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Mean ( Ϯ SD) perihematoma and contralateral homologous region cerebral blood flow, cerebral blood volume, cerebral perfusion pressure, and cerebrovascular reserve.
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Background and purpose:
Although blood pressure reduction has been postulated to result in a fall in cerebral perfusion pressure in patients with intracerebral hemorrhage, the latter is rarely measured. We assessed regional cerebral perfusion pressure in patients with intracerebral hemorrhage by using CT perfusion source data.
Materials and metho...
Contexts in source publication
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... perihematoma CBF in all 73 patients (38.7 11.9 mL/100 g/min; Fig 2) was significantly lower than that in contralateral homologous regions (44.1 11.1 mL/100 g/min, P .001). Mean ipsilateral hemispheric CBF (42.1 10.5 mL/100 g/min) was lower than that in the contralateral hemisphere (43.4 10.5 mL/ 100 g/min, P .001). ...
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... was a reduction in perihematoma CBV (3.65 0.70 mL/100 g; Fig 2) compared with the contralateral regions (4.21 1.53 mL/100 g, P .001). Mean ipsilateral hemispheric CBV (3.83 0.63 mL/100 g) was lower than that in the contralateral hemisphere (3.88 0.64 mL/100 g, P .033). ...
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... CPP (14.4 4.6 minutes 1 ) was similar to that in contralateral homologous regions (14.3 4.8 minutes 1 , P .93; Fig 2). Ipsilateral hemispheric CPP (14.6 4.6 minutes 1 ) was also comparable with that in the contralateral hemispheric CPP (14.8 4.9 minutes 1 , P .28). ...
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... in an antecubital vein. CTP images were acquired every 1 second for 50 seconds (80 KV[p], 200 mA per image), and all sections were 5-mm-thick. All patients had a repeat NCCT scan at 24 Ϯ 3 hours. Raw contrast-enhanced CT images were imported into the Perf- Scape analysis package (2.0 CT Edition; Olea Medical, La Ciotat, France) software. An arterial input function was manually selected over the contralateral anterior cerebral artery, while the venous output function was obtained over the confluence of the sinuses. Perfusion maps were derived from the tissue time-atten- uation curve on the basis of the change in x-ray attenuation, which is linearly related to iodinated contrast concentration on a per-voxel basis with time. Errors introduced by delay and disper- sion of the contrast bolus before arrival in the cerebral circulation were corrected for by using a block-circulant deconvolution algo- rithm. 22 Quantitative perfusion indices, including CBF and CBV, were calculated on a voxelwise basis and used to generate color- coded maps. All perfusion maps were transferred to the Analyze 11.0 software package (AnalyzeDirect, Overland Park, Kansas). 23 Maps of CPP and cerebrovascular resistance (CVR) were generated by using a voxelwise calculation of CBF/CBV and 1/CBV, respectively (Fig 1), as previously described. 18 The perimeter of the hematoma was outlined on the precontrast arrival CT source image by using a semiautomated intensity Hounsfield unit threshold technique, as previously described. 24 Internal and external BZ and 7-mm perihematoma ROIs were manually outlined (Fig 1). In cases in which the hematoma itself involved a BZ, the latter was not outlined. All voxels containing blood vessels were removed from the ROI by using an intensity-threshold function. On the basis of previous studies, voxels with CBF of Ͼ 100 mL/100 g/min or CBV of Ͼ 8 mL/100 g were assumed to contain vessels and removed from the ROI. 25-27 Mean perfusion indices were measured in all ROIs, contralateral homologous regions, and the entire hemispheres (excluding the hematoma) ipsilateral and contralateral to the hematoma. Statistical analysis was performed by using SPSS Statistics 21.0 2008 (IBM, Armonk, New York). Differences in perfusion parameters were assessed with paired t tests. Linear regression was used to assess the relationship between the perfusion parameters and blood pressure. Differences in perfusion parameters between treatment groups were assessed with indepen- dent-samples t tests. Seventy-five patients were randomized in ICH ADAPT. Two patients were excluded from this analysis due to inadequate qual- ity of raw CTP data required to complete CPP and CVR calculations. This study, therefore, included 73 patients (54 men), with a median age of 70 years (interquartile range, 60 – 80 years). Hematoma locations were as follows: 55 basal ganglia, 17 lobar, and 1 posterior fossa. Median time from symptom onset to CTP imag- ing was 9.8 hours (interquartile range, 6.0 –19.2 hours), and from the acute diagnostic CT to the CTP study, it was 4.8 hours (interquartile range, 3.4 –14.5 hours). The delay between the diagnostic CT and randomization was variable with a median of 2.3 hours (interquartile range, 1.0 –11.6 hours). Four patients in each treatment arm had antithrombotic-associated ICH (either antiplatelet or anticoagulant; Table 1). The mean systolic and diastolic BP at the time of the CTP scan was 150 Ϯ 20 and 77 Ϯ 15 mm Hg, respectively. The number of patients receiving each of the 3 antihypertensive therapies along with the mean dose is recorded in Table 1. The median acute Glasgow Coma Scale and NIHSS scores were 15 (range, 4 –15; interquartile range, 13–15) and 10 (range, 1–35; interquartile range, 6 –17), respectively. The mean intraparenchymal hematoma volume at the time of CTP imaging was 23.9 Ϯ 28.3 mL. Follow-up imaging was performed at a median of 21.8 hours (interquartile range, 21–23.7 hours) later. Mean hematoma volume at that time was 25.5 Ϯ 27.3 mL. Eleven patients (15%) had large-volume ICHs, with hematoma volumes of Ͼ 40 mL. Hematoma expansion of Ͼ 6 mL was seen in 16 patients (8 in each treatment group, P ϭ .86). Thirty-seven patients were randomized to a target BP of Ͻ 150 mm Hg, and 36, to a target BP of Ͻ 180 mm Hg. No significant differences in patient characteristics were seen between the treatment groups (Table 1). There were no differences in any clinical outcome events between the 2 groups (Table 1). Mortality was 19% in the 150-mm Hg treatment group and 11% in the 180-mm Hg treatment group ( P ϭ .52). Functional disability as measured by the modified Rankin Scale score was comparable between the 150-mm Hg (median, 3 mm Hg; interquartile range, 1.5–5.5 mm Hg) and 180-mm Hg (median, 4 mm Hg; interquartile range, 2–5 mm Hg) treatment groups ( P ϭ .43). No patient in the trial had an ischemic lesion on 24-hour follow-up CT. Mean perihematoma CBF in all 73 patients (38.7 Ϯ 11.9 mL/100 g/min; Fig 2) was significantly lower than that in contralateral homologous regions (44.1 Ϯ 11.1 mL/100 g/min, P Ͻ .001). Mean ipsilateral hemispheric CBF (42.1 Ϯ 10.5 mL/100 g/min) was lower than that in the contralateral hemisphere (43.4 Ϯ 10.5 mL/ 100 g/min, P Ͻ .001). There was a reduction in perihematoma CBV (3.65 Ϯ 0.70 mL/100 g; Fig 2) compared with the contralateral regions (4.21 Ϯ 1.53 mL/100 g, P ϭ .001). Mean ipsilateral hemispheric CBV (3.83 Ϯ 0.63 mL/100 g) was lower than that in the contralateral hemisphere (3.88 Ϯ 0.64 mL/100 g, P ϭ .033). Perihematoma CPP (14.4 Ϯ 4.6 minutes ) was similar to that in contralateral homologous regions (14.3 Ϯ 4.8 minutes Ϫ 1 , P ϭ .93; Fig 2). Ipsilateral hemispheric CPP (14.6 Ϯ 4.6 minutes Ϫ 1 ) was also comparable with that in the contralateral hemispheric CPP (14.8 Ϯ 4.9 minutes Ϫ 1 , P ϭ .28). There were no differences in CPP within the ipsilateral and contralateral external (15.0 Ϯ 4.6 and 15.6 Ϯ 5.3 minutes , respectively; P ϭ .15) or ipsilateral and contralateral internal (15.0 Ϯ 4.8 and 15.0 Ϯ 4.8 minutes Ϫ 1 , respectively; P ϭ .90) BZ regions. Similarly, there were no significant differences when the CPP in the above ipsilateral and contralateral external and internal BZ regions was compared with the mean bilateral hemispheric CPP (14.7 Ϯ 4.7 minutes Ϫ 1 , P Ն .29; Table 2). On linear regression analysis, CPP was not related to intraparenchymal hematoma volume (  ϭ Ϫ 0.001 [ Ϫ 0.002, 0.001]). Mean perihematoma CVR (0.34 Ϯ 0.11 g/mL) was slightly higher than that in contralateral homologous regions (0.30 Ϯ 0.10 g/mL, P Ͻ .001; Fig 2). Ipsilateral hemispheric CVR was also elevated (0.31 Ϯ 0.08) relative to the contralateral hemisphere (0.30 Ϯ 0.09 g/mL, P ϭ .04). There were no hemispheric differences in CVR within the external (0.34 Ϯ 0.12 versus 0.35 Ϯ 0.12 g/mL, P ϭ .53) or internal (0.41 Ϯ 0.15 versus 0.39 Ϯ 0.14 g/mL, P ϭ .17) BZ regions. At the time of CTP imaging, systolic BP was significantly lower in the Ͻ 150-mm Hg target group (140 Ϯ 19 mm Hg) than that in the Ͻ 180-mm Hg target group (162 Ϯ 12 mm Hg, P Ͻ .001). Mean CPP and CVR in the perihematoma and most BZ regions was similar between BP treatment groups (Table 2). Mean CPP in the ipsilateral internal BZ (13.5 Ϯ 4.6 minutes -1 ) in ...
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... contrast concentration on a per-voxel basis with time. Errors introduced by delay and disper- sion of the contrast bolus before arrival in the cerebral circulation were corrected for by using a block-circulant deconvolution algo- rithm. 22 Quantitative perfusion indices, including CBF and CBV, were calculated on a voxelwise basis and used to generate color- coded maps. All perfusion maps were transferred to the Analyze 11.0 software package (AnalyzeDirect, Overland Park, Kansas). 23 Maps of CPP and cerebrovascular resistance (CVR) were generated by using a voxelwise calculation of CBF/CBV and 1/CBV, respectively (Fig 1), as previously described. 18 The perimeter of the hematoma was outlined on the precontrast arrival CT source image by using a semiautomated intensity Hounsfield unit threshold technique, as previously described. 24 Internal and external BZ and 7-mm perihematoma ROIs were manually outlined (Fig 1). In cases in which the hematoma itself involved a BZ, the latter was not outlined. All voxels containing blood vessels were removed from the ROI by using an intensity-threshold function. On the basis of previous studies, voxels with CBF of Ͼ 100 mL/100 g/min or CBV of Ͼ 8 mL/100 g were assumed to contain vessels and removed from the ROI. 25-27 Mean perfusion indices were measured in all ROIs, contralateral homologous regions, and the entire hemispheres (excluding the hematoma) ipsilateral and contralateral to the hematoma. Statistical analysis was performed by using SPSS Statistics 21.0 2008 (IBM, Armonk, New York). Differences in perfusion parameters were assessed with paired t tests. Linear regression was used to assess the relationship between the perfusion parameters and blood pressure. Differences in perfusion parameters between treatment groups were assessed with indepen- dent-samples t tests. Seventy-five patients were randomized in ICH ADAPT. Two patients were excluded from this analysis due to inadequate qual- ity of raw CTP data required to complete CPP and CVR calculations. This study, therefore, included 73 patients (54 men), with a median age of 70 years (interquartile range, 60 – 80 years). Hematoma locations were as follows: 55 basal ganglia, 17 lobar, and 1 posterior fossa. Median time from symptom onset