PET OEF reactivity for hemodynamic compromise in occlusive vascular disease.

BACKGROUND AND PURPOSE: Hemodynamic compromise in symptomatic patients with occlusive vascular disease (OVD) identified by cerebrovascular reserve (CVR) and oxygen extraction fraction (OEF) is an independent predictor of high stroke risk. However, up to 60% of patients compromised by CVR have normal OEF indicating a high rate of discordance. CVR is measured with an acetazolamide challenge, and OEF reactivity (OEFR) to acetazolamide, ie, a hemodynamic challenge, may reveal hemodynamic compromise and less discordance with measurements of CVR. METHODS: Nine symptomatic patients with OVD were studied by positron emission tomography before and 15 minutes after 15 mg/kg intravenous acetazolamide in the middle cerebral artery territories of each hemisphere. RESULTS: A close correlation between hemispheric CVR and OEFR was observed. Two hemispheres from two different patients showed an increase in OEF to acetazolamide challenge despite a normal baseline OEF. The two hemispheres showing an increase in OEF in response to acetazolamide were also associated with the lowest CVR and severest white matter hyperintensities. CONCLUSIONS: These observations suggest that positive OEFR may distinguish hemispheres in hemodynamic compromise despite normal OEF and show less discordance with CVR. However, these preliminary observations require confirmation in a larger study.

Identifying regions of compromised hemodynamics in symptomatic carotid occlusion by cerebrovascular reactivity and oxygen extraction fraction.

OBJECTIVES: Oxygen extraction fraction (OEF) and cerebrovascular reserve (CVR) are both proven predictors of stroke risk in symptomatic patients with carotid occlusion. Accordingly, hemispheric comparisons of CVR and OEF are significantly correlated. However, there was also substantial disagreement: hemispheres identified as compromised by CVR were normal by OEF. Our aim was to determine whether regional comparisons could resolve the CVR-OEF discordance. We also studied the relationship between white matter (WM) infarction and hemodynamic compromise. METHODS: Quantitative CVR and OEF were measured in 12 symptomatic patients with internal carotid artery occlusion. CVR and OEF comparisons were made in the anterior watershed (AWS), middle cerebral artery (MCA) and WM territories using various thresholds for hemodynamic compromise. Associations with WM infarction were also recorded. RESULTS: Comparison of CVR and OEF for the AWS and MCA showed high sensitivity (100%) with specificities of 83 and 40%, respectively. There was also agreement (k=Cohen's Kappa) for the AWS (k=0.83) and MCA (k=0.39) territories. CVR-OEF discordance was reduced with regional analysis. Hemodynamic compromise was more often found in patients with WM infarction. DISCUSSION: Regional comparison of CVR and OEF reduced the discordance compared with hemispheric analysis, especially for the AWS territory. Despite the persistence of some regions with compromised CVR and normal OEF, CVR is able to identify all regions with elevated OEF making it a useful screening technology. Future studies are needed to understand whether those remaining regions with compromised CVR are also at increased stroke risk despite normal OEF.

Differentiating hemodynamic compromise by the OEF response to acetazolamide in occlusive vascular disease.

Identification of increased stroke risk in a population of symptomatic patients with occlusive vascular disease (OVD) is presently accomplished by measurement of oxygen extraction fraction (OEF) or cerebrovascular reserve (CVR). However, many regions identified by compromised CVR are not identified by OEF. Our aim was to determine whether the response of OEF to acetazolamide, namely, oxygen extraction fraction response (OEFR) would identify those hemispheres in hemodynamic compromise with normal OEF. Nine patients symptomatic with transient ischemic attacks and strokes, and with occlusive vascular disease were studied. Anatomical MRI scans and T2-weighted images were used to identify and grade subcortical white matter infarcts. PET cerebral blood flow (CBF) and OEF were measured after acetazolamide. The relationship between CVR and oxygen extraction fraction response (OEFR) showed that positive OEFR occurred after acetazolamide despite normal baseline OEF values. The two hemispheres with positive OEFR were also associated with severe (> 3 cm) subcortical white matter infarcts. We found that the OEFR was highly correlated with CVR and identified hemispheres that were hemodynamically compromised despite normal baseline OEF.

Identification of hemodynamic compromise by cerebrovascular reserve and oxygen extraction fraction in occlusive vascular disease.

Cerebrovascular reserve (CVR) and oxygen extraction fraction (OEF) are used to identify hemodynamic compromise in symptomatic patients with carotid occlusive vascular disease, but evidence suggests that they are not equivalent. The authors studied the relationship between CVR and OEF to evaluate their equivalence and stages of hemodynamic compromise. Symptomatic patients (N = 12) with carotid occlusion were studied by stable xenon-computed tomography CBF after intravenous acetazolamide administration for CVR, followed within 24 hours by positron emission tomography (PET) for OEF. Middle cerebral artery territories were analyzed by hemisphere and level. Hemispheric subcortical white matter infarctions were graded with magnetic resonance imaging. Both hemispheric and level analysis of CVR and OEF showed a significant (P = 0.001), negative linear relationship [CVR (%) = -1.5 (OEF) + 83.4, (r = -0.57, P = 0.001, n = 24]. However, 37.5% of the hemispheres showed compromised CVR but normal OEF and were associated (P = 0.019) with subcortical white matter infarction. CMRO2 was elevated in stage II hemodynamic compromise (CVR < 10%, OEF > 50%). CVR and OEF showed a significant negative linear relationship in stage II hemodynamic compromise but revealed hemispheres in hemodynamic compromise by CVR but normal OEF that were associated with subcortical white matter infarction.