Nevertheless, vertebral hypoplasia as a possible risk factor for pathology, particularly of stroke in the vertebrobasilar circulation territory, was little emphasized yet. The aim of this preliminary study is to evaluate a hypothesis of a possible causal link between the Ferroptosis mutation anatomical findings of VAH and the incidence of posterior circulation stroke. For this purpose, we assessed the relative

frequencies of posterior circulation strokes in patients with VAH as compared to patients without VAH, and also the relative frequencies of the conventional vascular risk factors (hypertension, diabetes, hyperlipidemia and smoking). Additionally, we determined the possible mechanism of stroke in our patients. A group of 44 patients (30 men, 14 women; mean age 67 years [range 44–88]) with acute ischemia in the vertebrobasilar territory had a full ultrasonographic examination of the extra- and intracranial arteries between September

2009 and February 2011. The location OSI 744 of the acute ischemic infarct was judged clinically and confirmed by CT scan or MRI. We excluded patients with transient ischemic attacks (TIA), patients with other vertebral artery findings (such as atheromatosis, stenosis or occlusion) or other cerebral lesions, as well as those in whom a full ultrasonographic examination of the vertebral arteries was not possible. We used a 7.5-MHz linear array transducer for the duplex ultrasonographic examination of the vertebral arteries (B-mode and color-coded duplex flow imaging). In the V1 (prevertebral) and V2 (intervertebral) segments of the extracranial vertebral artery the distance between the internal layers of the parallel walls of the vessel (caliber of VA) and the hemodynamic characteristics of blood flow were

measured. The diameter equal or less than 2.5 mm, respectively the side difference equal or greater than 1:1.7 were set as a feature of vertebral artery hypoplasia. Additionally, reduced flow velocities as compared to the contralateral side, and higher peripheral resistance ipsilaterally (RI equal or greater than 0.75) were considered. MRA, CTA or conventional angiography was performed to confirm the presence or absence of the anatomic variation of hypoplasia. We also investigated the occurrence of other concomitant vascular risk factors such as hypertension, diabetes, hyperlipidemia Chorioepithelioma and smoking. In the group of 44 posterior circulation stroke patients, 9 (20%) had a hypoplastic vertebral artery and 35 (80%) were without VAH (Fig. 1A). There was more frequent right-sided VAH in 7 (78%), as compared to left-sided VAH in 2 (22%) cases (Fig. 1B). One patient had bilateral VAH (both vertebral arteries had a diameter of less than 2.5 mm), more significant on the right side. None of the patients had basilar artery hypoplasia. In the group of non-VAH patients were 22 men and 13 women, in the VAH group 8 men and 1 woman (Fig. 1C). There was a slight difference for age between the non-VAH (mean age 68.