Abstract
BackgroundAtrial fibrosis creates a vulnerable tissue for atrial fibrillation (AF), but the spatial disarray of collagen fibers underlying atrial fibrosis is not fully elucidated.ObjectiveThis study hypothesizes that harmonics optical microscopy can illuminate the spatial mal-alignment of collagen fibers in AF via a layer-by-layer approach.Patients and MethodsAtrial tissues taken from patients who underwent open-heart surgery were examined by harmonics optical microscopy. Using the two-dimensional Fourier transformation method, a spectral-energy description of image texture was constituted and its entropy was used to quantify the mal-alignment of collagen fibers. The amount of collagen fiber was derived from its area ratio to total atrial tissue in each image. Serum C-terminal pro-collagen pro-peptide (CICP), pro-matrix metalloproteinase-1 (pro-MMP-1), and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) were also evaluated.Results46 patients were evaluated, including 20 with normal sinus rhythm and 26 with AF. The entropy of spectral-energy distribution of collagen alignment was significantly higher in AF than that in sinus rhythm (3.97±0.33 vs. 2.80±0.18, p<0.005). This difference was more significant in the permanent AF group. The amount of collagen was also significantly higher in AF patients (0.39±0.13 vs. 0.18±0.06, p<0.005) but serum markers of cardiac fibrosis were not significantly different between the two groups.ConclusionsHarmonics optical microscopy can quantify the spatial mal-alignment of collagen fibers in AF. The entropy of spectral-energy distribution of collagen alignment is a potential tool for research in atrial remodeling.
Highlights
Atrial fibrosis creates a vulnerable tissue for atrial fibrillation (AF) [1]
The entropy of spectral-energy distribution of collagen alignment was significantly higher in AF than that in sinus rhythm (3.9760.33 vs. 2.8060.18, p,0.005)
Harmonics optical microscopy can quantify the spatial mal-alignment of collagen fibers in AF
Summary
Atrial fibrosis creates a vulnerable tissue for atrial fibrillation (AF) [1]. Found that increased amounts of connective tissue between cardiomyocytes have high susceptibility for initiating AF [3,4]. AF maintenance is promoted by an atrial vulnerable tissue that is suitable for the initiation and continuation of the re-entering wavelets [5]. Accumulating fibrillar and non-fibrillar collagen leads to excessive atrial fibrosis and maintenance of AF [6]. In AF patients, increased serum degenerating products of collagen I, collagen III, and fibronectin all imply changes of collagen fibers [7,8,9]. The spatial disarray of collagen fibers underlying atrial fibrosis is not fully elucidated. Atrial fibrosis creates a vulnerable tissue for atrial fibrillation (AF), but the spatial disarray of collagen fibers underlying atrial fibrosis is not fully elucidated
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