© 2002 by European Society of Cardiology
Copyright © 2001, European Society of Cardiology
Atrial fibrillation-induced atrial contractile dysfunction: a tachycardiomyopathy of a different sort
aDepartment of Physiology, University Maastricht, P.O. Box 616, 6200 MD Maastricht, The Netherlands
bDepartment of Cardiology, University Hospital Aachen, Aachen, Germany
cThoracic and Cardiovascular Surgery, University Hospital Aachen, Aachen, Germany
* Corresponding author. Tel.: +31-43-388-1077; fax: +31-43-388-4166 schotten{at}fys.unimaas.nl
Objective: Although AF-induced atrial contractile dysfunction has significant clinical implications the underlying intracellular mechanisms are poorly understood. Methods: From the right atrial appendages of 59 consecutive patients undergoing mitral valve surgery (31 in SR, 28 in chronic AF) thin muscle preparations (diameter<0.7 mm) were isolated. Isometric force of contraction was measured in the presence of different concentrations of Ca2+ and isoprenaline. To assess the function of the sarcoplasmic reticulum, the force–frequency relationship and the post-rest potentiation were studied. The myocardial density of the ryanodine-sensitive calcium release channel (CRC) of the sarcoplasmic reticulum was determined by [3H]ryanodine binding. Myocardial content of SR-Ca2+-ATPase (SERCA), phospholamban (Plb), calsequestrin (Cals) and the Na+/Ca2+-exchanger (NCX) were analyzed by Western blot analysis. Adenylyl cyclase activity was measured with a radiolabeled bioassay using [32P]ATP as a tracer. Results: In 72 muscle preparations of SR patients contractile force was 10.9±1.8 mN/mm2 compared to 3.3±0.9 mN/mm2 (n=48, P<0.01) in AF patients. The positive inotropic effect of isoprenaline was diminished but the stimulatory effect on relaxation and the adenylyl cyclase were not altered in AF patients. The force–frequency relation and the post-rest potentiation were enhanced in atrial myocardium of AF patients. The protein levels of CRC, SERCA, Plb, and Cals were not different between the two groups. In contrast, the Na+/Ca2+-exchanger was upregulated by 67% in atria of AF patients. Conclusions: AF-induced atrial contractile dysfunction is not due to β-adrenergic desensitization or dysfunction of the sarcoplasmic reticulum and thus is based on different cellular mechanisms than a ventricular tachycardia-induced cardiomyopathy. Instead, downregulation or altered function of the L-type Ca2+-channel and an increased Ca2+ extrusion via the Na+/Ca2+-exchanger seem to be responsible for the depressed contractility in remodeled atria.
KEYWORDS Arrhythmia (mechanisms); Atrial function; Contractile function; SR (function)
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