BACKGROUND/AIMS: Changes in lipid profiles in patients infected with hepatitis C virus (HCV) during direct-acting antiviral therapy have been reported in recent years. However, the clinical aspects of disturbed lipid metabolism in chronic HCV infection have not been fully elucidated. METHODS: Dynamic changes in serum total, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) cholesterol and apolipoprotein levels in patients infected with HCV genotype 1b were examined during combination therapy with daclatasvir (DCV) and asunaprevir (ASV). RESULTS: Total, LDL−, and HDL-cholesterol levels increased rapidly and persistently after week 4. Apolipoprotein (apo) A-I, apo B, apo C-II, and apo C-III levels were significantly higher at week 4 than at week 0. In contrast, apo A-II and apo E levels were significantly lower. The differences in LDL− and HDL-cholesterol levels were positively correlated with those of apo B and apo A-I, respectively. Interestingly, in patients with non-sustained virological response, these cholesterol levels decreased rapidly after viral breakthrough or viral relapse. Furthermore, similar changes were observed for apo A-I, apo B and apo C-III levels. CONCLUSIONS: Clearance of HCV using combination therapy with DCV and ASV results in rapid changes in serum lipid profiles, suggesting an influence of HCV infection on disturbed lipid metabolism.
Apolipoprotein A-I ; Apolipoprotein A-II ; Apolipoprotein C-II ; Apolipoprotein C-III ; Apolipoproteins ; Apolipoproteins B ; Apolipoproteins E ; Cholesterol ; Genotype ; Hepacivirus* ; Hepatitis C* ; Hepatitis* ; Humans ; Lipid Metabolism ; Lipoproteins ; Recurrence

This case report describes our first experience performing percutaneous epicardial catheter ablation for Burugada syndrome in our hospital. We describe the good results achieved in this case. The patient was a man in his 30s with no remarkable medical history. However, his family history was notable for the sudden death of his grandfather at age 37 years and his father at age 27 years. While asleep, the patient experienced convulsions and lost consciousness. During emergency transportation, defibrillation was performed 7 times by the ambulance crew. When the patient arrived at our hospital, sinus rhythm was observed on ECG. During resuscitation, Burugada syndrome was diagnosed based on ECG findings. On hospital day 6, an internal cardioverter defibrillator was implanted. After discharge, the defibrillator operated 10 times, so we opted for ablation treatment. Fractionated potential of over 150 ms was confirmed in the right ventricular outflow tract. A low voltage zone of <1 mV could be mapped, and the same site was cauterized a total of 46 times. As a result, ST segment amplitude decreased significantly in lead V1 on ECG. Percutaneous epicardial catheter ablation performed with reference to Nademanee’s report achieved good results in this case of Burugada syndrome.