Assessment of carotid intima-media thickness and carotid plaque formation among patients with ischemic stroke and hepatitis C virus infection

Abstract Background Cerebrovascular diseases are well known all over the world to be among the top list of the causes of death. One third of ischemic stroke could be regarded to plaque rupture and embolization. The actual mechanisms have not been exactly understood, but inflammation plays a pathogenic role. Patients with hepatitis C virus (HCV) proved to have a high level of inflammation. Replication of HCV within the brain endothelial cells and carotid plaques and, recently, the consideration of HCV as playing a role in risking for atherosclerosis rose the question of the role of HCV in cerebrovascular diseases. Objective Evaluating the role of infection with HCV among patients with stroke through assessment of carotid atherosclerosis. Patients and methods A cross-sectional study was carried out on 100 patients with ischemic stroke, aged 40–60 years, enrolled from the Neuropsychiatry Department of Suez Canal University Hospital. Patients were classified into 50 HCV-positive patients and 50 HCV-negative patients. All patients were assessed for HCV and the traditional risk of stroke as they were subjected to complete neurological examination, assessment of vascular risk factors, and a full extracranial neurovascular ultrasonography. Features evaluated were isolated increase of common carotid artery mean intima-media thickness (IMT) and extracranial atheromatous plaques. Results Intima-media thickness (IMT) was significantly higher in HCV-positive patients (1.04) than in HCV-negative patients (0.71). The percentage of plaque formation was insignificantly more frequent in HCV-positive patients (20%) than HCV-negative patients (10%). IMT and plaque formation were significantly increased in HCV-positive patients with high viremia. The multivariate analysis statistics concluded that infection with HCV was independently a risk factor for stroke. Conclusion Patients with HCV infection are at higher and earlier risk of stroke. The key mediator is inflammation. Lastly, researchers and clinicians should take these new findings into their consideration