When Epidemics Collide

Atrial fibrillation (AF) and heart failure (HF) are two of the most common and increasingly prevalent cardiac disorders. Complicating an already difficult situation, AF and HF often occur together, and their combination increases morbidity and mortality compared with each disorder alone.

In terms of HF, it is a huge problem that will likely get worse as the population ages. An estimated 6.6 million US adults have HF, and an additional three million people are projected to have joined those ranks by the year 2030 — a 25 percent increase in HF prevalence from 2010.1 The Centers for Medicare and Medicaid Services already estimate that 14 percent of Medicare beneficiaries have HF, accounting for 43 percent of Medicare spending.

Then there’s AF. An estimated 2.3 million people in North America have AF. During the last 20 years, hospital admissions for AF have increased 66 percent, with a number of likely reasons, including the aging of the population, rising prevalence of chronic heart disease, and more frequent diagnosis as a result of increased monitoring.

In the Framingham Heart Study, 1,470 participants developed either new AF or HF between 1948 and 1995 and, among those participants, 383 people (26 percent) developed both AF and HF. This was a group of patients with moderate HF; evidence suggests AF occurs in up to 50% of patients with advanced HF.2

Dual Epidemics

While data vary, numerous studies suggest new-onset AF carries a particularly grave prognosis in patients with HF and, in general, the risk appears to be more than additive.

One reason may be the fact that the combination of HF and AF is a textbook example of a vicious cycle.3 The combination of an increase in resting heart rate associated with AF and the exaggerated heart rate response to exercise results in shorter diastolic filling time, leading to a reduction in cardiac output.

This is further affected by the irregularity of the ventricular response. The reduction in LV filling during short cycles is not completely compensated for by increased filling during longer cycles. The loss of effective atrial contractile function also contributes, especially in patients with diastolic dysfunction. The good news: restoration of sinus rhythm improves cardiac output, exercise capacity, and maximal oxygen consumption.

Similarly, HF can increase the risk for AF in several ways. Neurohormonal activation promotes structural remodeling and atrial fibrosis, thus altering atrial conduction properties and promoting AF. Also, HF leads to elevation of cardiac filling pressures, dysregulation of intracellular calcium, and autonomic and neuroendocrine dysfunction, all of which can promote the development of AF. Atrial stretch results in activation of stretch-activated ionic currents, leading to increased dispersion of refractoriness facilitating AF. The good news: optimal pharmacological therapy for HF has a beneficial impact on the progression of AF.

Targets for Risk Reduction

CardioSource WorldNews noted that preliminary data from the ongoing SAFETY study indicate that one of the best ways to reduce high rates of mortality and rehospitalization following discharge of patients treated for acute HF is team-based care that improves the transition home.4 Simon Stewart, PhD, and colleagues reported in a pilot study that this approach reduced rehospitalization by about one-quarter (27 percent) among those at high risk of rehospitalization.5

It will be years before sufficient data are generated to specifically guide practice when these two common disease processes intersect. Until that time, several concepts can help guide patient care. Individual goals include: optimal cardiac protection, including targeting risk of thromboembolic events and bleeding events; symptom control and improved quality of life; and efforts that will reduce morbidity and mortality.

One other approach is suggested by what we know about shared risk factors: the coexistence of these clinical entities can be explained to some degree by the presence of common risk factors such as age, hypertension, diabetes, and obesity, as well as valvular, ischemic, and nonischemic structural heart disease. This suggests targets for risk reduction.

Not so promising are the numerous variables that complicate the management of patients with these two disorders: advanced age, comorbidities, cognitive decline, and renal dysfunction. In addition, the standard conundrum of treatment risk versus treatment benefit is heightened.

It is most certainly a clinical challenge and, given the trends for both HF and AF, one that will not be lessening anytime soon.


  1. Roger VL, et al. Circulation. 2012;125:e2-e220.
  2. Maisel WH, et al. Am J Cardiol. 2003;91:2D-8D.
  3. Anter E, et al. Circulation. 2009;119:2516-25.
  4. Carrington MJ, et al. Int J Cardiol. 2011 Nov 11 [Epub ahead of print].
  5. Inglis S, et al. J Cardiovasc Nurs. 2004;19:118-27.

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