Patterns of cerebrovascular reactivity in patients with unilateral asymptomatic carotid artery stenosis.

BACKGROUND AND PURPOSE

Intracranial hemodynamic status varies in patients with unilateral significant carotid artery stenosis. It ranges from normal, because of sufficient collaterals, to poor, because of a severely reduced blood supply that puts the patient at an increased risk of stroke or cerebral ischemia. The present study examined patterns of abnormal cerebrovascular hemodynamics in patients with asymptomatic carotid artery stenosis.

METHODS

The CO2 reactivity of the cerebral resistance index (CRi) and of mean blood flow velocity (vmean) was determined via transcranial Doppler sonography in 91 patients with unilateral high-grade to threadlike carotid artery stenosis and in 37 control subjects. The interhemispheric asymmetry of CRi reactivity of the control group was used to differentiate between normal and abnormal findings.

RESULTS

We found that 64.8% of the patients demonstrated normal CRi asymmetry with comparable CRi reactivity (ipsilateral, 4.42 +/- 0.44 %CRi/vol%CO2; contralateral, 4.51 +/- 0.39 %CRi/vol%CO2) and vmean reactivity (ipsilateral, 0.080 +/- 0.004 m/s per vol%CO2; contralateral, 0.079 +/- 0.005 m/s per vol%CO2) at both hemispheres. In 16.5% of the patients, CRi reactivity was supranormal at the affected hemisphere. This phenomenon was due to an exaggerated dilatory response of the ipsilateral hemisphere and was combined with an absent CRi reactivity of the contralateral hemisphere (ipsilateral, 6.63 +/- 1.03 %CRi/vol%CO2; contralateral, -1.16 +/- 1.78 %CRi/vol%CO2). In contrast, hemispheric vmean reactivities were comparable (ipsilateral, 0.078 +/- 0.008 m/s per vol%CO2; contralateral, 0.077 +/- 0.008 m/s per vol%CO2). The remaining 18.7% showed severely diminished ipsilateral CRi reactivity (ipsilateral, 1.91 +/- 0.83 %CRi/vol%CO2; contralateral, 8.48 +/- 1.00 %CRi/vol%CO2) and vmean reactivity (ipsilateral, 0.073 +/- 0.007 m/s per vol%CO2; contralateral, 0.108 +/- 0.012 m/s per vol%CO2; P < .01), compatible with a significantly reduced perfusion pressure at the poststenotic hemisphere.

CONCLUSIONS

Most asymptomatic patients do not suffer from severely abnormal hemodynamics at the poststenotic hemisphere. One small subgroup of patients presented with severely disturbed ipsilateral hemodynamics; another small subgroup demonstrated a steal phenomenon with secondary dilation of large cerebral vessels at the contralateral hemisphere. These subgroups require specific evaluation of proper treatment.