Better assessment of acute stroke using a revised strategy for bolus-tracking perfusion imaging and a novel volumetric analysis methodology

Bibliography: p. 172-186Some pages are in colour

Early hematoma retraction in intracerebral hemorrhage is uncommon and does not predict outcome.

BACKGROUND:Clot retraction in intracerebral hemorrhage (ICH) has been described and postulated to be related to effective hemostasis and perihematoma edema (PHE) formation. The incidence and quantitative extent of hematoma retraction (HR) is unknown. Our aim was to determine the incidence of HR between baseline and time of admission. We also tested the hypothesis that patients with HR had higher PHE volume and good prognosis. METHODS:This was a retrospective single-centre study in which serial planimetric volume measurements of the total hematoma volume (parenchymal (IPH) and intraventricular (IVH)) and PHE were performed in ICH patients with baseline non-contrast computed tomography (CT) completed within 6 hours of onset and follow-up CT 24 (±12) hours from symptom onset. HR was defined as a decrease in volume of >3ml or >15%, and hematoma expansion (HE) as an increase of >6ml or >30%. All other patients were categorized as stable hematoma (HS). Good outcome was defined as modified Rankin Scale (mRS) 0-2 at 90 days. RESULTS:A total of 136 patients (mean age = 69.3±13.39 years, 58.1% male) were included. Median (interquartile range) baseline total hematoma volume was 14.96 (7.80, 31.88) ml. HR >3ml and >15% occurred in 6 (4.4%) and 8 (5.9%) patients, respectively. Neither definition of HR was associated with follow-up PHE (p>0.297) or good outcome (p>0.249). IVH was the only independent predictor of HR (p<0.0241). CONCLUSIONS:Early HR is rare and associated with IVH, but not with PHE or clinical outcome. There was no relationship between HR, PHE, and patient prognosis. Therefore, HR is unlikely to be a useful endpoint in clinical ICH studies

Blood–Brain Barrier Compromise Does Not Predict Perihematoma Edema Growth in Intracerebral Hemorrhage

There are limited data on the extent of blood-brain barrier (BBB) compromise in acute intracerebral hemorrhage patients. We tested the hypotheses that BBB compromise measured with permeability-surface area product (PS) is increased in the perihematoma region and predicts perihematoma edema growth in acute intracerebral hemorrhage patients. Patients were randomized within 24 hours of symptom onset to a systolic blood pressure (SBP) treatment of <150 (n=26) or <180 mm Hg (n=27). Permeability maps were generated using computed tomographic perfusion source data acquired 2 hours after randomization, and mean PS was measured in the hematoma, perihematoma, and hemispheric regions. Hematoma and edema volumes were measured on noncontrast computed tomographic scans obtained at baseline, 2 hours and 24 hours after randomization. Patients were randomized at a median (interquartile range) time of 9.3 hours (14.1) from symptom onset. Treatment groups were balanced with respect to baseline SBP and hematoma volume. Perihematoma PS (5.1±2.4 mL/100 mL per minute) was higher than PS in contralateral regions (3.6±1.7 mL/100 mL per minute; P<0.001). Relative edema growth (0-24 hours) was not predicted by perihematoma PS (β=-0.192 [-0.06 to 0.01]) or SBP change (β=-0.092 [-0.002 to 0.001]). SBP was lower in the <150 target group (139.2±22.1 mm Hg) than in the <180 group (159.7±12.3 mm Hg; P<0.0001). Perihematoma PS was not different between groups (4.9±2.4 mL/100 mL per minute for the <150 group, 5.3±2.4 mL/100 mL per minute for the <180 group; P=0.51). BBB permeability is focally increased in the hematoma and perihematoma regions of acute intracerebral hemorrhage patients. BBB compromise does not predict acute perihematoma edema volume or edema growth. SBP reduction does not affect BBB permeability. URL: http://www.clinicaltrials.gov. Unique identifier: NCT00963976

Aggressive blood pressure reduction is not associated with decreased perfusion in leukoaraiosis regions in acute intracerebral hemorrhage patients.

Leukoaraiosis regions may be more vulnerable to decreases in cerebral perfusion. We aimed to assess perfusion in leukoaraiosis regions in acute intracerebral hemorrhage (ICH) patients. We tested the hypothesis that aggressive acute BP reduction in ICH patients is associated with hypoperfusion in areas of leukoaraiosis. In the ICH Acutely Decreasing Arterial Pressure Trial (ICH ADAPT), patients with ICH <24 hours duration were randomized to two systolic BP (SBP) target groups (<150 mmHg vs. <180 mmHg). Computed tomography perfusion (CTP) imaging was performed 2h post-randomization. Leukoaraiosis tissue volumes were planimetrically measured using semi-automated threshold techniques on the acute non-contrast CT. CTP source leukoaraiosis region-of-interest object maps were co-registered with CTP post-processed maps to assess cerebral perfusion in these areas. Seventy-one patients were included with a mean age of 69±11.4 years, 52 of whom had leukoaraiosis. The mean relative Tmax (rTmax) of leukoaraiotic tissue (2.3±2s) was prolonged compared to that of normal appearing white matter in patients without leukoaraiosis (1.1±1.2s, p = 0.04). In the 52 patients with leukoaraiosis, SBP in the aggressive treatment group (145±20.4 mmHg, n = 27) was significantly lower than that in the conservative group (159.9±13.1 mmHg, n = 25, p = 0.001) at the time of CTP. Despite this SBP difference, mean leukoaraiosis rTmax was similar in the two treatment groups (2.6±2.3 vs. 1.8±1.6 seconds, p = 0.3). Cerebral perfusion in tissue affected by leukoaraiosis is hypoperfused in acute ICH patients. Aggressive BP reduction does not appear to acutely aggravate cerebral hypoperfusion