Author + information
- Jagmeet P. Singh, MD, DPhil∗ ( and )
- Sunu S. Thomas, MD, MSc
- ↵∗Reprint requests and correspondence:
Dr. Jagmeet P. Singh, Cardiology Division, Massachusetts General Hospital Heart Center, 55 Fruit Street, GRB 842, Boston, Massachusetts 02114.
“Eagles do not beget Doves”
Atrial fibrillation (AF) and heart failure (HF) as individual cardiac conditions are associated with morbidity and mortality in epidemic proportions. Indeed, with at least 3 million patients with AF (1) and 5 million with HF (2) in the United States, the clinical effect and the health economic burden cannot be underestimated. Importantly, several studies have demonstrated the concurrent prevalence of these conditions; in particular, incident AF in patients with HF is associated with worse outcomes and is consequently a significant drain on health care resources (3). These statistics will only further be compounded by the anticipated increasing prevalence of both conditions as overall cardiac survival continues to improve with advances in medical and device-based cardiac therapies.
Much of the evidence for the coexistence of these conditions is related to a similar clinical risk profile with interplay of physiology where one condition may precipitate the other (Figure 1). As such, both HF and AF are associated with shared structural and molecular changes. What remains to be further characterized is a refinement in our understanding of the intimate relationship from which one condition may be borne of the other. Although several studies have focused on stroke prevention in patients with AF, there has been a paucity of effort directed toward predicting and preventing incident HF in this cohort of patients.
In this issue of JACC: Heart Failure, Pandey et al. (4) provide further evidence to implicate the shared predispositions and clinical effect of documented AF and de novo HF. Using a contemporary cohort derived from the ORBIT-AF (Outcomes Registry for Informed Treatment of Atrial Fibrillation) observational study, they report a 3.6% incidence of HF over a 2-year follow-up in 6,545 patients with documented AF. At least two-thirds of new-onset HF was due to a HF with preserved ejection fraction syndrome, albeit in a study population that was under-represented for systolic HF. The probability of incident HF was cumulative over the study period and was associated with permanent AF and baseline higher heart rates. Notably, the risk of new-onset HF was further accentuated by a broader cardiac vulnerability arising from older age, nonprivate insurance coverage, renal failure, anemia, and coronary artery and valvular disease. Importantly, the incidence of HF in this cohort of patients with AF portended a poorer prognosis with a higher rate of all-cause death and hospitalization.
Despite the limitations of a registry, this investigative effort appropriately highlights the need to further understand the overlap between these 2 clinical entities and to motivate strategic advancements for optimization of AF care. Clearly, there is a subset of patients with AF who are predisposed to HF. Identifying the exact phenotype is challenging due to the complexity of many contributing parameters, whereby the development of an acute HF state arises from a structural predisposition (i.e., hypertrophy with diastolic dysfunction), a demand issue (due to ischemia), a filling problem (due to higher heart rates), or a combination of these. However, within the current study, the proportion of patients with structural heart disease, including ventricular hypertrophy and left atrial dilation, and its severity and prognostic effect on HF incidence requires further elaboration. Although registry studies may be challenged by clinical heterogeneity, defining the atrial fibrillation patient who is at risk for HF may further establish the evolving clinical phenotype of the vulnerable cardiac substrate.
Although the current analysis has aimed to evaluate the risk of developing HF in patients with AF, an alternative perspective on the study question could well relate to the effect of AF on subclinical HF. Of those patients with AF with incident HF, 54.2% were concurrently on diuretic agents at the time of enrollment, thereby potentially confounding the true incidence of de novo HF in this study. Verily, this registry may have had a subset of patients with subclinical HF who, with concurrent AF, went on to develop overt HF. Nevertheless, the interplay of risk factors is self-evident, and the argument as to whether AF begets HF, or vice versa, may remain circular. There is growing evidence that a high-risk subset of patients with prevalent AF may progress to HF (5). Therefore, is it time to develop a risk score, akin to a CHA2DS2-VASc model for stroke prediction, for predicting and preventing HF in the AF population? Alternatively, should our prognostic modeling of stage B HF also include AF as an electrical vulnerability to progression of mechanical ventricular dysfunction?
To further emphasize the need for AF-HF risk stratification, the incidence of all-cause death among patients with AF in the current study who developed HF was high (8.24 per 100 patient-years) reflecting the vulnerability of the patient population carrying both diagnoses. Earlier recognition and interventions seem like plausible and necessary strategies. Evident from the subanalysis, patients at risk for incident HF had progression of their AF, higher heart rates, and lower use of rhythm control strategies; this makes a case for the early use of rhythm control approaches with medications or catheter ablation (i.e., pulmonary vein isolation). Such early interventions may prevent adverse left atrial electrical and mechanical remodeling, thereby maintaining normal sinus rhythm and possibly reducing the predisposition to HF progression.
Additionally, the study patients for this registry were derived from practices involving internists, cardiologists, and electrophysiologists with no mention of HF specialists. The temporal and linear relationship between AF and incident HF should encourage a multidisciplinary approach to patient care. Such clinical care models exist for patients with systolic HF and ventricular conduction abnormalities requiring defibrillator and cardiac resynchronization therapies (CRT). In our experience, such an integrated approach involving arrhythmia and HF specialists has resulted in improved clinical outcomes for patients with HF with reduced ejection fraction (6). Accordingly, the current study suggests that a novel integrated clinical pathway engaging clinical providers specializing in both AF and HF with preserved ejection fraction may prove valuable in improving outcomes and reducing the use of health care resources. This is timely, as several health care organizations are looking at separately developing chronic disease management platforms for HF and AF.
We would like to congratulate the authors for a well-conducted analysis and for highlighting an oft-ignored relationship between prevalent AF and incident HF. This study reinforces the fact that both of these disease entities share common risk factors from which either condition may be borne. However, chronicity of either condition predisposes to the other, reflecting a vulnerable and evolving state of cardiac dysfunction. Because AF may beget HF, there is much to be gained by predicting and preventing the consequent cascade of physiological stressors that may trigger the vicious cycle for this double whammy.
↵∗ Editorials published in JACC: Heart Failure reflect the views of the authors and do not necessarily represent the views of JACC: Heart Failure or the American College of Cardiology.
Dr. Singh has served as a consultant for Biotronik, Boston Scientific, Medtronic, St. Jude Medical, Liva Nova Group, Respicardia Inc., and Impulse Dynamics. Dr. Thomas has reported that he has no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation
- January C.T.,
- Wann L.S.,
- Alpert J.S.,
- et al.
- Go A.S.,
- Mozaffarian D.,
- Roger V.L.,
- et al.
- Pandey A.,
- Kim S.,
- Moore C.,
- et al.
- Santhanakrishnan R.,
- Wang N.,
- Larson M.G.,
- et al.
- Altman R.K.,
- Parks K.A.,
- Schlett C.L.,
- et al.