Original Article practice head CT is still and will probably remain for many years the first step of stroke imaging. The last update of guidelines of the European Stroke Organization states that non-enhanced cranial CT is generally sufficient to conduct thrombolysis, the only one approved specific therapy for acute stroke [3]. This imaging technique identifies subtle, early signs associated with brain ischemia as: loss of gray- -white matter differentiation in cortical gyri, basal ganglia or insula; focal hypoattenuation of brain structures; cortical sulcal effacement and hyperattenuation of vessel [4]. Most of them are related to the territory supplied by the middle cerebral artery (MCA). However, infarction of the region in the posterior cerebral artery (PCA) supply is not rare – according to various sources the prevalence is from 10% to 20% of all types of stroke [5]. From the above mentioned early CT signs of brain ischemia, the hyperdense MCA seems to be more reliable than parenchyma abnormalities [4]. The same phenomenon could occur in other intracranial vessels including the PCA. However, the number of studies which showed a hyperdense posterior cerebral artery (HPCA) sign in posterior circulation infarction is relatively small [6,7]. In the present study we focused on the occurrence of the HPCA sign on CT in a large group of stroke patients, and on the association of this sign with neurological status. Additionally we investigated the association between the HPCA sign and important cerebrovascular risk factors inc- luding pro-thrombotic and inflammatory markers which have not been studied before. The aim of this study was to determine the prevalence of the HPCA sign in associa- tion with PCA infarction noticeable on CT scans, density of affected vessels and the correlations with the ischemic lesion volume and fibrinogen and C-reactive protein levels. Material and Methods The prospective trial included 376 patients with an acute (<24 hours of symptoms onset) ischemic stroke consecutively admitted to ED in two regional hospitals between December 2006 and November 2007. Written informed consent was collected from all study participants. The protocol was approved by the Local Ethics Committee, Poznań University of Medical Sciences. Demographic data, cerebrovascular risk factors, drugs, neurological deficits, type of stroke were collected. Every patient was assigned to one of the syndro- mes according to the Oxfordshire Community Stroke Project (OCSP) classification. The NIH Stroke Scale (NIHSS) was used to assess the clinical status of patients at admission. At the time of collecting data hospitalized patients had not been tre- ated by thrombolysis, so only patients with general stroke treatment are the subject of this study. We retrospectively analyzed unenhanced brain CT scans (Picker PQ 5000 and Toshiba Aquilion TSX 101A) perfor- med at the admission to hospital. All scans were obtained based on a standard protocol for CT examination in acute stroke suspected patient: 130-kvP tube voltage, 512×512 pixel matrix, and axial 5 mm section thickness for the enti- re brain (from occipital foramen to the vertex). The reviewers (clinical neurologist (WA) and neuroanato- my expert (WLN) with experience in stroke neuroimaging interpretation) were aware that the results of CT scan come 14 © Pol J Radiol, 2011; 76(2): 13-17 from patients with acute stroke suspicion but they were blinded to the clinical information. The HPCA sign was assessed as present (according to previously defined crite- ria [7]) when: 1. it was unilateral, 2. PCA was denser than the surrounding brain and counterpart on the contralate- ral site, 3. the other early ischemic changes (brain tissue hypoattenuation and loss of precise delineation of the gray- -white interface) were present. In the case of disagreement a second review was conducted to achieve consensus. The average density of the affected vessels and their intact counterparts was calculated in Hounsfield units (HU). The area of a visible acute ischemia lesion in the PCA territory on every slice was contoured manually and based on the number of slices, the slice thickness and the marked area, the volume of lesion was automatically calculated by the StrokeCAD developed in house [8,9]. Statistics The interobserver agreement for the HPCA sign was assessed between the two readers using kappa statistics. Statistical analysis of categorical data was performed with Fisher’s exact test or a c2 test when appropriate. For con- tinuous data, we used the t test and Shapiro Wilk test for normal distribution of data. The non-parametric Wilcoxon rank-sum (or Kruskal-Wallis) test was also used to confirm the significant differences between subgroups. Finally, to assess the independent contribution of the parameters with significant differences across the classes in a univariate analysis to the risk of the presence of the HPCA sign we used multivariate logistic regression analysis. The results are expressed as adjusted odds ratio and corresponding 95% confidence intervals. A p value of less than 0.05 was considered significant. All tests were 2-sided and computed with the SPSS software, ver.15. Results Based on clinical symptoms 376 patients were assigned to OCSP classification: 71 (19%) subjects had a total anterior circulation syndrome, 176 (47%) partial anterior circulation syndrome, 72 (19%) lacunar syndrome and 57 (15%) poste- rior circulation syndrome. However, the 221 (58%) patients had visible early signs of brain ischemia in CT examina- tion. Within this group 55 (24%) patients had noticeable acute infarcts lesions in brain tissue supplied by the poste- rior cerebral arteries. In turn in this subgroup we iden- tified 12 (22%) patients with the HPCA sign (Figure 1) in the CT exam. The reviewers had disagreement regarding two cases. The kappa value which expresses the inter- -observer agreement for the HPCA sign was 0.81 (a very good strength of agreement). The baseline characteristics (demographic, clinical and biochemical data) according to appearance or absence of the HPCA sign are presented in Table 1. The average density of the affected PCA was 46.5 (±8.8) comparing to 20.2 HU (±6.7) of the intact vessel (p<0.0001) in a univariate non-parametric analysis. The HPCA sign was unilateral to the affected hemisphere in all patients. In the univariate analysis patients with the HPCA sign had a significantly larger volume of ischemic lesion (mean