Atrial fibrillation-induced atrial contractile dysfunction: a tachycardiomyopathy of a different sort.

Content Provider	Semantic Scholar
Author	Schotten, Ulrich Greiser, Maura Benke, Dirk Buerkel, Kai Ehrenteidt, Britta Stellbrink, Christoph Vazquez-Jimenez, Jaime Francisco Schoendube, Friedrich Hanrath, Peter
Copyright Year	2002
Abstract	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 Ca(2+) 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-Ca(2+)-ATPase (SERCA), phospholamban (Plb), calsequestrin (Cals) and the Na(+)/Ca(2+)-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/mm(2) compared to 3.3+/-0.9 mN/mm(2) (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(+)/Ca(2+)-exchanger was upregulated by 67% in atria of AF patients. CONCLUSIONS AF-induced atrial contractile dysfunction is not due to beta-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 Ca(2+)-channel and an increased Ca(2+) extrusion via the Na(+)/Ca(2+)-exchanger seem to be responsible for the depressed contractility in remodeled atria.
Starting Page	192
Ending Page	201
Page Count	10
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PubMed reference number	11744028v1
Volume Number	53
Issue Number	1
Journal	Cardiovascular research
Language	English
Access Restriction	Open
Subject Keyword	Adenylate Cyclase Atrial Fibrillation Biological Assay CA8 gene Calcium Calsequestrin Cardiomyopathies Chronic Obstructive Airway Disease Depressive disorder Down-Regulation Fifty Nine Heart Atrium Isoproterenol Mitral Valve Muscle PLN gene Patients Ryanodine Sarcoplasmic Reticulum Structure of auricular appendage Structure of myocardium of atrium Tachycardia Tachycardia, Ventricular Tracer Western Blot chemosensitization/potentiation hypersensitivity desensitization
Content Type	Text
Resource Type	Article