to CTP imag- ing was 9.8 hours (interquartile range, 6.0 –19.2 hours), and from the acute diagnostic CT to the CTP study, it was 4.8 hours (interquartile range, 3.4 –14.5 hours). The delay between the diagnostic CT and randomization was variable with a median of 2.3 hours (interquartile range, 1.0 –11.6 hours). Four patients in each treatment arm had antithrombotic-associated ICH (either antiplatelet or anticoagulant; Table 1). The mean systolic and diastolic BP at the time of the CTP scan was 150 Ϯ 20 and 77 Ϯ 15 mm Hg, respectively. The number of patients receiving each of the 3 antihypertensive therapies along with the mean dose is recorded in Table 1. The median acute Glasgow Coma Scale and NIHSS scores were 15 (range, 4 –15; interquartile range, 13–15) and 10 (range, 1–35; interquartile range, 6 –17), respectively. The mean intraparenchymal hematoma volume at the time of CTP imaging was 23.9 Ϯ 28.3 mL. Follow-up imaging was performed at a median of 21.8 hours (interquartile range, 21–23.7 hours) later. Mean hematoma volume at that time was 25.5 Ϯ 27.3 mL. Eleven patients (15%) had large-volume ICHs, with hematoma volumes of Ͼ 40 mL. Hematoma expansion of Ͼ 6 mL was seen in 16 patients (8 in each treatment group, P ϭ .86). Thirty-seven patients were randomized to a target BP of Ͻ 150 mm Hg, and 36, to a target BP of Ͻ 180 mm Hg. No significant differences in patient characteristics were seen between the treatment groups (Table 1). There were no differences in any clinical outcome events between the 2 groups (Table 1). Mortality was 19% in the 150-mm Hg treatment group and 11% in the 180-mm Hg treatment group ( P ϭ .52). Functional disability as measured by the modified Rankin Scale score was comparable between the 150-mm Hg (median, 3 mm Hg; interquartile range, 1.5–5.5 mm Hg) and 180-mm Hg (median, 4 mm Hg; interquartile range, 2–5 mm Hg) treatment groups ( P ϭ .43). No patient in the trial had an ischemic lesion on 24-hour follow-up CT. Mean perihematoma CBF in all 73 patients (38.7 Ϯ 11.9 mL/100 g/min; Fig 2) was significantly lower than that in contralateral homologous regions (44.1 Ϯ 11.1 mL/100 g/min, P Ͻ .001). Mean ipsilateral hemispheric CBF (42.1 Ϯ 10.5 mL/100 g/min) was lower than that in the contralateral hemisphere (43.4 Ϯ 10.5 mL/ 100 g/min, P Ͻ .001). There was a reduction in perihematoma CBV (3.65 Ϯ 0.70 mL/100 g; Fig 2) compared with the contralateral regions (4.21 Ϯ 1.53 mL/100 g, P ϭ .001). Mean ipsilateral hemispheric CBV (3.83 Ϯ 0.63 mL/100 g) was lower than that in the contralateral hemisphere (3.88 Ϯ 0.64 mL/100 g, P ϭ .033). Perihematoma CPP (14.4 Ϯ 4.6 minutes ) was similar to that in contralateral homologous regions (14.3 Ϯ 4.8 minutes Ϫ 1 , P ϭ .93; Fig 2). Ipsilateral hemispheric CPP (14.6 Ϯ 4.6 minutes Ϫ 1 ) was also comparable with that in the contralateral hemispheric CPP (14.8 Ϯ 4.9 minutes Ϫ 1 , P ϭ .28). There were no differences in CPP within the ipsilateral and contralateral external (15.0 Ϯ 4.6 and 15.6 Ϯ 5.3 minutes , respectively; P ϭ .15) or ipsilateral and contralateral internal (15.0 Ϯ 4.8 and 15.0 Ϯ 4.8 minutes Ϫ 1 , respectively; P ϭ .90) BZ regions. Similarly, there were no significant differences when the CPP in the above ipsilateral and contralateral external and internal BZ regions was compared with the mean bilateral hemispheric CPP (14.7 Ϯ 4.7 minutes Ϫ 1 , P Ն .29; Table 2). On linear regression analysis, CPP was not related to intraparenchymal hematoma volume (  ϭ Ϫ 0.001 [ Ϫ 0.002, 0.001]). Mean perihematoma CVR (0.34 Ϯ 0.11 g/mL) was slightly higher than that in contralateral homologous regions (0.30 Ϯ 0.10 g/mL, P Ͻ .001; Fig 2). Ipsilateral hemispheric CVR was also elevated (0.31 Ϯ 0.08) relative to the contralateral hemisphere (0.30 Ϯ 0.09 g/mL, P ϭ .04). There were no hemispheric differences in CVR within the external (0.34 Ϯ 0.12 versus 0.35 Ϯ 0.12 g/mL, P ϭ .53) or internal (0.41 Ϯ 0.15 versus 0.39 Ϯ 0.14 g/mL, P ϭ .17) BZ regions. At the time of CTP imaging, systolic BP was significantly lower in the Ͻ 150-mm Hg target group (140 Ϯ 19 mm Hg) than that in the Ͻ 180-mm Hg target group (162 Ϯ 12 mm Hg, P Ͻ .001). Mean CPP and CVR in the perihematoma and most BZ regions was similar between BP treatment groups (Table 2). Mean CPP in the ipsilateral internal BZ (13.5 Ϯ 4.6 minutes -1 ) in ...
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... France) software. An arterial input function was manually selected over the contralateral anterior cerebral artery, while the venous output function was obtained over the confluence of the sinuses. Perfusion maps were derived from the tissue time-atten- uation curve on the basis of the change in x-ray attenuation, which is linearly related to iodinated contrast concentration on a per-voxel basis with time. Errors introduced by delay and disper- sion of the contrast bolus before arrival in the cerebral circulation were corrected for by using a block-circulant deconvolution algo- rithm. 22 Quantitative perfusion indices, including CBF and CBV, were calculated on a voxelwise basis and used to generate color- coded maps. All perfusion maps were transferred to the Analyze 11.0 software package (AnalyzeDirect, Overland Park, Kansas). 23 Maps of CPP and cerebrovascular resistance (CVR) were generated by using a voxelwise calculation of CBF/CBV and 1/CBV, respectively (Fig 1), as previously described. 18 The perimeter of the hematoma was outlined on the precontrast arrival CT source image by using a semiautomated intensity Hounsfield unit threshold technique, as previously described. 