BACKGROUND: Several chronic infections have been associated with cardiovascular diseases, including Chlamydia pneumoniae, human immunodeficiency virus and viral hepatitis. This review evaluates the literature on the association between chronic hepatitis C virus (HCV) infection and the risk of coronary artery disease (CAD). METHODS: Studies were identified using several databases. Only studies on CAD in patients with HCV infection were included. A set of criteria for evaluating potential biases was made, based on known confounders and biases in observational research. Data were not synthesized because of the large heterogeneity in the included studies. RESULTS: Twelve eligible references were identified. Nine did not comply with our criteria of minimizing bias, and six studies were evaluated as potentially heavily biased. The studies of the highest quality showed a trend towards association of HCV with CAD. Five studies showed this association (three studies significantly), while one showed that HCV was a protective factor against CAD. CONCLUSION: Our findings suggest an increased risk of CAD in HCV-infected individuals. Further studies are needed to confirm this and to evaluate the magnitude of the association. Clinicians should be aware of this and strive to reduce CAD risk factors in patients with chronic HCV infection.
BACKGROUND: Several chronic infections have been associated with cardiovascular diseases, including Chlamydia pneumoniae, human immunodeficiency virus and viral hepatitis. This review evaluates the literature on the association between chronic hepatitis C virus (HCV) infection and the risk of coronary artery disease (CAD). METHODS: Studies were identified using several databases. Only studies on CAD in patients with HCV infection were included. A set of criteria for evaluating potential biases was made, based on known confounders and biases in observational research. Data were not synthesized because of the large heterogeneity in the included studies. RESULTS: Twelve eligible references were identified. Nine did not comply with our criteria of minimizing bias, and six studies were evaluated as potentially heavily biased. The studies of the highest quality showed a trend towards association of HCV with CAD. Five studies showed this association (three studies significantly), while one showed that HCV was a protective factor against CAD. CONCLUSION: Our findings suggest an increased risk of CAD in HCV-infected individuals. Further studies are needed to confirm this and to evaluate the magnitude of the association. Clinicians should be aware of this and strive to reduce CAD risk factors in patients with chronic HCV infection.
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