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