24 Internal and external BZ and 7-mm perihematoma ROIs were manually outlined (Fig 1). In cases in which the hematoma itself involved a BZ, the latter was not outlined. All voxels containing blood vessels were removed from the ROI by using an intensity-threshold function. On the basis of previous studies, voxels with CBF of Ͼ 100 mL/100 g/min or CBV of Ͼ 8 mL/100 g were assumed to contain vessels and removed from the ROI. 25-27 Mean perfusion indices were measured in all ROIs, contralateral homologous regions, and the entire hemispheres (excluding the hematoma) ipsilateral and contralateral to the hematoma. Statistical analysis was performed by using SPSS Statistics 21.0 2008 (IBM, Armonk, New York). Differences in perfusion parameters were assessed with paired t tests. Linear regression was used to assess the relationship between the perfusion parameters and blood pressure. Differences in perfusion parameters between treatment groups were assessed with indepen- dent-samples t tests. Seventy-five patients were randomized in ICH ADAPT. Two patients were excluded from this analysis due to inadequate qual- ity of raw CTP data required to complete CPP and CVR calculations. This study, therefore, included 73 patients (54 men), with a median age of 70 years (interquartile range, 60 – 80 years). Hematoma locations were as follows: 55 basal ganglia, 17 lobar, and 1 posterior fossa. Median time from symptom onset to CTP imag- ing was 9.8 hours (interquartile range, 6.0 –19.2 hours), and from the acute diagnostic CT to the CTP study, it was 4.8 hours (interquartile range, 3.4 –14.5 hours). The delay between the diagnostic CT and randomization was variable with a median of 2.3 hours (interquartile range, 1.0 –11.6 hours). Four patients in each treatment arm had antithrombotic-associated ICH (either antiplatelet or anticoagulant; Table 1). The mean systolic and diastolic BP at the time of the CTP scan was 150 Ϯ 20 and 77 Ϯ 15 mm Hg, respectively. The number of patients receiving each of the 3 antihypertensive therapies along with the mean dose is recorded in Table 1. The median acute Glasgow Coma Scale and NIHSS scores were 15 (range, 4 –15; interquartile range, 13–15) and 10 (range, 1–35; interquartile range, 6 –17), respectively. The mean intraparenchymal hematoma volume at the time of CTP imaging was 23.9 Ϯ 28.3 mL. Follow-up imaging was performed at a median of 21.8 hours (interquartile range, 21–23.7 hours) later. Mean hematoma volume at that time was 25.5 Ϯ 27.3 mL. Eleven patients (15%) had large-volume ICHs, with hematoma volumes of Ͼ 40 mL. Hematoma expansion of Ͼ 6 mL was seen in 16 patients (8 in each treatment group, P ϭ .86). Thirty-seven patients were randomized to a target BP of Ͻ 150 mm Hg, and 36, to a target BP of Ͻ 180 mm Hg. No significant differences in patient characteristics were seen between the treatment groups (Table 1). There were no differences in any clinical outcome events between the 2 groups (Table 1). Mortality was 19% in the 150-mm Hg treatment group and 11% in the 180-mm Hg treatment group ( P ϭ .52). Functional disability as measured by the modified Rankin Scale score was comparable between the 150-mm Hg (median, 3 mm Hg; interquartile range, 1.5–5.5 mm Hg) and 180-mm Hg (median, 4 mm Hg; interquartile range, 2–5 mm Hg) treatment groups ( P ϭ .43). No patient in the trial had an ischemic lesion on 24-hour follow-up CT. Mean perihematoma CBF in all 73 patients (38.7 Ϯ 11.9 mL/100 g/min; Fig 2) was significantly lower than that in contralateral homologous regions (44.1 Ϯ 11.1 mL/100 g/min, P Ͻ .001). Mean ipsilateral hemispheric CBF (42.1 Ϯ 10.5 mL/100 g/min) was lower than that in the contralateral hemisphere (43.4 Ϯ 10.5 mL/ 100 g/min, P Ͻ .001). There was a reduction in perihematoma CBV (3.65 Ϯ 0.70 mL/100 g; Fig 2) compared with the contralateral regions (4.21 Ϯ 1.53 mL/100 g, P ϭ .001). Mean ipsilateral hemispheric CBV (3.83 Ϯ 0.63 mL/100 g) was lower than that in the contralateral hemisphere (3.88 Ϯ 0.64 mL/100 g, P ϭ .033). Perihematoma CPP (14.4 Ϯ 4.6 minutes ) was similar to that in contralateral homologous regions (14.3 Ϯ 4.8 minutes Ϫ 1 , P ϭ .93; Fig 2). Ipsilateral hemispheric CPP (14.6 Ϯ 4.6 minutes Ϫ 1 ) was also comparable with that in the contralateral hemispheric CPP (14.8 Ϯ 4.9 minutes Ϫ 1 , P ϭ .28). There were no differences in CPP within the ipsilateral and contralateral external (15.0 Ϯ 4.6 and 15.6 Ϯ 5.3 minutes , respectively; P ϭ .15) or ipsilateral and contralateral internal (15.0 Ϯ 4.8 and 15.0 Ϯ 4.8 minutes Ϫ 1 , respectively; P ϭ .90) BZ regions. Similarly, there were no significant differences when the CPP in the above ipsilateral and contralateral external and internal BZ regions was compared with the mean bilateral hemispheric CPP (14.7 Ϯ 4.7 minutes Ϫ 1 , P Ն .29; Table 2). On linear regression analysis, CPP was not related to intraparenchymal hematoma volume (  ϭ Ϫ 0.001 [ Ϫ 0.002, 0.001]). Mean perihematoma CVR (0.34 Ϯ 0.11 g/mL) was slightly higher than that in contralateral homologous regions (0.30 Ϯ 0.10 g/mL, P Ͻ .001; Fig 2). Ipsilateral hemispheric CVR was also elevated (0.31 Ϯ 0.08) relative to the contralateral hemisphere (0.30 Ϯ 0.09 g/mL, P ϭ .04). There were no hemispheric differences in CVR within the external (0.34 Ϯ 0.12 versus 0.35 Ϯ 0.12 g/mL, P ϭ .53) or internal (0.41 Ϯ 0.15 versus 0.39 Ϯ 0.14 g/mL, P ϭ .17) BZ regions. At the time of CTP imaging, systolic BP was significantly lower in the Ͻ 150-mm Hg target group (140 Ϯ 19 mm Hg) than that in the Ͻ 180-mm Hg target group (162 Ϯ 12 mm Hg, P Ͻ .001). Mean CPP and CVR in the perihematoma and most BZ regions was similar between BP treatment groups (Table 2). Mean CPP in the ipsilateral internal BZ (13.5 Ϯ 4.6 minutes -1 ) in ...
