Histopathological substrate for chronic atrial fibrillation in humans.
Histopathological substrate for chronic atrial fibrillation in humans.
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DOI:
10.1016/j.hrthm.2009.01.010
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发表时间:
2009-04
期刊:
影响因子:
5.5
通讯作者:
Masroor, Saqib
中科院分区:
文献类型:
--
作者:
Nguyen, Bich Lien;Fishbein, Michael C.;Chen, Lan S.;Chen, Peng-Sheng;Masroor, Saqib
There is a lack of understanding of the substrate for microreentrant circuits and triggered activity of the pulmonary vein (PV) muscle sleeves and atria, in patients with atrial fibrillation (AF). To examine the histological substrate of patients with chronic AF. We stained 23 biopsies taken from the PV-LA junction and RAA from 5 chronic AF patients and 3 sinus rhythm (SR) patients undergoing mitral valve surgery using periodic acid-Schiff (PAS), and antibodies to hyperpolarization-activated cyclic nucleotide-gated potassium channel 4 (HCN4), CD117/c-kit, myoglobin, tyrosine hydroxylase (TH), growth-associated protein 43, cholineacetyltransferase, and synaptophysin, as well as trichrome. As opposed to being clustered together in the subendocardial layer in SR patients, PAS-positive cells were separated from each other by inflammatory infiltrate and collagen fibers in AF patients. These cells stained positively for HCN4 and myoglobin, indicating they were cardiomyocytes that might have a potential pacemaking function, but different from CD117/c-kit-positive interstitial Cajal-like cells (ICLC). In AF patients, the intercellular space was occupied by a lymphomononuclear infiltrate (100% vs. 33% in SR patients, p=0.002), and a greater amount of interstitial fibrosis (37±5.6% vs. 7.4±2.8%, p=0.009). Nerve densities did not differ between AF and SR patients. However, the density of sympathetic nerve twigs in AF patients was significantly greater as compared to the others nerves (p=0.03). HCN4-/PAS-positive cardiomyocytes, and CD117/c-kit-positive ICLC scattered among abundant inflammatory infiltrate, fibrous tissue, and sympathetic nerve structures in the atria and at the PV-LA junctions might be a substrate for the maintenance of chronic AF.
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影响因子:
24
作者:
Ogawa, Masahiro;Zhou, Shengmei;Chen, Peng-Sheng
通讯作者:
Chen, Peng-Sheng
影响因子:
37.8
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Haïssaguerre, M;Shah, DC;Clémenty, J
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Clémenty, J
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37.8
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Hamabe, A;Okuyama, Y;Chen, PS
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Chen, PS
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5.7
作者:
Ho, SY;Cabrera, JA;Sánchez-Quintana, D
通讯作者:
Sánchez-Quintana, D
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37.8
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Chou, CC;Nihei, M;Chen, PS
通讯作者:
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