Non-ischemic Cardiomyopathy Secondary to Pegylated Interferon in a Patient with Chronic Hepatitis C

Abstract

Purpose: Reversible cardiomyopathy is a side effect of interferon treatment, typically described as being associated with high-dose standard interferon. Pegylated INF has a polyethylene glycol molecule attached to the protein, which results in a reduction in its rate of absorption, renal clearance, and immunogenicity following subcutaneous injection. We present a rare case of PEG interferon-induced dilated cardiomyopathy. A 65-year-old female with hepatitis C (HCV), mononeuritis multiplex, mixed cryoglobulinemia, and hypertension presented with complaints of shortness of breath with minimal exertion, which was gradually worsening. She denied any chest pain, palpitations, fever, chills, blood loss, weight loss, or history of smoking. She was started on treatment for HCV in June of 2012, with telapravir, PEG interferon, and ribavirin. Her viral load was detectable at week four, and undetectable at weeks 12 and 24. Her renal function was normal at the start of treatment. During the therapy, her renal function started to deteriorate. Doses of ribavirin and interferon were reduced secondary to her anemia and neutropenia, respectively. Despite dose reduction, treatment was stopped at week 33 due to treatment intolerance. Prior to treatment, the patient had a cardiac catheterization, which showed an ejection fraction (EF) of 50% and non-obstructive coronary artery disease. An echocardiogram done in following treatment showed an EF of 30-35%, with moderate mitral regurgitation (MR) and global left ventricular hypokinesia, stage three diastolic dysfunction, left ventricular dilatation, moderate left atrial dilatation, trace tricuspid regurgitation, and a pulmonary artery pressure of 40 mmHg. A transesophageal echocardiogram (TEE) confirmed the global hypokinesia, and the EF had decreased to 15-20%, with moderate MR. Repeat cardiac catheterization showed global hypokinesia, patent coronary arteries, and an EF of 25-30%. The right ventricular systolic pressure was 41 mmHg. Cryoglobulins were absent, and the rheumatoid factor had decreased to 45 from 200 prior to treatment. An autoimmune work-up was negative. The patient denied any flu-like illness during treatment. A myocardial biopsy was not performed to confirm the diagnosis; however, after ruling out other causes of cardiomyopathy, we attributed the cardiomyopathy to interferon therapy. We believe that the deterioration in renal function may have caused elevated concentrations of interferon, resulting in cardiotoxicity. The sudden worsening of the cardiomyopathy and its chronology in relation to the use of pegylated interferon and deteriorating renal function further support our impression.