Heart rate is associated with progression of atrial fibrillation, independent of rhythm.
OBJECTIVE
Atrial fibrillation (AF) often progresses from paroxysmal or persistent to more sustained forms, but the rate and predictors of AF progression in clinical practice are not well described.


METHODS
Using the Outcomes Registry for Better Informed Treatment of AF, we analysed the incidence and predictors of progression and tested the discrimination and calibration of the HATCH (hypertension, age, TIA/stroke, chronic obstructive pulmonary disease, heart failure) and CHA₂DS₂VASc scores for identifying AF progression.


RESULTS
Among 6235 patients with paroxysmal or persistent AF at baseline, 1479 progressed, during follow-up (median 18 (IQR 12-24) months). These patients were older and had more comorbidities than patients who did not progress (CHADS₂ 2.3±1.3 vs 2.1±1.3, p<0.0001). At baseline, patients with AF progression were more often on a rate control as opposed to a rhythm control strategy (66 vs 56%, p<0.0001) and had higher heart rate (72(64-80) vs 68(60-76) bpm, p<0.0001). The strongest predictors of AF progression were AF on the baseline ECG (OR 2.30, 95% CI 1.95 to 2.73, p<0.0001) and increasing age (OR 1.16, 95% CI1.09 to 1.24, p<0.0001, per 10 increase), while patients with lower heart rate (OR 0.84, 95% CI 0.79 to 0.89, p<0.0001, per 10 decrease ≤80) were less likely to progress. There was no significant interaction between rhythm on baseline ECG and heart rate (p=0.71). The HATCH and CHA₂DS₂VASc scores had modest discriminatory power for AF progression (C-indices 0.55 (95% CI 0.53 to 0.58) and 0.55 (95% CI 0.52 to 0.57)).


CONCLUSIONS
Within 1.5 years, almost a quarter of the patients with paroxysmal or persistent AF progress to a more sustained form. Progression is strongly associated with heart rate, and age.
Duke Clinical Research Institute, Durham, North Carolina, USA.
Fredrik
F
Holmqvist
Duke Clinical Research Institute, Durham, North Carolina, USA.
Sunghee
S
Kim
Duke Clinical Research Institute, Durham, North Carolina, USA.
Benjamin A
http://orcid.org/0000-0002-4729-7820
BA
Steinberg
Columbia University, New York, New York, USA.
James A
JA
Reiffel
Department of Medicine, Stanford University, Stanford, California, USA.
Kenneth W
KW
Mahaffey
Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Bernard J
BJ
Gersh
Ahmanson-UCLA Cardiomyopathy Center, Los Angeles, California, USA.
Gregg C
GC
Fonarow
Penn State Milton S. Hershey Medical Center, Hershey, Pennsylvania, USA.
Gerald V
GV
Naccarelli
Janssen Pharmaceuticals, Inc., Raritan, New Jersey, USA.
Paul
P
Chang
Department of Internal Medicine, Cardiovascular Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.
James V
JV
Freeman
Lankenau Hospital and Medical Research Center, Philadelphia, Pennsylvania, USA.
Peter R
PR
Kowey
Duke Clinical Research Institute, Durham, North Carolina, USA.
Laine
L
Thomas
Duke Clinical Research Institute, Durham, North Carolina, USA.
Eric D
ED
Peterson
Duke Clinical Research Institute, Durham, North Carolina, USA.
Jonathan P
JP
Piccini
D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D001281:Atrial Fibrillation / Q000503:physiopathology*; D015331:Cohort Studies; D018450:Disease Progression; D005260:Female; D006333:Heart Failure / Q000503:physiopathology; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology; D008297:Male; D012307:Risk Factors