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Atrial fibrillation (AF) and heart failure (HF) frequently occur together, and their coexistence is associated with a poor prognosis. AF and HF share risk factors, but their relationship involves complex hemodynamic, neurohormonal, inflammatory, ultrastructural, and electrophysiologic processes that extend beyond epidemiological associations. The shared mechanisms underlying AF and HF have important implications for the treatment of AF in patients with HF. This article focuses on reviewing contemporary data as it pertains to AF management in patients with HF and provides insight into investigational therapies currently under development.

Anthracycline-based chemotherapeutics have long been recognized as effective agents for treating a wide range of malignancies. However, their use is not without significant adverse cardiotoxic side effects. Strategies for prevention involve limiting free-radical production and subsequent cardiac myocyte damage. Dexrazoxane remains the most widely studied cardioprotective medication. Alternative agents may reduce cardiotoxicity but may still cause significant cardiovascular problems. The role of β-blockers and angiotensin-converting enzyme inhibitors in the treatment of heart failure is well proven. The role of these medications in the prevention and treatment of chemotherapy-induced cardiotoxicity is not well established.

Heart failure (HF) and atrial fibrillation (AF) are 2 of the most common cardiovascular diseases encountered in clinical practice, and the prevalence of these diseases continues to grow worldwide with the aging of the global population. While recognizing that AF is a heterogeneous disorder, we submit that the parallels between AF and HF may arise because many cases of AF and HF result from the cumulative exposure of the atria and ventricles to a common set of systemic cardiovascular risk factors. Over time, exposure to risk factors promotes development of atrial and ventricular structural and functional abnormalities through activation of several biologic pathways in concert: upregulation of neurohormonal signaling cascades, release of inflammatory mediators, programmed cell death, and fibrosis. Cardiac structural remodeling occurs in concert with electrophysiologic remodeling, both of which contribute to atrial and ventricular rhythm disturbances, including AF. AF and HF, instead of representing distinct disease processes, often represent different endpoints along a disease continuum. By reviewing some of the mechanistic parallels between AF and HF, we hope to emphasize the connection between established cardiovascular risk factors, cardiac remodeling and AF, with a view to promote strategies for AF prevention.