Atrial fibrillation in heart failure: epidemiology, pathophysiology, and rationale for therapy

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Abstract

Heart failure (HF) affects almost 5 million patients in the United States and is a leading cause of morbidity and mortality. Atrial fibrillation (AF), like HF, affects millions of patients and markedly increases in prevalence with age. As the US population ages, the number of patients afflicted with HF and AF will continue to grow. HF with preserved ejection fraction is particularly common in the elderly population. The prevalence of AF in patients with HF increases from <10% in those with New York Heart Association (NYHA) functional class I HF to approximately 50% in those with NYHA functional class IV HF. The pathophysiologic changes that occur in patients with HF and AF are complex and incompletely understood. Alterations in neurohormonal activation, electrophysiologic parameters, and mechanical factors conspire to create an environment in which HF predisposes to AF and AF exacerbates HF. Mechanisms include atrial remodeling and tachycardia-induced myopathy. The development of AF in HF appears to independently predict death resulting from pump failure and total mortality. Although the currently available therapeutic options for AF in patients with HF are varied, their effect on prognosis remains unknown and is the subject of ongoing clinical trials. It will be critical to define and plan therapies specifically for those patients with AF, HF, and preserved ejection fraction in addition to the population with low ejection fraction that has dominated previous investigations.

Section snippets

Prevalence of atrial fibrillation in patients with heart failure

The prevalence of AF increases as the severity of HF increases (Figure 1). 9, 10, 11, 12, 13, 14, 15, 16 Patients with New York Heart Association (NYHA) functional class I symptoms have an AF prevalence of ≤5%.10 For example, the Studies of Left Ventricular Dysfunction (SOLVD) Prevention Trial enrolled 4,228 participants with asymptomatic or minimally symptomatic (67% NYHA class I; 33% NYHA class II) reduction in LVEF (≤0.35).10, 11 The baseline prevalence of AF was 4.0%.11 On the other end of

Heart failure begets atrial fibrillation/atrial fibrillation begets heart failure

The pathophysiologic changes that occur in patients with HF and AF are complex and incompletely understood. Alterations in neurohormonal activation, electrophysiologic parameters, and mechanical factors participate in the development of an environment in which changes that occur as a result of HF promote the development and maintenance of AF, and changes that occur because of AF in turn predispose to the development and exacerbation of HF (Figure 2).

Effect of atrial fibrillation on prognosis in patients with heart failure

AF is a marker of increased mortality in patients with underlying cardiac disease.5 Most evidence suggests that patients with HF and AF have a worse prognosis than patients with HF but no AF.10, 17, 19, 41

The SOLVD Prevention Trial and Treatment Trial studied 6,517 patients with HF, including 419 patients with AF, and followed them for an average of almost 3 years.10 Patients with AF at baseline had greater all-cause mortality than patients with sinus rhythm at baseline (34% vs 23%; p <0.001),

Rationale and options for therapy

The continued cycle of HF predisposing to AF and AF exacerbating HF argues for interventions to break the cycle. Patients with severe HF and AF have reduced cardiac output and reduced peak exercise performance compared with patients with HF in sinus rhythm.32 This suggests that restoration or maintenance of sinus rhythm may contribute to improved cardiac output, improved exercise performance, better quality of life, and perhaps even improved survival.32 The data, however, to support

Summary

Ongoing clinical trials will provide insight into the management of AF in patients with HF. Our improved understanding of the pathophysiology of AF and HF and our increased understanding of their complex interactions may provide avenues for future intervention. For example, therapies that interfere with signal transduction or directly prevent ion channel alterations could prevent or reduce atrial remodeling.31 Other potential targets, such as inhibition of extracellular matrix fibrosis by

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