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... (Fig 1). In cases in which the hematoma itself involved a BZ, the latter was not outlined. All voxels containing blood vessels were removed from the ROI by using an intensity-threshold function. On the basis of previous studies, voxels with CBF of Ͼ 100 mL/100 g/min or CBV of Ͼ 8 mL/100 g were assumed to contain vessels and removed from the ROI. 25-27 Mean perfusion indices were measured in all ROIs, contralateral homologous regions, and the entire hemispheres (excluding the hematoma) ipsilateral and contralateral to the hematoma. Statistical analysis was performed by using SPSS Statistics 21.0 2008 (IBM, Armonk, New York). Differences in perfusion parameters were assessed with paired t tests. Linear regression was used to assess the relationship between the perfusion parameters and blood pressure. Differences in perfusion parameters between treatment groups were assessed with indepen- dent-samples t tests. Seventy-five patients were randomized in ICH ADAPT. Two patients were excluded from this analysis due to inadequate qual- ity of raw CTP data required to complete CPP and CVR calculations. This study, therefore, included 73 patients (54 men), with a median age of 70 years (interquartile range, 60 – 80 years). Hematoma locations were as follows: 55 basal ganglia, 17 lobar, and 1 posterior fossa. Median time from symptom onset to CTP imag- ing was 9.8 hours (interquartile range, 6.0 –19.2 hours), and from the acute diagnostic CT to the CTP study, it was 4.8 hours (interquartile range, 3.4 –14.5 hours). The delay between the diagnostic CT and randomization was variable with a median of 2.3 hours (interquartile range, 1.0 –11.6 hours). Four patients in each treatment arm had antithrombotic-associated ICH (either antiplatelet or anticoagulant; Table 1). The mean systolic and diastolic BP at the time of the CTP scan was 150 Ϯ 20 and 77 Ϯ 15 mm Hg, respectively. The number of patients receiving each of the 3 antihypertensive therapies along with the mean dose is recorded in Table 1. The median acute Glasgow Coma Scale and NIHSS scores were 15 (range, 4 –15; interquartile range, 13–15) and 10 (range, 1–35; interquartile range, 6 –17), respectively. The mean intraparenchymal hematoma volume at the time of CTP imaging was 23.9 Ϯ 28.3 mL. Follow-up imaging was performed at a median of 21.8 hours (interquartile range, 21–23.7 hours) later. Mean hematoma volume at that time was 25.5 Ϯ 27.3 mL. Eleven patients (15%) had large-volume ICHs, with hematoma volumes of Ͼ 40 mL. Hematoma expansion of Ͼ 6 mL was seen in 16 patients (8 in each treatment group, P ϭ .86). Thirty-seven patients were randomized to a target BP of Ͻ 150 mm Hg, and 36, to a target BP of Ͻ 180 mm Hg. No significant differences in patient characteristics were seen between the treatment groups (Table 1). There were no differences in any clinical outcome events between the 2 groups (Table 1). Mortality was 19% in the 150-mm Hg treatment group and 11% in the 180-mm Hg treatment group ( P ϭ .52). Functional disability as measured by the modified Rankin Scale score was comparable between the 150-mm Hg (median, 3 mm Hg; interquartile range, 1.5–5.5 mm Hg) and 180-mm Hg (median, 4 mm Hg; interquartile range, 2–5 mm Hg) treatment groups ( P ϭ .43). No patient in the trial had an ischemic lesion on 24-hour follow-up CT. Mean perihematoma CBF in all 73 patients (38.7 Ϯ 11.9 mL/100 g/min; Fig 2) was significantly lower than that in contralateral homologous regions (44.1 Ϯ 11.1 mL/100 g/min, P Ͻ .001). Mean ipsilateral hemispheric CBF (42.1 Ϯ 10.5 mL/100 g/min) was lower than that in the contralateral hemisphere (43.4 Ϯ 10.5 mL/ 100 g/min, P Ͻ .001). There was a reduction in perihematoma CBV (3.65 Ϯ 0.70 mL/100 g; Fig 2) compared with the contralateral regions (4.21 Ϯ 1.53 mL/100 g, P ϭ .001). Mean ipsilateral hemispheric CBV (3.83 Ϯ 0.63 mL/100 g) was lower than that in the contralateral hemisphere (3.88 Ϯ 0.64 mL/100 g, P ϭ .033). Perihematoma CPP (14.4 Ϯ 4.6 minutes ) was similar to that in contralateral homologous regions (14.3 Ϯ 4.8 minutes Ϫ 1 , P ϭ .93; Fig 2). Ipsilateral hemispheric CPP (14.6 Ϯ 4.6 minutes Ϫ 1 ) was also comparable with that in the contralateral hemispheric CPP (14.8 Ϯ 4.9 minutes Ϫ 1 , P ϭ .28). There were no differences in CPP within the ipsilateral and contralateral external (15.0 Ϯ 4.6 and 15.6 Ϯ 5.3 minutes , respectively; P ϭ .15) or ipsilateral and contralateral internal (15.0 Ϯ 4.8 and 15.0 Ϯ 4.8 minutes Ϫ 1 , respectively; P ϭ .90) BZ regions. Similarly, there were no significant differences when the CPP in the above ipsilateral and contralateral external and internal BZ regions was compared with the mean bilateral hemispheric CPP (14.7 Ϯ 4.7 minutes Ϫ 1 , P Ն .29; Table 2). On linear regression analysis, CPP was not related to intraparenchymal hematoma volume (  ϭ Ϫ 0.001 [ Ϫ 0.002, 0.001]). Mean perihematoma CVR (0.34 Ϯ 0.11 g/mL) was slightly higher than that in contralateral homologous regions (0.30 Ϯ 0.10 g/mL, P Ͻ .001; Fig 2). Ipsilateral hemispheric CVR was also elevated (0.31 Ϯ 0.08) relative to the contralateral hemisphere (0.30 Ϯ 0.09 g/mL, P ϭ .04). There were no hemispheric differences in CVR within the external (0.34 Ϯ 0.12 versus 0.35 Ϯ 0.12 g/mL, P ϭ .53) or internal (0.41 Ϯ 0.15 versus 0.39 Ϯ 0.14 g/mL, P ϭ .17) BZ regions. At the time of CTP imaging, systolic BP was significantly lower in the Ͻ 150-mm Hg target group (140 Ϯ 19 mm Hg) than that in the Ͻ 180-mm Hg target group (162 Ϯ 12 mm Hg, P Ͻ .001). Mean CPP and CVR in the perihematoma and most BZ regions was similar between BP treatment groups (Table 2). Mean CPP in the ipsilateral internal BZ (13.5 Ϯ 4.6 minutes -1 ) in ...
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The early hematoma expansion of intracerebral hemorrhage (ICH) indicates a poor prognosis. This paper studies the relationship between cerebral blood flow (CBF) around the hematoma and hematoma expansion (HE) in the acute stage of intracerebral hemorrhage. A total of 50 patients with supratentorial cerebral hemorrhage were enrolled in this study. T...
