Atrial fibrillation coincides with the advanced glycation end product N(ε)-(carboxymethyl)lysine in the atrium

M.P.V. Begieneman, L. Rijvers, B. Kubat, W.J. Paulus, A.B.A. Vonk, A.C. van Rossum, C.G. Schalkwijk, W. Stooker, H.W.M. Niessen, P.A.J. Krijnen

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Presence of advanced glycation end products (AGEs) in the heart induces a proinflammatory phenotype. However, the presence of AGEs within atrial tissue of atrial fibrillation (AF) patients is unknown and was analyzed here. Left atrial appendage tissue from 33 AF patients and 9 controls was analyzed for the presence of the major AGEs N(ε)-(carboxymethyl)lysine (CML), VCAM-1, neutrophilic granulocytes, lymphocytes, and macrophages in both the fat tissue and myocardium separately. The total amount of fibrosis was also analyzed. Presence of CML was significantly higher in blood vessels of the left atrial appendage in AF patients as compared to controls, independent of diabetes mellitus. In AF patients, VCAM-1 expression in blood vessels and the numbers of infiltrated neutrophilic granulocytes, lymphocytes, and macrophages significantly increased compared to controls, and were highest in the fat tissue; there was no significant difference in fibrosis compared to controls. Interestingly, total amount of CML and fibrosis in AF and control patients correlated positively. Finally, there was no difference between AF patients based on AF type or surgical indication in the presence of CML, VCAM-1 expression, inflammatory cells, and fibrosis. Our results indicate that in AF the intramyocardial blood vessels of the left atrial appendage have an increased CML presence and proinflammatory status coinciding with a local increase in the number of inflammatory cells.

Original languageEnglish
Pages (from-to)2096-2104
Number of pages9
JournalThe American Journal of Pathology
Volume185
Issue number8
DOIs
Publication statusPublished - Aug 2015

Cite this

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title = "Atrial fibrillation coincides with the advanced glycation end product N(ε)-(carboxymethyl)lysine in the atrium",
abstract = "Presence of advanced glycation end products (AGEs) in the heart induces a proinflammatory phenotype. However, the presence of AGEs within atrial tissue of atrial fibrillation (AF) patients is unknown and was analyzed here. Left atrial appendage tissue from 33 AF patients and 9 controls was analyzed for the presence of the major AGEs N(ε)-(carboxymethyl)lysine (CML), VCAM-1, neutrophilic granulocytes, lymphocytes, and macrophages in both the fat tissue and myocardium separately. The total amount of fibrosis was also analyzed. Presence of CML was significantly higher in blood vessels of the left atrial appendage in AF patients as compared to controls, independent of diabetes mellitus. In AF patients, VCAM-1 expression in blood vessels and the numbers of infiltrated neutrophilic granulocytes, lymphocytes, and macrophages significantly increased compared to controls, and were highest in the fat tissue; there was no significant difference in fibrosis compared to controls. Interestingly, total amount of CML and fibrosis in AF and control patients correlated positively. Finally, there was no difference between AF patients based on AF type or surgical indication in the presence of CML, VCAM-1 expression, inflammatory cells, and fibrosis. Our results indicate that in AF the intramyocardial blood vessels of the left atrial appendage have an increased CML presence and proinflammatory status coinciding with a local increase in the number of inflammatory cells.",
author = "M.P.V. Begieneman and L. Rijvers and B. Kubat and W.J. Paulus and A.B.A. Vonk and {van Rossum}, A.C. and C.G. Schalkwijk and W. Stooker and H.W.M. Niessen and P.A.J. Krijnen",
note = "Copyright {\circledC} 2015 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.",
year = "2015",
month = "8",
doi = "10.1016/j.ajpath.2015.04.018",
language = "English",
volume = "185",
pages = "2096--2104",
journal = "The American Journal of Pathology",
issn = "0002-9440",
publisher = "Elsevier Inc.",
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Atrial fibrillation coincides with the advanced glycation end product N(ε)-(carboxymethyl)lysine in the atrium. / Begieneman, M.P.V.; Rijvers, L.; Kubat, B.; Paulus, W.J.; Vonk, A.B.A.; van Rossum, A.C.; Schalkwijk, C.G.; Stooker, W.; Niessen, H.W.M.; Krijnen, P.A.J.

