Background:
Treatment of hypertension during acute intracerebral hemorrhage (ICH) is controversial. There are concerns that in the context of disrupted cerebral autoregulation, blood pressure (BP) reduction may cause decreased cerebral blood flow (CBF), particularly in the perihematoma region. CBF was assessed using serial CT perfusion (CTP) studies. We hypothesized that CBF would remain stable following BP reduction.
Methods:
Acute primary ICH patients were imaged pre and post BP treatment. Perfusion maps were calculated from CTP source images. Mean CBF was measured in a 1cm perihematoma region, contralateral homologous regions and in both hemispheres. Mean cerebral blood volume (CBV), mean transit time (MTT), and time to drain (TTD) were calculated in the same manner. Relative measures (i.e. rCBF) were calculated as ratios/differences between ipsilateral and contralateral regions.
Results:
Sixteen patients (median age 75 (54-91)) were imaged with CTP (median time from onset 19.4 (2.0-72.2) h) and re-imaged 2.0 (1.1-3.3) h later. Median NIHSS at baseline was 9 (2-24); this remained stable at the time of the second CTP (10 (2-24), P=0.14). Baseline hematoma volume was 24.8±19.9 ml and there was no change at the time of the second CTP (26.3±22.1 ml, P=0.16). Patients were recruited from an ongoing trial, in which they were randomly treated to a target systolic BP of <150mmHg (n=9) or <180mmHg (n=7). Four patients received no antihypertensives as BP was below target at the time of randomization. Mean systolic BP in treated patients (n=12) decreased significantly between the first (165±23 mmHg) and second (143±18 mmHg, P<0.0001) CTP scans. Mean perihematoma CBF in treated patients was stable with BP reduction (pre=35.1±7.1 vs. post=35.4±6.2 ml/100g/min, P=0.87). Ipsilateral hemispheric CBF was also stable (pre=47.3±7.2 vs. post=46.4±7.1 ml/100g/min, P=0.66). Although perihematoma CBF was lower than in contralateral homologous regions (rCBF=0.72±0.11), BP reduction did not decrease this further (0.74±0.14 post-treatment, P=0.58). Ipsilateral hemispheric rCBF (0.96±0.06) was also unaffected by BP treatment (0.95±0.08, P=0.64). Perihematoma rCBF decreased in 5 treated patients, but never by >12%. Linear regression showed no relationship between changes in systolic BP and perihematoma rCBF (R=-0.002, [-0.005, 0.001], P=0.18). Perihematoma rCBV (pre=0.77±0.11 vs. post=0.79±0.10, P=0.20), rMTT (pre=0.51±0.54s vs. post=0.70±0.65s, P=0.26) and rTTD (pre=0.71±1.01s vs. post=0.89±0.84s, P=0.42) also remained stable following BP treatment.
Conclusions:
Acute BP reduction does not appear to exacerbate perihematoma oligaemia. Stability of CBF following acute BP treatment suggests preservation of cerebral autoregulation in ICH, within the range of arterial pressures studied. These findings support the safety of early BP treatment in ICH.
Brain hemorrhage after endovascular reperfusion therapy of ischemic stroke: a threshold-finding whole-brain perfusion CT study