Background:
Acute ischemic stroke treatment with intravenous thrombolysis(IVT) is restricted to a time window of 4.5 hours after known or presumed onset. Recently, MRI-guided treatment decision in wake-up stroke(WUS) was shown to be effective. The aim of this study was to determine the safety and outcome of IVT in patients with a time window beyon...
Background
Subacute ischemic lesions in intracerebral hemorrhage ( ICH ) have been hypothesized to result from hypoperfusion. Although studies of cerebral blood flow ( CBF ) indicate modest hypoperfusion in ICH , these investigations have been limited to early time points. Arterial spin labeling ( ASL ), a magnetic resonance imaging technique, can...
Citations
... Moreover, the SBP in a small number of ICH patients is controlled at the target value within 24 h. The blood flow of the brain tissue around the hematoma can be maintained by autoregulation (Gould et al., 2014;Tanaka et al., 2014;Tamm et al., 2016). With the progress of INTERACT2 and ATACH2 experiments, Gould et al. (2014) demonstrated that the blood perfusion around the hematoma, perihematoma tissue area and watershed tissue area of early ICH (<2 h) was below the ischemic threshold by CTP, but there was no significant correlation between intensive hypotension and hypoperfusion area. ...
Background
Antihypertensive therapy in the acute phase of intracerebral hemorrhage (ICH) can reduce hematoma expansion. Numerous studies have demonstrated that blood pressure variability secondary to antihypertensive therapy has adverse effects on neurological outcomes, but the conclusions are diverse, and the mechanism of this occurrence is unknown. The aim of this research was to analyze the impact of blood pressure variability after antihypertensive treatment on the prognosis of patients with acute ICH, along with the possible mechanism.
Materials and methods
A total of 120 patients within 20 h of onset of ICH were divided into a good prognosis group (mRS ≤ 2 points) and a poor prognosis group (mRS ≥ 3 points) according to their 90-day mRS scores. The basic patient information, NIHSS score, GCS score, mRS score at 90 days after admission, head CT examination at admission and 24 h and CTP examination at 24 h were collected from some patients. The blood pressure values of patients were collected within 24 h, and multiple blood pressure variation (BPV) parameters within 1 and 24 h were calculated.
Results
(1) After excluding confounding factors such as age, whether the hematoma ruptured into the ventricle, confounding signs, amount of bleeding, edema around the hematoma, NIHSS on admission, operation or non-operation, and 24-h hematoma increment, the fourth quartile systolic blood pressure (SBP) maximum and minimum difference within 1 h [OR: 5.069, CI (1.036–24.813) P = 0.045] and coefficient of continuous variation (SV) within 24 h [OR: 2.912 CI (1.818–71.728) P = 0.009] were still independent factors affecting the 90-day mRS in ICH patients. (2) There was a negative correlation between SBP SV and CBF in terms of the difference between the contralateral side and the perihematomal region at 24 h (Rs = −0.692, P = 0.013).
Conclusion
Blood pressure variability after antihypertensive therapy in acute ICH is one of the influencing factors for 90-day mRS in patients. A 1-h dramatic drop in SBP and 24-h SBP SV may affect the long-term prognosis of patients by reducing whole cerebral perfusion.
... The perfusion pressure (Pp) is the difference between the inlet and outlet pressure of the cerebral perfusion circuit but it is calculated as the differential between the mean arterial pressure and the intracranial pressure due to the strict coupling of cortical vein pressure and ICp at bridge vein level, with the latter easier to monitor in clinical settings. The perfusion pressure is approximately 50-70 mmHg [67]. The cerebral blood flow remains proportional to Pp, which therefore must remain unchanged despite the continuous However, this dynamic would reduce the cerebral perfusion pressure, and thus the blood flow, if it were not promptly compensated by a corresponding and almost simultaneous increase in arteriolar caliber, which keeps the perfusion pressure unchanged. ...
Besides representing the place where a migraine attack generates, what is the physiological role of peptidergic control of arteriolar caliber within the trigemino-vascular system? Considering that the shared goal of most human CGRP-based neurosensory systems is the protection from an acute threat, especially if hypoxic, what is the end meaning of a migraine attack? In this paper, we have reviewed available evidence on the possible role of the trigemino-vascular system in maintaining cerebral perfusion pressure homeostasis, despite the large physiological fluctuations in intracranial pressure occurring in daily life activities. In this perspective, the migraine attack is presented as the response to a cerebral hypoxic threat consequent to a deranged intracranial pressure control aimed at generating a temporary withdrawal from the environment with limitation of physical activity, a condition required to promote the restoration of cerebral fluids dynamic balance.
... Patient numbers ranged from 1 to 385. Nine studies included patients with ICH only [18][19][20][22][23][24][25][26][27]; the remaining nine studies included other brain injury patients as well as ICH patients. These studies included patients with subarachnoid haemorrhage (SAH), traumatic brain injury, acute ischaemic stroke, hypoxic brain injury, anoxia, encephalitis and arteriovenous malformation [16,21,[28][29][30][31][32][33][34]. ...
... The mean age of patients varied from 43 years to 70 years. Two studies randomized patients to a control or placebo group [16,24], whilst one study randomized patients to different blood pressure targets [20]. ...
... The main findings of the included studies are presented in Table 1. Overall, sixteen studies included ICP measures [18,19,[21][22][23][24][25][26][27][28][29][30][31][32][33][34], eleven studies included ICP and CPP measures [19, 22-24, 26-28, 30-33], and two studies included CPP [16,20]. Dihydropyridine calcium channel blockers (CCBs) were the main agent used to lower BP, with six studies using these agents and including ICP measures [18,22,27,28,31,32]. ...
IntroductionIntracerebral haemorrhage (ICH) is associated with high morbidity and mortality. Blood pressure (BP) control is one of the main management strategies in acute ICH. Limited data currently exist regarding intracranial pressure (ICP) in acute ICH. The relationship between BP lowering and ICP is yet to be fully elucidated.Methods
We conducted a systematic review to investigate the effects of BP lowering on ICP in acute ICH. The study protocol was registered on PROSPERO (CRD42019134470).ResultsFollowing PRISMA guidelines, MEDLINE, EMBASE and CENTRAL were searched for studies on ICH with BP and ICP or surrogate measures. 1096 articles were identified after duplicates were removed; 18 studies meeting the inclusion criteria. Dihydropyridine calcium channel blockers (CCBs) were the most common agent used to lower BP, but had a varying effect on ICP. Other BP-lowering agents used also had a varying effect on ICP.Discussion and Conclusion
Further work, including large observational or randomized interventional studies, is needed to develop a better understanding of the effect of BP lowering on ICP in acute ICH, which will assist the development of more effective management strategies.Trial RegistrationThe study protocol was registered on PROSPERO (CRD42019134470) on 29/05/2019.
