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Introduction: We investigated whether baseline CT angiography (CTA) and CT perfusion (CTP) in acute ischemic stroke could improve prediction of infarct presence and infarct volume on follow-up imaging., Methods: We analyzed 906 patients with suspected anterior circulation stroke from the prospective multicenter Dutch acute stroke study (DUST). All patients underwent baseline non-contrast CT, CTA, and CTP and follow-up non-contrast CT/MRI after 3 days. Multivariable regression models were developed including patient characteristics and non-contrast CT, and subsequently, CTA and CTP measures were added. The increase in area under the curve (AUC) and R (2) was assessed to determine the additional value of CTA and CTP., Results: At follow-up, 612 patients (67.5%) had a detectable infarct on CT/MRI; median infarct volume was 14.8 mL (interquartile range (IQR) 2.8-69.6). Regarding infarct presence, the AUC of 0.82 (95% confidence interval (CI) 0.79-0.85) for patient characteristics and non-contrast CT was improved with addition of CTA measures (AUC 0.85 (95% CI 0.82-0.87); p < 0.001) and was even higher after addition of CTP measures (AUC 0.89 (95% CI 0.87-0.91); p < 0.001) and combined CTA/CTP measures (AUC 0.89 (95% CI 0.87-0.91); p < 0.001). For infarct volume, adding combined CTA/CTP measures (R (2) = 0.58) was superior to patient characteristics and non-contrast CT alone (R (2) = 0.44) and to addition of CTA alone (R (2) = 0.55) or CTP alone (R (2) = 0.54; all p < 0.001)., Conclusion: In the acute stage, CTA and CTP have additional value over patient characteristics and non-contrast CT for predicting infarct presence and infarct volume on follow-up imaging. These findings could be applied for patient selection in future trials on ischemic stroke treatment.

Introduction: Our aim was to compare infarct core volume on whole brain CT perfusion (CTP) with several limited coverage sizes (i.e., 3, 4, 6, and 8 cm), as currently used in routine clinical practice., Methods: In total, 40 acute ischemic stroke patients with non-contrast CT (NCCT) and CTP imaging of anterior circulation ischemia were included. Imaging was performed using a 320-multislice CT. Average volumes of infarct core of all simulated partial coverage sizes were calculated. Infarct core volume of each partial brain coverage was compared with infarct core volume of whole brain coverage and expressed using a percentage. To determine the optimal starting position for each simulated CTP coverage, the percentage of infarct coverage was calculated for every possible starting position of the simulated partial coverage in relation to Alberta Stroke Program Early CT Score in Acute Stroke Triage (ASPECTS 1) level., Results: Whole brain CTP coverage further increased the percentage of infarct core volume depicted by 10% as compared to the 8-cm coverage when the bottom slice was positioned at the ASPECTS 1 level. Optimization of the position of the region of interest (ROI) in 3 cm, 4 cm, and 8 cm improved the percentage of infarct depicted by 4% for the 8-cm, 7% for the 4-cm, and 13% for the 3-cm coverage size., Conclusion: This study shows that whole brain CTP is the optimal coverage for CTP with a substantial improvement in accuracy in quantifying infarct core size. In addition, our results suggest that the optimal position of the ROI in limited coverage depends on the size of the coverage.

Smoking and hypertension are risk factors for aneurysmal subarachnoid hemorrhage (aSAH), but also for other cardiovascular diseases and cancer. Few prospective data are available on the very long term risks of vascular diseases and vascular, cancer-related and overall death after aSAH. We determined vascular events and survival status in 1,765 patients with aSAH admitted to our center from 1985 to 2010. Cumulative risks were estimated with survival analysis. We compared risks of vascular, cancer-related and all-cause death with the general population with standardized mortality ratios (SMRs). Incidences of vascular events and death were compared with those after TIA/minor stroke. Conditional on surviving 3 months after aSAH, the risk of death was 8.7 % (95 % CI 7.3-10.1) within 5 years, 17.9 % (16.1-19.9) within 10 years, 29.5 % (27.3-31.8) within 15 years, and 43.6 % (41.2-46.1) within 20 years after SAH. The SMR for all-cause death was 1.8 (1.6-2.1), for vascular death 2.0 (95 % CI 1.6-2.5) and for cancer-related death 1.2 (0.9-1.5; sensitivity analysis 1.4; 95 % CI 1.1-1.8). The increased SMR for all-cause death persevered up to 20 years after aSAH. Compared with TIA/minor stroke patients, the age- and sex-adjusted cumulative incidence on vascular events was lower for aSAH patients [hazard ratio (HR) 0.48; 95 % CI 0.40-0.57); the HR for all-cause death was 0.96 (95 % CI 0.84-1.10). After aSAH, risks of vascular events and death, and probably also that of cancer-related death, are higher than in the general population. Although the long-term risk of vascular events was lower in aSAH patients than in TIA/minor stroke patients, the risk of death was similar.

