The synergism between atrial fibrillation and heart failure.
BACKGROUND
Atrial fibrillation (AF) is a common comorbidity in heart failure (HF) patients and is classically associated with acceleration in the rate of HF progression. The precise mechanism for this interaction is unclear, but comprises "bidirectional" aspects in which AF promotes HF and HF also increases the likelihood of AF. We therefore studied the relationship between AF in an ovine model of pacing-induced congestive HF, in an attempt to identify the mechanisms that underpin the apparent synergistic relationship between AF and HF.


RESULTS
Sixteen adult sheep were paced at 190 beats/min for 21 days (HF). AF was induced in 8 of these animals at 14 days' pacing using programmed extrastimuli (HF + AF). Left ventricular hemodynamics and the pattern of cardiac neurohormonal activation, via coronary sinus (CS) sampling, were determined at rest and during submaximal exercise testing in both groups at 21 days and after AF reversion (by atrial defibrillation) at 21 days. CS norepinephrine (NE), endothelin (ET-1), and brain natriuretic peptide (BNP) levels were significantly increased in HF + AF animals, whereas LV end-diastolic pressure (EDP) and LV dP/dt max were significantly reduced compared with moderate HF alone. Cardioversion significantly reduced CS NE and BNP levels and improved contractility in AF + HF animals. In a further 6 animals, we explored the mechanism by which HF increases susceptibility to AF, with specific emphasis on the influence of functional mitral regurgitation. The elimination of MR in HF animals using a percutaneous mitral annular reduction device significantly decreased the inducibility of AF.


CONCLUSIONS
AF induction significantly depresses left ventricular function and causes activation of myocardial neurohormones. In conjunction, the presence of functional MR increases susceptibility to AF and this may be attenuated by MR reduction by percutaneous mitral annular reduction.
Byrne
Melissa
M
Baker Heart Research Institute, Melbourne, Victoria,Australia.
Kaye
David M
DM
Power
John
J
D000818:Animals; D001281:Atrial Fibrillation / Q000097:blood / Q000503:physiopathology*; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure; D015897:Comorbidity; D018450:Disease Progression; D004554:Electric Countershock; D019332:Endothelin-1 / Q000097:blood; D006333:Heart Failure / Q000097:blood / Q000503:physiopathology*; D006339:Heart Rate; D023421:Models, Animal; D020097:Natriuretic Peptide, Brain / Q000097:blood; D009638:Norepinephrine / Q000097:blood; D012307:Risk Factors; D012756:Sheep; D013997:Time Factors
D015415:Biomarkers; D019332:Endothelin-1; D020097:Natriuretic Peptide, Brain; D009638:Norepinephrine