Parameter Age, years Female Baseline NIHSS Hematocrit at baseline (%) WBC (K/uL) Glucose at baseline (mg/dL) C-reactive protein (mg/L) Fibrinogen (g/L) Time to CT scan from onset (h) Infarct’s volume (cm3) Secondary hemorrhage Diabetes Coronary artery disease Previous stroke or TIA Atrial fibrillation Hyperlipidemia Current smoking Variable Infarct’s volume C-reactive protein Hematocrit Fibrinogen Secondary hemorrhage Original Article Table 1. The baseline characteristics of patients with a presence or absence of the HPCA sign. © Pol J Radiol, 2011; 76(2): 13-17 HPCA Sign (n=12) no HPCA Sign (n=43) P-value 72 4 3 4.8 11.5 17.6 3 3 6 4 1 5 7 45.2 (42.5–50.5) 9.95 (7.3–12.4) 117.5 (103.5–174.5) 17.2 (8.05–28.6) (62–79) (33%) (2–4.5) (3.7–5.04) (7.5–22) (4.6–31.8) (25%) (25%) (50%) (33%) (8%) (42%) (58%) 65 15 3 42.6 8.1 2.6 3.8 9.5 4.3 1 12 20 11 8 12 24 136 (104.5–172) (58–75) (34%) (2–5) (40–45.4) (6.5–10.8) (0.7–7.9) (3.0–4.4) (5–21.5) (1.5–14.1) (2.3%) (28%) (45%) (25%) (19%) (28%) (56%) NS NS NS 0.05 NS NS 0.02 0.02 NS 0.02 0.03 NS NS NS NS NS NS Values are median (interquartile range) or n (%). NIHSS – NIH Stroke Scale, mRS – modified Rankin Score, NS – not significant. Table 2. Evaluation of independent factors associated with the HPCA sign by a multinomial logistic regression analysis. Odds Ratio 95% Confidence Interval 1.07 1.01 1.22 1.14 9.48 0.99–1.13 0.98–1.03 0.99–1.5 0.56–2.29 0.9–105.6 Significance P=0.04 NS NS p=0.05 p=0.07 NS – not significant. the infarct size is inconsistent as some studies have not shown any correlation [15] while in others the patients with the HMCA sign have a significantly larger infarct volume compared to the patients without this feature [16]. We found that the HPCA sign was significantly related (but only in the univariate analysis) to higher fibrinogen and CRP levels. To our best knowledge no previous report revealed an association between a hyperdense artery sign appearance and the considered acute phase markers, howe- ver, a strong association between inflammation, prothrom- botic state and stroke is well established [5,17]. We also know that the increase of CRP levels correlates with the lesion volume [18]. That is why we assume that the link between the HPCA and acute phase markers levels comes from a more intense inflammatory state in stroke with a larger infarct area. Another explanation could be that 16 pro-inflammatory and prothrombic states predispose to a hyperdense sign appearance – we know that the signal augmentation of artery in stroke is indicative of an intra- -luminal thromboembolic clot [19]. Further population stu- dies are necessary. Previous studies have indicated that the hyperdense arte- ry was related to a severe clinical status [15,20], however, most of them have been referred to the hyperdense MCA sign and stroke in an area supplied by the MCA. The results of published large trials have shown that the mean baseli- ne NIHSS score was lower among posterior than anterior circulation stroke patients [21]. Our results are consistent with the above mentioned study because the baseline mean clinical status was relatively good. This could explain why we did not find any association between the presence of the HPCA sign and the baseline NIHSS score. The other possible