Background: Bilateral severe obstruction of the internal carotid artery is a hemodynamically critical state. We aimed to (1) analyze dynamic cerebral autoregulation (DCA) in affected patients, and (2) to correlate DCA data with different collateral flow patterns.
Methods: DCA was assessed noninvasively by transfer function analysis (phase shift) of respiratory-induced oscillations at 0.1 Hz of arterial blood pressure (Finapres method) and cerebral blood flow velocity (transcranial Doppler) in 30 patients with severe bilateral carotid stenosis (> or =75%) or occlusion. CO(2)-reactivity was measured via inhalation of 7% CO(2). 30 patients with unilateral stenosis were recruited as controls.
Results: Patients with bilateral 75-89% stenosis had a virtually preserved phase shift. A pronounced reduction was found in bilateral critical stenosis or obstruction (90-100%). Patients with ipsilateral 90-100% and contralateral 75-89% stenosis had a significantly less severe reduction of phase shift on the ipsilateral side. CO(2)-reactivity showed a less marked reduction in patients with bilateral critical stenosis or occlusion. Phase shift was best if "Willisian" collaterals were present. Significantly reduced values were found if only secondary collaterals (ophthalmic artery, leptomeningeal flow) were detected. Poorest values occurred with recruitment of functionally stenosed "Willisian" collaterals. CO(2)-reactivity showed poor values with sole recruitment of secondary collaterals, whereas functionally stenosed primary collaterals did not show values as poor as for phase shift. Clinically symptomatic patients had significantly lower phase shift and CO(2)-reactivity values.
Conclusions: DCA is severely impaired in bilateral critical carotid stenosis or occlusion. Sole recruitment of secondary collaterals and signs of a functional stenosis in primary ("Willisian") collaterals reflect insufficient collateral supply with a poor hemodynamic status. CO(2)-reactivity assessing the vasodilatory reserve and DCA represent different information for characterizing cerebral hemodynamic impairment. Determining transfer function phase might be a physiologically well supported approach for analysis of cerebral hemodynamic compromise.