... Brain edema in the perihematoma area was reported to contribute a lot on ICHmediated brain damage and closely associated with poor clinical outcomes, such as deterioration or even death [2][3][4]. Brain edema destroys the blood-brain barrier (BBB), resulting in inflammatory factors releasing into the blood circulation, further leading to the dysfunction of cerebral blood flow (CBF) automatic regulation, and finally, reducing the CBF in the perihematoma area [5]. Therefore, CBF improvement and brain tissue protection in the perihematoma area may be important targets in ICH treatment. ...
... Imaging assessment After confirming the diagnosis of acute ICH by CT scan (GE 256-row ultra-high-end spiral CT, USA), patients will continue to undergo CTA and CTP scanning within 1 h to obtain baseline data. CTA maps will be used to assess the presence of vascular malformations such as aneurysms and arteriovenous malformations [5]. CTP map will be used to evaluate cerebral perfusion, including the parameters of cerebral blood flow (CBF), mean transition time (MTT), time to peak (TTP), and brain CT (Fig. 2). ...
... Hypo-perfusion and hypoxia in the perihematoma area are the major mechanisms of ICH-mediated brain tissue injury, which may result from cerebral parenchyma microcirculation insufficiency caused by the compressing of hematoma or the toxicity of the bleeding released metabolites [5,26]. Whereby, to rescue the perihematoma area by correcting hypo-perfusion, hypoxia may be the key step to obtain a good outcome. ...
Background
All of the existing medication and surgical therapies currently cannot completely inhibit intracerebral hemorrhage (ICH)-mediated brain damage, resulting in disability in different degrees in the involved patients. Normobaric oxygenation (NBO) was reported attenuating ischemic brain injury. Herein, we aimed to explore the safety and efficacy of NBO on rescuing the damaged brain tissues secondary to acute ICH, especially those in the perihematoma area being threatened by ischemia and hypoxia.
Methods
A total of 150 patients confirmed as acute spontaneous ICH by computed tomography (CT) within 6 h after symptoms onset, will enroll in this study after signing the informed consent, and enter into the NBO group or control group randomly according to a random number. In the NBO group, patients will inhale high-flow oxygen (8 L/min, 1 h each time for 6 cycles daily) and intake low-flow oxygen (2 L/min) in intermittent periods by mask for a total of 7 days. While in the control group, patients will breathe in only low-flow oxygen (2 L/min) by mask for 7 consecutive days. Computed tomography and perfusion (CT/CTP) will be used to evaluate cerebral perfusion status and brain edema. CT and CTP maps in the two groups at baseline and day 7 and 14 after NBO or low-flow oxygen control will be compared. The primary endpoint is mRS at both Day14 post-ICH and the end of the 3rd month follow-up. The secondary endpoints include NIHSS and plasma biomarkers at baseline and Day-1, 7, and 14 after treatment, as well as the NIHSS at the end of the 3rd month post-ICH and the incidence of bleeding recurrence and the mortalities within 3 months post-ICH.
Discussion
This study will provide preliminary clinical evidence about the safety and efficacy of NBO on correcting acute ICH and explore some mechanisms accordingly, to offer reference for larger clinical trials in the future.
Trial registration
ClinicalTrials.gov NCT04144868 . Retrospectively registered on October 29, 2019.
... Exclusion criteria were (1) presence on MRI-2 of parenchymal hematoma (ECASS classification 33 ), which may hinder assessment of ASL maps; 34 (2) re-occlusion, new intracranial occlusion or ipsi-or contralateral ICA or MCA ! 50% stenosis on MR angiography (MRA)-2, which may affect brain perfusion; and (3) un-interpretable ASL images due to movement artifacts, technical problems, or inordinately low whole brain CBF (<20 mL/100 g/min). ...
Despite early thrombectomy, a sizeable fraction of acute stroke patients with large vessel occlusion have poor outcome. The no-reflow phenomenon, i.e. impaired microvascular reperfusion despite complete recanalization, may contribute to such "futile recanalizations". Although well reported in animal models, no-reflow is still poorly characterized in man. From a large prospective thrombectomy database, we included all patients with intracranial proximal occlusion, complete recanalization (modified thrombolysis in cerebral infarction score 2c-3), and availability of both baseline and 24 h follow-up MRI including arterial spin labeling perfusion mapping. No-reflow was operationally defined as i) hypoperfusion ≥40% relative to contralateral homologous region, assessed with both visual (two independent investigators) and automatic image analysis, and ii) infarction on follow-up MRI. Thirty-three patients were eligible (median age: 70 years, NIHSS: 18, and stroke onset-to-recanalization delay: 208 min). The operational criteria were met in one patient only, consistently with the visual and automatic analyses. This patient recanalized 160 min after stroke onset and had excellent functional outcome. In our cohort of patients with complete and stable recanalization following thrombectomy for intracranial proximal occlusion, severe ipsilateral hypoperfusion on follow-up imaging associated with newly developed infarction was a rare occurrence. Thus, no-reflow may be infrequent in human stroke and may not substantially contribute to futile recanalizations.
... The dynamic coupling of intracranial pressure and cortical vein pressure: the role of the bridge vein It is well-known that the ICp and the cortical vein pressure (CVp) are very close, with the latter always a few mmHg higher than ICp [29][30][31], to the point that the clinical estimation of cerebral perfusion pressure (CPp), i.e., the difference between arterial pressure and venous pressure, is routinely calculated as the difference between mean arterial pressure (Ap) and ICp [32]. How this dynamic coupling of ICp and CVp is generated? ...
Headache is the most frequent and often the most severe symptom of idiopathic intracranial hypertension (IIH) clinical presentation, although pain characteristics are very variable among sufferers and the pain may even lack in some cases. Whatever the headache features, refractoriness to treatments, pain worsening in the recumbent position, and frequent awakenings with severe headache late in the night are the specific complains of such patients. However, a migraine or probable migraine headache, mostly with a chronic headache pattern, can be diagnosed in about 2/3 of the cases. In IIH cases without papilledema (IIHWOP), this leads to a high rate of misdiagnosis with primary chronic migraine (CM). Mechanisms responsible for the shared migrainous presentation of CM and IIH/IIHWOP may rely on a pathologic CGRP release from the rich trigemino-vascular innervated dural sinuses, congested in the course of raised intracranial pressure. The possible role of IIHWOP as a powerful and modifiable risk factor for migraine progression is discussed. Further studies investigating the possible efficacy of anti CGRP/receptor antibodies in IIH/IIHWOP headache treatment are needed.
