Electrical and structural remodeling: role in the genesis and maintenance of atrial fibrillation.
Atrial fibrillation (AF) and congestive heart failure (CHF) are 2 frequently encountered conditions in clinical practice. Both lead to changes in atrial function and structure, an array of processes known as atrial remodeling. This review provides an overview of ionic, electrical, contractile, neurohumoral, and structural atrial changes responsible for initiation and maintenance of AF. In the last decade, many studies have evaluated atrial remodeling due to AF or CHF. Both conditions often coexist, which makes it difficult to distinguish the contribution of each. Because of atrial stretch in the setting of hypertension or CHF, atrial remodeling frequently occurs long before AF arises. Alternatively, AF may lead to electrical remodeling, that is, shortening of refractoriness due to the high atrial rate itself. In many experimental AF or rapid atrial pacing studies, the ventricular rate was uncontrolled. In those studies, atrial stretch due to CHF may have interfered with the high atrial rate to produce a mixed type of electrical and structural remodeling. Other studies have dissected the individual role of AF or atrial tachycardia from the role CHF plays in atrial remodeling. Atrial fibrillation itself does not lead to structural remodeling, whereas this is frequently produced by hypertension or CHF, even in the absence of AF. Primary and secondary prevention programs should tailor treatment to the various types of remodeling.
Schoonderwoerd
Bas A
BA
Department of Cardiology, Thoraxcenter, University Medical Center Groningen, University of Groningen, RB Groningen, The Netherlands. b.a.schoonderwoerd@thorax.umcg.nl
Van Gelder
Isabelle C
IC
Van Veldhuisen
Dirk J
DJ
Van den Berg
Maarten P
MP
Crijns
Harry J G M
HJ
D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D001281:Atrial Fibrillation / Q000473:pathology / Q000503:physiopathology*; D016275:Atrial Function / Q000502:physiology*; D006325:Heart Atria / Q000503:physiopathology* / Q000648:ultrastructure; D006801:Humans; D008854:Microscopy, Electron; D009200:Myocardial Contraction