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1 Division of Cardiology, Department of Internal Medicine, 2 Institute of Experimental Internal Medicine, 3 Institute of Pathology, 4 Department of Cardiovascular Surgery, and 5 Institute of Immunology, University Hospital Magdeburg, 39120 Magdeburg, Germany
Atrial fibrillation (AF) is accompanied
by intracellular calcium overload. The purpose of this study was to
assess the role of calcium-dependent calpains and cytokines during AF.
Atrial tissue samples from 32 patients [16 with chronic AF and 16 in sinus rhythm (SR)] undergoing open heart surgery were studied. Atrial
expression of calpain I and II, calpastatin, troponin T (TnT), troponin
C (TnC), and cytokines [interleukin (IL)-1
, IL-2, IL-6, IL-8,
IL-10, transforming growth factor (TGF)-1, and tumor necrosis
factor-
] 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 ± 17.7 vs. 12.4 ± 9.2 units, P < 0.05). In
contrast to TnC, TnT levels were reduced in fibrillating atria by 26%
(P < 0.05), corresponding to the myofilament
disintegration seen by electron microscopy. Small amounts of only IL-2
and TGF-1 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 contractile dysfunction,
whereas there is no evidence of activation of tissue cytokines.
fibrillation; calcium; contractile proteins; cytokine; inflammation
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