Abstract
Background: CT Perfusion (CTP) defined hemodynamic parameters used to delineate admission infarct core can be affected by truncated data acquisition, recanalization status and reactive hyperemia. We determined the optimal CTP parameter for infarct demarcation while taking these variables into account. Methods: 30 patients had CTP/NCCT scanning within 6 hours of ictus, a 24 hour CTA and an NCCT at 3 months post stroke to define final infarct. Patients were analyzed according to: 1) the percent wash out (truncation) of the ischemic time density curve (ITDC) and 2) recanalization status defined using the 24 hour CTA. CTP functional maps were generated using delay insensitive CTP software (GE Healthcare). For all patients, the total ischemic lesion (infarct+penumbra+benign oligemia) was defined using the contrast delay plus mean transit time map. Cerebral blood flow (CBF), cerebral blood volume (CBV) and the product of CBF and CBV (CBFxCBV) were used to define the infarct core defect, according to established thresholds, and compared with the infarct volume defined on the 3 month NCCT. The coefficients of correlation (R2) of linear regression models were used for the comparisons. Results: R2 values for admission CBF, CBV, and CBFxCBV defect versus final infarct volume for patients with and without truncation of the ITDC were 0.89, 0.49, 0.65 and 0.90, 0.42, 0.68, respectively; while R2 values for patients with and without recanalization at 24 hours were 0.73, 0.33, 0.44 and 0.84, 0.54, 0.45, respectively. In addition, for the recanalization group with and without truncation of the ITDC, R2 for CBF, CBV, CBFxCBV versus final infarct volume were 0.73, 0.12, 0.31 and 0.79, 0.58, 0.56, respectively. Hyperemia, defined as an increase in CBV relative to the contralateral hemisphere, was observed in 30% of patients. Both hyperemia and ITDC truncation led to poor correlation between the CBV defect and NCCT defined infarct volume. Conclusion: CBF is the optimal parameter for determining the size of the acute infarct core as it is not affected by truncation of the ITDC and autoregulatory vasodilation causing reactive hyperemia.
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