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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
Electrophysiology
Cardiovascular Research
Maastricht University
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Ulrich Schotten (Tue,) studied this question.
synapsesocial.com/papers/69d9c72f1ad561c6736851ba — DOI: https://doi.org/10.1016/s0008-6363(01)00453-9