Heart Failure with Etanercept Therapy: A Case Report

Khan Ma,Dormand H,Neyses L

doi:10.4172/2155-9880.1000236

Abstract

Tumour Necrosis Factor-alpha antagonists constitute an important part of the therapeutic armamentarium available for managing autoimmune diseases such as rheumatoid arthritis and psoriatic arthropathy. Here, we present the case of a 68-year old male with severe rheumatoid arthritis who developed chest pains and severe left ventricular systolic dysfunction following etanercept therapy. Etanercept was discontinued while he was commenced on standard heart failure treatment. This, consequently, led to complete resolution of his symptoms and recovery of left ventricular function to near normal. Previous literature involving similar case reports is reviewed and implications for clinical practice are discussed with emphasis on the need for a screening protocol when commencing such therapy.

Highlights

Etanercept is a tumour necrosis factor-alpha (TNF-α) antagonist. It was the first member of a family of cytokine modulators subsequently used as disease modifying agents for a variety of autoimmune conditions including rheumatoid arthritis, polyarticular juvenile rheumatoid arthritis, ankylosing spondylitis and psoriasis
In the Studies of Left Ventricular Dysfunction (SOLVD) trial TNF-α was increased in patients in NYHA functional classes I to III as compared to healthy controls with levels correlated to NYHA class [4]
In contrast to previous reports, this was an acute presentation with left ventricular dysfunction and chest pains following etanercept therapy

Summary

Introduction

Etanercept is a tumour necrosis factor-alpha (TNF-α) antagonist. It was the first member of a family of cytokine modulators subsequently used as disease modifying agents for a variety of autoimmune conditions including rheumatoid arthritis, polyarticular juvenile rheumatoid arthritis, ankylosing spondylitis and psoriasis. In the Studies of Left Ventricular Dysfunction (SOLVD) trial TNF-α was increased in patients in NYHA functional classes I to III as compared to healthy controls with levels correlated to NYHA class [4]. This association between TNF-α and heart failure severity led to the assessment of TNF as a potential target in heart failure. We repeated echocardiography following a period of 6 months, which revealed improved left ventricular dimension (LVEDD 5.7 cm), mild mitral regurgitation and LVEF of 40% He remained asymptomatic from a heart failure perspective and the chest pains had not recurred.

Discussion

Findings

Conclusion