Atherosclerosis is a chronic inflammatory disease of large- and medium-sized arteries characterized by the development of atherosclerotic plaque.1 Atherosclerotic changes are initiated by the passage of cholesterol into arterial walls and its engulfment by macrophages, which leads to the formation of foam cells and plaque. 2 Globally, atherosclerosis-induced ischemic heart disease and stroke are the leading causes of mortality.3 Increasing age (> 45 years old), metabolic syndrome and smoking are considered as the major risks of atherosclerosis,4,5 however, alcohol consumption had an inverse association with atherosclerosis.6 Coronary calcium determined through computed tomography (CT) is a suggested marker for predicting coronary heart disease and stroke events.7 Epidemiological studies have reported significant associations of aortic calcification with coronary heart disease, stroke, and peripheral vascular disease.8, 9, 10, 11 Moreover, compared with the carotid intima–media thickness and ankle–brachial index, atherosclerotic calcification is more accurate in predicting future cardiovascular events.12,13

In a systematic, global meta-analysis of 341,739 people with hepatitis C virus (HCV) infection, chronic HCV infection was associated with a 1.28-fold (95% confidence interval [CI]: 1.18–1.39) risk of cardiovascular disease.14 HCV infection can cause hepatic and systemic inflammation, which are associated with increased levels of proatherogenic chemokines and cytokines potentially involved in atherosclerosis development.15 In addition, HCV infection is significantly associated with insulin resistance (IR), diabetes mellitus, hepatic steatosis, cryoglobulinemia, and endotoxemia, all of which are linked to atherosclerosis and cardiovascular disease.16, 17, 18 Although metabolic disorder is not directly linked to HCV infection, there is a substantial interaction with metabolic syndrome. Similar to metabolic syndrome, HCV is associated with insulin resistance, indicating a significant interplay between HCV infection and different aspects of lipid and glucose metabolism. It is clear that while HCV and metabolic syndrome may not be directly associated, they certainly demonstrate a noteworthy interconnection.19 Another study identified HCV RNA sequences in carotid plaque tissue, indicating the prominent influence of HCV infection on atherosclerosis development.20 The signal-to-cutoff (S/CO) ratio of anti-HCV antibody mainly to HCV core NS3 fusion protein and nonstructural proteins (c200, c100, NS5) has been used to predict 95% probability of true positivity of HCV infection 21. Some studies revealed that decline S/CO ratio was associated with spontaneous HCV RNA clearance through humoral immune response22,23 that was totally different from those HCV eradicated by direct-acting antiviral agent (DAA) whose S/CO ratio was still high while HCV RNA being negative. Whether the range of S/CO ratio in those without history of HCV treatment associated with the severity of atherosclerosis remain unknown.

The Society of Cardiovascular Computed Tomography (CT) and the Society of Thoracic Radiology recommend low-dose chest multi-detector CT (MDCT) for the detection of coronary and thoracic aortic calcification.24 Low-dose (0.6-1.1 mSv) chest ECG-ungated non-contrast is reported to have high concordant with electrocardiographically (ECG)-gated non-contrast CT (radiation exposure 1.0 to 1.25 mSv) for prediction of the presence of thoracic and coronary artery calcification and assessment of Agatston score.25,26 Coronary CT angiography has been used in the diagnosis of coronary artery atherosclerosis; however, because of the requirement for the injection of an iodine-containing contrast material and the high radiation dose (13.8 mSv), Coronary CT angiography is recommended for symptomatic patients only on an individual basis.27 The aim of present study was to investigate the association between HCV infection and central coronary, thoracic artery atherosclerosis detected from MDCT. We assess the severity of liver fibrosis and levels of anti-HCV S/CO ratio in HCV infection interacting with metabolic syndrome that correlate with coronary and thoracic artery atherosclerosis.