Introduction: Vasospasm after aneurysmal subarachnoid hemorrhage (SAH) is thought to cause ischemia. To evaluate the contribution of vasospasm to delayed cerebral ischemia (DCI), we investigated the effect of vasospasm on cerebral perfusion and the relationship of vasospasm with DCI., Methods: We studied 37 consecutive SAH patients with CT angiography (CTA) and CT perfusion (CTP) on admission and within 14 days after admission or at time of clinical deterioration. CTP values (cerebral blood volume, cerebral blood flow (CBF) and mean transit time), degree of vasospasm on CTA, and occurrence of DCI were recorded. Vasospasm was categorized as follows: no spasm (0-25% decrease in vessel diameter), moderate spasm (25-50% decrease), and severe spasm (>50% decrease). The correspondence of the flow territory of the most spastic vessel with the least perfused region was evaluated, and differences in perfusion values and occurrence of DCI between degrees of vasospasm were calculated with 95% confidence intervals (95% CI)., Results: Fourteen patients had no vasospasm, 16 were moderate, and seven were severe. In 65% of patients with spasm, the flow territory of the most spastic vessel corresponded with the least perfused region. There was significant CBF (milliliters per 100 g per minute) difference (-21.3; 95% CI, -37 <--> -5.3) between flow territories of severe and no vasospasm. Four of seven patients with severe, six of 16 with moderate, and three of 14 patients with no vasospasm had DCI., Conclusion: Vasospasm decreases cerebral perfusion, but corresponds with the least perfused region in only two thirds of our patients. Furthermore, almost half of patients with severe vasospasm do not have DCI. Thus, although severe vasospasm can decrease perfusion, it may not result in DCI.

Introduction: The pathogenesis of delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) is unclear. We assessed whether DCI relates to focal or global cerebral perfusion on admission and on follow-up imaging., Materials and Methods: Twenty-seven SAH patients underwent computed tomography (CT) perfusion (CTP) on admission and at clinical deterioration or 1 week after admission in clinically stable patients. We compared global and focal (least perfused territory) perfusion in patients with DCI (n = 12), clinically stable patients (n = 7), and patients with non-DCI-related deterioration (n = 8)., Results: Global cerebral blood flow (CBF) increased on follow-up: 29% (95% confidence interval (CI) 15% to 43%) in patients with DCI, 12% (95%CI -1% to 25%) in stable patients, and 20% (95%CI 4% to 36%) in patients with non-DCI-related deterioration. Focal CBF decreased in patients with DCI, (-23%; 95%CI -58% to 12%) but increased in patients with non-DCI-related deterioration (23%; 95%CI -26% to 55%) and stable patients (7%; 95%CI -30% to 45%).On follow-up, global CBF was lower in patients with DCI (70.0 ml per 100 g/min) than in clinically stable patients (81.6; difference 11.6; 95%CI 0.8 to 22.5 ml per 100 g/min) but comparable to patients with non-DCI-related deterioration (67.6; difference -2.4; 95%CI -11.9 to 7.2 ml per 100 g/min). Focal CBF was lower in patients with DCI (30.7) than in clinically stable patients (53.6; difference 22.9; 95%CI 5.1 to 40.6 ml per 100 g/min) and patients with non-DCI-related deterioration (46.6; difference 15.9; 95%CI -2.6 to 28.4 ml per 100 g/min), Conclusion: Our results suggest that DCI is more likely a focal than a global process.