Bilateral increase in CO2 reactivity after unilateral carotid endarterectomy.
BACKGROUND AND PURPOSE: A low or absent CO2 reactivity is considered indicative of a compromised hemodynamic compensatory capacity in patients with internal carotid artery (ICA) stenosis or occlusion. The aim of the present study was to investigate whether patients with preoperatively decreased or absent CO2 reactivity show an improvement of CO2 reactivity 3 months after carotid endarterectomy (CEA) and whether the preoperative CO2 reactivity is correlated with clinical classification and hemodynamic factors. METHODS: A group of 65 patients with > 70% ICA stenosis was studied. CO2 reactivity was measured by bilateral transcranial Doppler sonography before and 3 months after CEA. RESULTS: The preoperative CO2 reactivity was not significantly different in subgroups formed according to the presenting clinical symptoms. Patients with severe ICA stenosis with contralateral ICA occlusion had mean low preoperative CO2 reactivity on both sides. Furthermore, patients with reversed flow in the ophthalmic artery had low mean preoperative CO2 reactivity on the same side. The CO2 reactivity was not significantly different in the subgroups of patients with signs of collateral blood flow through the anterior or posterior communicating artery. In particular, patients with low preoperative CO2 reactivity (approximately < 30%) showed an evident increase after the operation. Such an inverse correlation was found bilaterally, although it was more pronounced on the CEA side. CONCLUSIONS: CEA can increase CO2 reactivity in both hemispheres. This effect is most pronounced in patients with low (< 30%) preoperative CO2 reactivity. If this group represents patients who would be at risk from low-flow stroke, then testing of CO2 reactivity might help select a subset of patients with an especially high probability of benefit from CEA.[1]References
- Bilateral increase in CO2 reactivity after unilateral carotid endarterectomy. Visser, G.H., van Huffelen, A.C., Wieneke, G.H., Eikelboom, B.C. Stroke (1997) [Pubmed]
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