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Acute changes in cardiac function by direct acting antiviral therapy for hepatitis C-infected patients with
Arezoo Khosravi1,2,3, Hamidreza Karimi-Sari1,2,4, Mahdi Abedi-Andani1,2,3
1Baqiyatallah Research Center for Gastroenterology and Liver Diseases (BRCGL), Baqiyatallah University of Medical Sciences, Tehran, Iran.
Insights
Direct-acting antiviral therapy for hepatitis C virus (HCV) in thalassemia patients showed safety and efficacy. While cardiac function parameters changed, ejection fraction remained stable, suggesting careful monitoring for those with pre-existing cardiac issues.
Area of Science:
- Cardiology
- Hepatology
- Hematology
Background:
- Thalassemia patients often experience cardiac complications due to congenital issues, anemia, and iron overload.
- Hepatitis C virus (HCV) infection can exacerbate cardiac abnormalities in thalassemia patients.
Purpose of the Study:
- To evaluate the impact of direct-acting antiviral (DAA) therapy on cardiac function in HCV-infected thalassemia patients.
- To assess the safety and efficacy of sofosbuvir-based regimens in this specific patient population.
Main Methods:
- A prospective study involving HCV-infected thalassemia patients treated with sofosbuvir-based DAA regimens (ledipasvir or daclatasvir ± ribavirin).
- Echocardiography was performed before and after treatment to assess cardiac function.
- Patients were monitored for cardiac events for 12 weeks post-treatment.
Main Results:
- All 32 patients achieved a sustained virological response.
- Significant increases were observed in left ventricular end-systolic diameter and volume, global longitudinal strain, and right ventricle size post-treatment.
- No significant changes were noted in other echocardiographic parameters, including ejection fraction, and changes did not correlate with myocardial iron load.
Conclusions:
- Sofosbuvir-based DAA therapy is safe and effective for HCV-infected thalassemia patients.
- While some cardiac dimensions changed, overall cardiac function (ejection fraction) remained stable.
- Specialized echocardiographic evaluation is recommended for patients with a history of cardiac abnormalities or iron overload.
Background:
Patients with thalassemia may also have cardiac abnormalities due to congenital problems, anemia, and increased burden of iron in their myocardium. This study was designed to evaluate the effects of direct acting antiviral (DAA) therapy on the cardiac function of hepatitis C virus (HCV)-infected patients with thalassemia.
Method:
HCV-infected thalassemia patients were enrolled to this prospective evaluation. Daily tablets of 90 mg Ledipasvir (or 60 mg Daclatasvir) plus 400 mg Sofosbuvir (±ribavirin) were prescribed for the patients according to the Iran Hepatitis Network's guidelines. An echocardiography fellow collected the echocardiography findings before and after the treatment of all the patients. The patients were followed up for any cardiac events within 12 weeks after finishing the treatment.
Results:
Thirty-two patients with the mean age of 24.2 ± 6.4 years were evaluated. All patients showed a sustained virological response at the 12th week after finishing the treatment. The patients' left ventricular end systolic diameter (3.0 vs 3.24; P = 0.003) and volume (33.8 vs 43.6; P = 0.001), global longitudinal strain of the left ventricle (-22.0 vs -20.6, P = 0.046), and average (-21.4 vs -20.3; P = 0.048), and the right ventricle size (3.12 vs 3.31; P = 0.012) were significantly increased after finishing the treatment. Changes in the abovementioned parameters were not correlated with the patients' myocardium iron load. There were no significant differences in other echocardiographic parameters ( P > 0.05) before and after the treatment.
Conclusion:
Sofosbuvir-based regimens for HCV treatment were safe for our HCV-infected patients with thalassemia. Our patients' ejection fraction remained unchanged. Hence, more specialized echocardiographic evaluations were recommended for those with a history of cardiac abnormalities, cardiac iron overload, and in case of any cardiac adverse event during DAA therapy in patients with thalassemia.
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