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Mechanistic differences from ventricular models suggest caution extrapolating therapies to AF atrial dysfunction; leaves open atrial-specific Ca2+ channel research.
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.
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Ulrich Schotten (2002) studied this question.
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