ACE–inhibitor treatment attenuates atrial structural remodeling in patients with lone chronic atrial fibrillation
Tóm tắt
Chronic atrial fibrillation (AF) is characterized by a
remodeling process which involves the development of fibrosis. Since
angiotensin II has been suspected to be involved in this process, the aim of
our study was to investigate a possible influence of an ACE–I therapy in
patients with chronic AF regarding the occurrence of left atrial structural
remodeling. Atrial tissue samples were obtained from patients with
lone chronic AF or sinus rhythm (SR). Collagen I, vascular endothelial growth
factor (VEGF) and basic fibroblast growth factor (bFGF) protein expression
were measured by quantitative Western Blotting techniques and calculated
as mean ± SEM. Histological tissue samples were used for calculating microvessel
density (microvessel/mm2 ± SEM). In AF, the collagen amount
was higher (1.78 ± 0.21; p = 0.01) vs. SR (0.37 ± 0.07) accompanied by declining
microcapillary density (AF: 145 ± 13 vs. SR: 202 ± 9; p = 0.01). Additionally,
a negative correlation (p = 0.01) between collagen content and microcapillary
density was observed. To investigate the influence of an ACE–I therapy
on this remodeling process, patient groups were divided into AF and SR
both with or without ACE–I. Interestingly, there was a significantly lower
expression of collagen I in AF with ACE–I (1.04 ± 0.26) vs. AF without ACE–I
treatment (2.07 ± 0.24, p = 0.02). The microcapillaries were not diminished
in AF with ACE–I (180 ± 15) vs. SR with ACE–I (196 ± 9), but there was a significant rarification in AF without ACE–I (123 ± 18; p = 0.03). The expression
of VEGF and bFGF did not reveal any significant differences. In
patients undergoing ACE–I treatment: atrial structural remodeling was attenuated
and the loss of atrial microcapillaries was prevented.
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