Related Experiment Video
Updated: Apr 16, 2026
A Protocol for Analyzing Hepatitis C Virus Replication
Published on: June 26, 2014
Higher Prevalence and More Severe Coronary Artery Disease in Hepatitis C Virus-infected Patients: A Case Control
Sanjaya K Satapathy1, Yun Ju Kim2, Ashish Kataria2
1Division of Gastroenterology, NSLIJ Hofstra School of Medicine, Long Island Jewish Medical Center, 270-05 76th Avenue, New Hyde Park, NY 11040, USA ; Division of Gastroenterology, NSLIJ Hofstra School of Medicine, North Shore University Hospital, 225 Community Drive, Manhasset, NY, USA.
Insights
Hepatitis C (HCV) patients show higher rates and severity of coronary artery disease (CAD) compared to non-infected individuals. HCV may be a significant risk factor for developing CAD.
Area of Science:
- Cardiology
- Hepatology
- Epidemiology
Background:
- The link between hepatitis C virus (HCV) infection and coronary artery disease (CAD) requires further investigation.
- Existing data on the association between HCV and CAD are inconclusive.
Purpose of the Study:
- To determine the prevalence and severity of CAD in HCV patients.
- To compare CAD rates and severity in HCV patients versus matched controls without HCV.
Main Methods:
- A retrospective study comparing 63 HCV patients with 63 matched controls undergoing coronary angiography.
- CAD was defined as >50% blockage in proximal coronary arteries.
- Severity was assessed using the modified Reardon scoring system.
Main Results:
- HCV patients had a significantly higher prevalence of CAD (69.8% vs. 47.6%, P=0.01).
- The Reardon severity score was significantly higher in the HCV group (6.26 ± 5.39 vs. 2.6 ± 3.03, P < 0.0005).
- Multivessel CAD was more common in HCV patients (57.1% vs. 15.9%, P < 0.0005).
Conclusions:
- HCV patients exhibit increased prevalence and severity of CAD compared to non-HCV individuals.
- Hepatitis C virus infection is a potential risk factor for coronary artery disease.
Background:
An association of Coronary artery disease (CAD) with hepatitis C (HCV) has been suggested, but definitive data are still lacking.
Aim:
Our study sought to estimate the prevalence and severity of CAD in HCV patients compared to with age-, sex-, and race-matched controls without HCV infection.
Subjects And Methods:
63 HCV-infected patients were compared with 63 age, race, and sex-matched controls without HCV infection undergoing coronary angiography for evaluation of CAD. CAD was defined as more than a 50% blockage in any of the proximal coronary arteries on angiogram. The severity of the stenosis was defined by the modified Reardon severity scoring system: <50% stenosis of the luminal diameter, 1 point; 50-74%, 2 points; 75-99%, 3 points; 100% or total obstruction, 4 points. The points for each lesion in the proximal coronary circulation were summed to give the score for severity.
Results:
A significantly higher prevalence of CAD was noted in the HCV population (69.8% vs. 47.6%, = 0.01). The combined Reardon's severity score in the HCV group was significantly higher compared to the controls (6.26 ± 5.39 vs. 2.6 ± 3.03, P < 0.0005). Additionally, significant multivessel CAD (>50% stenosis and ≥2 vessels involved) was also noted significantly more commonly in the HCV group compared to controls (57.1% vs. 15.9%, P < 0.0005).
Conclusion:
In this retrospective study the prevalence and severity of CAD was higher in HCV patients who were evaluated for CAD by angiogram compared with matched non-HCV patients. HCV-positive status is potentially a risk factor for CAD.
Related Concept Videos
01:25Hepatitis
01:30Coronary Artery Disease I: Introduction
01:30Coronary Artery Disease III: Clinical Manifestations
01:26Effect of Hepatic Disease on Pharmacokinetics: Drug Dosing and Hepatic Blood Flow
01:26Diseases of the Liver and Gallbladder
Cirrhosis is characterized by the scarring of hepatic lobules in the liver, which are replaced by fibrous tissue, affecting the liver's normal functioning. NAFLD, on the other hand, is caused by an excessive build-up of fat in the liver, not...
01:26Coronary Artery Disease II: Pathophysiology