... The outcome of ICH is affected by several factors, such as low serum magnesium [50], inflammatory response (higher neutrophils and lower lymphocytes) [51], maintenance of cerebral perfusion pressure and drug actions [52,53] through the influence of neurovascular recovery and systemic complications. ...
Intracerebral hemorrhage (ICH) causes an accumulation of blood in the brain parenchyma that disrupts the normal neurological function of the brain. Despite extensive clinical trials, no medical or surgical therapy has shown to be effective in managing ICH, resulting in a poor prognosis for the patients. Urocortin (UCN) is a 40-amino-acid endogenous neuropeptide that belongs to the corticotropin-releasing hormone (CRH) family. The effect of UCN is activated by binding to two G-protein coupled receptors, CRH-R1 and CRH-R2, which are expressed in brain neurons and glial cells in various brain regions. Current research has shown that UCN exerts neuroprotective effects in ICH models via anti-inflammatory effects, which generally reduced brain edema and reduced blood-brain barrier disruption. These effects gradually help in the improvement of the neurological outcome, and thus, UCN may be a potential therapeutic target in the treatment of ICH. This review summarizes the data published to date on the role of UCN in ICH and the possible protective mechanisms underlined.
... -индекс локального церебрального перфузионного давления (index of local cerebral perfusion pressure, iCPP): CBF/CBV [16,17]; -индекс цереброваскулярной резистентности (index of cerebrovascular resistance, iCVR): 1/CBV [18]; -индекс цереброваскулярной резистентности с учетом среднего артериального давления -АД (CVRi): (диастолическое АД + (систолическое АД -диастолическое АД)/3)/CBF, измеренные при поступлении [19]; ...
Цель исследования. Комплексная оценка перфузионных данных с учетом шкалы Hemorrhagic Transformation Index (HTI) для предикции геморрагической трансформации у больных ишемическим инсультом. Материал и методы. На основе сопоставления оценок склонности ретроспективно отобрали 21 пару «случай-контроль» из 71 последовательного пациента с ишемическим инсультом в бассейне средней мозговой артерии. Всем больным в первые 12 ч от дебюта симптомов проводили перфузионную компьютерную томографию (КТ) с исследованием проницаемости гематоэнцефалического барьера. В ядре инфаркта и пенумбре оценивали среднее время прохождения контрастного вещества (MTT), объем (CBV) и скорость (CBF) мозгового кровотока, а также коэффициент проницаемости гематоэнцефалического барьера (PS). Конечной точкой исследования служила любая геморрагическая трансформация, выявленная на КТ головного мозга в динамике в течение 2 нед от начала ишемического инсульта. Результаты. Логистический регрессионный анализ показал, что PS является независимым предиктором геморрагической трансформации в ядре инфаркта (отношение шансов 8; 95% доверительный ин-тервал-ДИ: 1,32-48,4; p=0,023). Пороговое значение PS составило 2,88 мл/100 г/мин (95% нормализованный ДИ (НДИ): 2,41-3,34), чувствительность-0,95 (95% НДИ: 0,87-1,0), специфичность-1 (95% НДИ: 0,95-1,0), площадь под ROC-кривой-0,98 (95% НДИ: 0,94-1,0). Однако независимых предикторов геморрагической трансформации в пенумбре не обнаружено. Анализ с помощью обобщенной линейной модели установил, что шкала HTI является предиктором CBV, CBF и PS в ядре инфаркта и пенумбре. По мере повышения риска геморрагической трансформации по шкале HTI в ядре инфаркта происходит снижение CBV и CBF и повышение PS; размеры ядра инфаркта при этом также увеличиваются. В то же время в пенумбре наблюдается прогрессирующее снижение CBF, но повышение CBV и PS; MTT-CBV несоответствие при этом уменьшается. Заключение. Источником геморрагической трансформации, наиболее вероятно, является ядро инфаркта. PS в ядре инфаркта является независимым предиктором геморрагической трансформации. Шкала HTI позволяет спрогнозировать не только вероятность развития геморрагической трансформации, но и перфузионные показатели головного мозга. По мере увеличения риска геморрагической трансформации перфузионные нарушения в ядре инфаркта и пенумбре усугубляются.
The reported incidence of persistent hypoperfusion despite complete recanalization as surrogate for impaired microvascular reperfusion (IMR) has varied widely among clinical studies, possibly due to differences in i) definition of complete recanalization, with only recent Thrombolysis in Cerebral Infarction (TICI) grading schemes allowing distinction between complete (TICI3) and partial recanalization with distal occlusions (TICI2c); ii) operational definition of IMR; and iii) consideration of potential alternative causes for hypoperfusion, notably carotid stenosis, re-occlusion and post-thrombectomy hemorrhage. We performed a systematic review to identify clinical studies that carried out brain perfusion imaging within 72 hrs post-thrombectomy for anterior circulation stroke and reported hypoperfusion rates separately for TICI3 and TICI2c grades. Authors were contacted if this data was missing. We identified eight eligible articles, altogether reporting 636 patients. The incidence of IMR after complete recanalization (i.e., TICI3) tended to decrease with the number of considered alternative causes of hypoperfusion: range 12.5–42.9%, 0–31.6% and 0–9.1% in articles that considered none, two or all three causes, respectively. No study reported the impact of IMR on functional outcome separately for TICI-3 patients. Based on this systematic review, IMR in true complete recanalization appears relatively rare, and reported incidence highly depends on definition used and consideration of confounding factors.
Hypertension is still the number one global killer. No matter what causes are, lowering blood pressure can significantly reduce cardiovascular complications, cardiovascular death, and total death. Unfortunately, some hypertensive individuals simply do not know having hypertension. Some knew it but either not being treated or treated but blood pressure does not achieve goal. The reasons for inadequate control of blood pressure are many. One important reason is that we are not very familiar with antihypertensive agents and less attention has been paid to comorbidities, complications as well as the hypertension-modified target organ damage in patients with hypertension. The right antihypertensive drug was not given to the right hypertensive patients at right time. This reviewer studied comprehensively the literature, hopefully that the review will help improve antihypertensive drug selection and antihypertensive therapy.
