseline to 122 (109 to 143) mm Hg and 136 (121 to 143) mm Hg at 8 and 24 hours after CAS (P < .001). No changes in baroreflex sensitivity or in autonomic activity were observed after CEA. Conclusions: These preliminary data suggest that CAS is associated with parasympathetic predominance postoperatively and may probably explain the lower systolic arterial pressure observed after CAS.