Impaired cerebral vasoreactivity correlates with recent symptomaticity in severe carotid artery disease

Abstract

P62 OBJECTIVE: Impaired cerebral vasomotor reactivity has been proposed as a measure of exhausted vascular reserve in patients with carotid artery stenosis or occlusion. We tested this hypothesis by measuring vasoreactivity in patients with asymptomatic or recently symptomatic severe carotid artery disease. METHODS: Fourteen patients with severe carotid artery disease (5 with occlusion, 9 with stenosis 80–99%, 8 symptomatic, 6 asymptomatic within 2 years) and 7 healthy controls had continuous bilateral monitoring of mean flow velocity (MFV) in the MCAs by transcranial Doppler (TCD). End-tidal CO2 was measured continuously with an in-line capnometer connected via snorkel mouthpiece, nasal airway occluded by noseclip. After baseline measurements, subjects held their breath for 30 seconds. A breath holding index (BHI) was calculated (% change in MFV/seconds held). After return to baseline MFV, subjects breathed a 5% CO2 gas mixture for 2 minutes. CO2 reactivity was calculated as percent rise in MFV per mmHg PCO2 once the MFV curve plateaued. ANOVA was used to calculate differences between symptomatic, asymptomatic and control groups for CO2 reactivity and BHI. RESULTS: There was a highly significant difference in vasoreactivity by CO2 inhalation in the symptomatic group (2.02±.80 %/mmHg) versus the asymptomatic group (4.45±1.9 %/mmHg) and controls (3.69±.95 %/mmHg) (F 2,18 =7.85, p=.004). A linear relationship was seen between MFV and PCO2, taking multiple MFV measurements at various PCO2 levels throughout the study period (average r 2 =.60 for patients, .77 for controls). BHI did not distinguish between the groups (p=.37). CONCLUSIONS: Measuring cerebral vasoreactivity by CO2 inhalation with continuous TCD monitoring provides an important physiological index of the clinical status of patients with carotid artery disease which may help guide treatment algorithms. The linear relationship between MCA MFV and end-tidal CO2 enables confirmation of the baseline and maximum measurements used to calculate CO2 reactivity, and provides the opportunity to investigate further the link between physiology and clinical state.