Atrial fibrillation is in human patients is associated with increased collagen V and TGFbeta1

Sava Costin (Neuruppin)1, M. Richter (Bad Nauheim)2, N. Gancheva (Bad Nauheim)2, B. Sasko (Neuruppin)1, T. Giannakopoulos (Neuruppin)1, O. Ritter (Neuruppin)1, Z. Szalay (Bad Nauheim)2, N. Pagonas (Neuruppin)1

1Medizinische Hochschule Brandenburg Theodor Fontane Kardiologie Neuruppin, Deutschland; 2Kerckhoff-Klinik Cardiac Surgery Bad Nauheim, Deutschland


Background and aim. Atrial fibrosis is an important factor in initiating and maintaining atrial fibrillation (AF). Collagen V belongs to fibrillar collagens. There are, however no data on collagen V in AF. The aim of this work was to study the quantity of collagen V and its relationship with the number of fibroblasts and TGF-b1 expression in patients in sinus rhythm (SR) and in patients with AF.

Methods. We used quantitative immuhistochemistry to study collagen V in right and left atrial biopsies obtained from 35 patients in SR, 35 patients with paroxysmal AF (pAF) and 27 patients with chronic, long-standing persistent AF (cAF). In addition, we have quantified the number of vimentin-positive fibroblasts and expression levels of TGF-b1.

Results. Compared to patients in SR, collagen V was increased 1.8- and 3.1-fold in patients with pAF and cAF, respectively. In comparison with SR patients, the number of vimentin-positive cells increased significantly 1.46- and 1.8-fold in pAF and cAF patients, respectively.

Compared to SR patients, expression levels of TGF-ß1, expressed as fluorescence units per tissue area, was significantly increased by 77% and 300% in patients with pAF and cAF, respectively. Similar to intensity measurements, the number of TGFß1-positive cells per 1mm2 atrial tissue increased significantly from 35.5 ± 5.5 cells in SR patients to 61.9 ± 12.4 cells in pAF and 131.5 ± 23.5 cells in cAF. In both types of measurements, there was a statistically significant difference between pAF and cAF groups.

Conclusions. This is the first study to show that AF is associated with increased expression levels of collagen V and TGF-ß1indicating its role in the pathogenesis of atrial fibrosis. In addition, increases in collagen V correlate with increased number of fibroblasts and TGF-b1 and are more pronounced in cAF patients than those in pAF patients.
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