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Articles in PresS, published online ahead of print February 7, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00505.2001
Submitted on June 8, 2001
Accepted on January 31, 2002
1 Division of Cardiology, University Hospital Magdeburg, Magdeburg, Germany
2 Institute of Experimental Internal Medicine, University Hospital Magdeburg, Magdeburg, Germany
3 Institute of Pathology, University Hospital Magdeburg, Magdeburg, Germany
4 Institute of Immunology, University Hospital Magdeburg, Magdeburg, Germany
5 Cardiovascular Surgery, University Hospital Magdeburg, Magdeburg, Germany
* To whom correspondence should be addressed. E-mail: andreas.goette{at}medizin.uni-magdeburg.de.
Atrial fibrillation (AF) is accompanied by intracellular calcium overload. The purpose of this study was to assess the role of calcium-dependent calpains and inflammation during AF. Atrial tissue samples from 32 patients (16 with chronic AF, 16 with sinus rhythm; SR) undergoing open heart surgery were studied. Atrial expression of calpain I and II, calpastatin, troponins T (TnT), C (TnC), and of the cytokines (IL-1ß,-2,-6,-8,-10, TGF-ß1, TNF-
)were determined. Expression of calpain I was increased during AF (461±201% vs 100±34%; p<0.05). Amounts of calpain II and calpastatin were unchanged. Total calpain enzymatic activity was more than doubled during AF (35.2±17.7U vs 12.4±9.2U; p<0.05). In contrast to TnC, TnT levels were reduced in fibrillating atria by 26% (p<0.05) corresponding to a myofilament disintegration seen by electron microscopy. Small amounts of only IL-2 and TGF-ß1 mRNA and protein were detected, regardless of the underlying cardiac rhythm. In conclusion, atria of patients with permanent AF show evidence of calpain I activation, that might contribute to structural remodeling and contractyle dysfunction, whereas there is no evidence of activation of tissue cytokines.
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