Interplay between chronic hepatitis B and atherosclerosis: Innovative perspectives and theories

Abstract

Elaboration of carotid atherosclerosis in the setting of hepatitis B virus (HBV) infection should emphasize the significance of extrahepatic manifestations of the infection pathogenesis. Diverse processes comprise the pathoevolution of HBV infection, rendering it a multi-systemic disease in its essence. Our work not only exemplified atherosclerosis as an often-underestimated contributor to the severity of HBV infection but has also highlighted the bidirectional relationship between the two. Therefore, it is suggested that HBV-induced inflammation is one of the root causes of atherosclerosis, which in turn has a consequent effect on the severity of the chronic infection disease state, creating a vicious cycle. Additionally, we coupled prior data with the current concepts of HBV infection to postulate intriguing perspectives and theories.

Keywords: Hepatitis B virus infection; Carotid atherosclerosis; Hepatitis B e antigen; Arterial inflammation; Perspectives and trends

Core Tip: Hepatitis B virus (HBV) infection is a multifaceted disease, with significant cardiovascular morbidity. Our innovative approach to this pathophysiologic relationship harbors several key ideas. First, HBV infection may carry a specific atherosclerosis distribution pattern, with predilection for carotid arteries. Second, we propose wider use of more sensitive inflammatory markers, such as high-sensitivity C-reactive protein and homocysteine. Third, macrophage phenotype function should be investigated, utilizing its potential role as an atherosclerosis biomarker in HBV infection and therapeutic target. Last but not least, we reason that statins should be exploited more in current practice, due to their favorable pleotropic effects.