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Atrial Dysfunction in Patients With HFpEF and AF
Quick Takes
- In patients with HFpEF, as the burden of AF increases from none, to paroxysmal, and to permanent, there is progressive worsening of LA compliance, remodeling, and contractile function.
- Furthermore, there is worsening biventricular systolic function, poorer cardiac output, higher filling pressures, and more severe pulmonary vascular disease.
- Progression to permanent AF was common in patients with paroxysmal AF and the risk was greater in patients with more severe reductions in LA strain and compliance.
- Increasing AF burden was associated with increased mortality.
Study Questions:
In patients with heart failure with preserved ejection fraction (HFpEF), do left atrial (LA) compliance and mechanics decline with increasing burden of atrial fibrillation (AF)?
Methods:
Between 2000 and 2015, consecutive outpatients undergoing evaluation for exertional dyspnea via invasive hemodynamic exercise testing and echocardiography were enrolled. HFpEF patients were defined by standard criteria, while control subjects had normal rest and exercise pulmonary capillary wedge pressure, no history of AF, and left ventricular ejection fraction (LVEF) >50%. In the HFpEF group, patients were classified as permanent AF (HFpEFperm-AF) if they were in AF at the time of evaluation; paroxysmal AF (HFpEFparox-AF) if they were in sinus rhythm but with a history of documented AF; and no AF (HFpEFno-AF) if there was no prior history of AF.
Echocardiographic measurements included LA volume, strain, total heart volumes, and pericardial restraint (total heart volume increase out of proportion to pericardial volume). Right heart catheterization was performed at rest and during exercise. There was also integrated assessment of LA function, combining both echocardiographic and invasive measurements to provide an integrated pressure-volume index.
Results:
Of 285 HFpEF patients, 181 (65%) had HFpEFno-AF, 49 (18%) had HFpEFparox-AF, and 48 (17%) had HFpEFperm-AF. There were 146 control subjects without HFpEF or history of AF. LA volumes and E/e’ ratio increased progressively across the four groups (control, HFpEFno-AF, HFpEFparox-AF, and HFpEFperm-AF, p < 0.0001), while LA compliance and reservoir strain progressively decreased (p < 0.0001), with the latter based on both echocardiographic and invasive hemodynamic measurements. These LA changes were coupled to greater ventricular interdependence and pericardial restraint. HFpEFperm-AF patients had the highest biventricular filling pressures, lowest cardiac index, and highest pulmonary vascular resistance and pulmonary artery systolic pressures (p < 0.0001).
Beyond hemodynamic measurements, 10-year survival was highest in the control group (94% and progressively declined across the three categories of HFpEF patients (73% in HFpEFno-AF, 62% in HFpEFparox-AF, and 38% in HFpEFperm-AF, p < 0.001). Finally, HFpEF patients had higher rates of new-onset AF over 10-year follow-up (31% of HFpEFno-AF patients vs. 1% in the control group, p < 0.001) and high rates of progression to permanent AF (52% of the HFpEFparox-AF patients).
Conclusions:
In HFpEF patients, as the burden of AF increases, there is progressive worsening of LA compliance, remodeling, and contractile function. Furthermore, there is worsening biventricular systolic function, poorer cardiac output, higher filling pressures, and more severe pulmonary vascular disease. Progression to permanent AF was common in patients with paroxysmal AF and the risk was greater in patients with more severe reductions in LA strain and compliance. Increasing AF burden was associated with increased mortality.
Perspective:
This is a relatively large and comprehensive study, in which consecutive patients were enrolled, followed for 10 years, and evaluated with an impressive battery of invasive hemodynamic and echocardiographic measurements. While cohorts were not matched, the progressive increases and decreases in relevant measures across the three groups of HFpEF patients suggests that AF promotes not only LA dysfunction, but elevation of ventricular filling pressures, pulmonary hypertension, and even mortality. These data question the equivalence of rate versus rhythm control of AF in HFpEF patients.
Of course, associative data provide no information as to the benefit of more stringent rhythm versus rate control. That said, they provide strong justification for future randomized studies of antiarrhythmics, cardioversion, and AF ablation to determine if these interventions might improve long-term outcomes. Likewise, the results may motivate the search for novel therapies targeting the metabolic and inflammatory stresses associated with chronic AF, as they may have therapeutic benefit in these patients.
Of note, the choice of a control group without HFpEF or AF was curious and precludes any conclusion regarding specific interaction between these variables (i.e., similar trends may be seen in no AF vs. paroxysmal AF vs. permanent AF groups without HFpEF). Likewise, the study fails to account for an important potential confounder, obstructive sleep apnea, likely due to the fact that its interdependent relationship with AF was not fully appreciated when this study was initiated.
Clinical Topics: Arrhythmias and Clinical EP, Heart Failure and Cardiomyopathies, Noninvasive Imaging, Implantable Devices, SCD/Ventricular Arrhythmias, Atrial Fibrillation/Supraventricular Arrhythmias, Acute Heart Failure, Echocardiography/Ultrasound
Keywords: Arrhythmias, Cardiac, Atrial Fibrillation, Blood Pressure, Cardiac Catheterization, Diagnostic Imaging, Dyspnea, Echocardiography, Exercise Test, Heart Failure, Hemodynamics, Stroke Volume, Vascular Resistance, Ventricular Function, Left
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