In: The American Journal of Pathology, Vol. 185, No. 8, 08.2015, p. 2096-2104.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - Atrial fibrillation coincides with the advanced glycation end product N(ε)-(carboxymethyl)lysine in the atrium

AU - Begieneman, M.P.V.

AU - Rijvers, L.

AU - Kubat, B.

AU - Paulus, W.J.

AU - Vonk, A.B.A.

AU - van Rossum, A.C.

AU - Schalkwijk, C.G.

AU - Stooker, W.

AU - Niessen, H.W.M.

AU - Krijnen, P.A.J.

N1 - Copyright © 2015 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.

PY - 2015/8

Y1 - 2015/8

N2 - Presence of advanced glycation end products (AGEs) in the heart induces a proinflammatory phenotype. However, the presence of AGEs within atrial tissue of atrial fibrillation (AF) patients is unknown and was analyzed here. Left atrial appendage tissue from 33 AF patients and 9 controls was analyzed for the presence of the major AGEs N(ε)-(carboxymethyl)lysine (CML), VCAM-1, neutrophilic granulocytes, lymphocytes, and macrophages in both the fat tissue and myocardium separately. The total amount of fibrosis was also analyzed. Presence of CML was significantly higher in blood vessels of the left atrial appendage in AF patients as compared to controls, independent of diabetes mellitus. In AF patients, VCAM-1 expression in blood vessels and the numbers of infiltrated neutrophilic granulocytes, lymphocytes, and macrophages significantly increased compared to controls, and were highest in the fat tissue; there was no significant difference in fibrosis compared to controls. Interestingly, total amount of CML and fibrosis in AF and control patients correlated positively. Finally, there was no difference between AF patients based on AF type or surgical indication in the presence of CML, VCAM-1 expression, inflammatory cells, and fibrosis. Our results indicate that in AF the intramyocardial blood vessels of the left atrial appendage have an increased CML presence and proinflammatory status coinciding with a local increase in the number of inflammatory cells.

AB - Presence of advanced glycation end products (AGEs) in the heart induces a proinflammatory phenotype. However, the presence of AGEs within atrial tissue of atrial fibrillation (AF) patients is unknown and was analyzed here. Left atrial appendage tissue from 33 AF patients and 9 controls was analyzed for the presence of the major AGEs N(ε)-(carboxymethyl)lysine (CML), VCAM-1, neutrophilic granulocytes, lymphocytes, and macrophages in both the fat tissue and myocardium separately. The total amount of fibrosis was also analyzed. Presence of CML was significantly higher in blood vessels of the left atrial appendage in AF patients as compared to controls, independent of diabetes mellitus. In AF patients, VCAM-1 expression in blood vessels and the numbers of infiltrated neutrophilic granulocytes, lymphocytes, and macrophages significantly increased compared to controls, and were highest in the fat tissue; there was no significant difference in fibrosis compared to controls. Interestingly, total amount of CML and fibrosis in AF and control patients correlated positively. Finally, there was no difference between AF patients based on AF type or surgical indication in the presence of CML, VCAM-1 expression, inflammatory cells, and fibrosis. Our results indicate that in AF the intramyocardial blood vessels of the left atrial appendage have an increased CML presence and proinflammatory status coinciding with a local increase in the number of inflammatory cells.

U2 - 10.1016/j.ajpath.2015.04.018

DO - 10.1016/j.ajpath.2015.04.018

M3 - Article

VL - 185

SP - 2096

EP - 2104

JO - The American Journal of Pathology

JF - The American Journal of Pathology

SN - 0002-9440

IS - 8

ER -