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Patterns of cerebrovascular reactivity in patients with unilateral asymptomatic carotid artery stenosis
H Fürst1, W H Hartl, I Janssen
1Department of Surgery, Klinikum Grosshadern, Ludwig-Maximilian University Munich, FRG.
Insights
Most patients with asymptomatic carotid artery stenosis have normal intracranial hemodynamics. However, some show abnormal cerebrovascular reactivity, including a steal phenomenon, requiring specific treatment evaluation.
Area of Science:
- Neurology
- Vascular Medicine
- Medical Imaging
Background:
- Intracranial hemodynamics vary significantly in patients with carotid artery stenosis.
- Hemodynamic status can range from normal (due to collaterals) to poor (reduced blood supply), increasing stroke risk.
- Understanding these variations is crucial for managing patients with asymptomatic carotid artery stenosis.
Purpose of the Study:
- To investigate patterns of abnormal cerebrovascular hemodynamics in patients with asymptomatic carotid artery stenosis.
- To analyze CO2 reactivity of cerebral resistance index (CRi) and mean blood flow velocity (vmean).
- To differentiate between normal and abnormal hemodynamic findings using interhemispheric asymmetry.
Main Methods:
- Transcranial Doppler sonography was used to measure CO2 reactivity of CRi and vmean.
- The study included 91 patients with unilateral high-grade to threadlike carotid artery stenosis and 37 controls.
- Interhemispheric asymmetry of CRi reactivity in controls served as a baseline for normal findings.
Main Results:
- 64.8% of patients exhibited normal CRi asymmetry and comparable reactivity in both hemispheres.
- 16.5% showed supranormal CRi reactivity in the affected hemisphere, indicating an exaggerated dilatory response.
- 18.7% displayed severely diminished ipsilateral CRi and vmean reactivity, suggesting reduced perfusion pressure.
Conclusions:
- Most asymptomatic carotid stenosis patients maintain normal hemodynamics.
- A small subgroup experiences severely disturbed ipsilateral hemodynamics.
- Another subgroup presents a steal phenomenon, necessitating tailored treatment strategies.
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.