Mast cells are increased in the media of coronary lesions in patients with myocardial infarction and may favor atherosclerotic plaque instability

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• 作者：Koba Kupreishvili ; MD^a ; ^b ; ¹ ; Wessel W. Fuijkschot ; MD^a ; ^b ; ^c ; ¹ ; Alexander B.A. Vonk ; MD ; PhD^d ; Yvo M. Smulders ; MD ; PhD^b ; ^c ; Wim Stooker ; MD ; PhD^b ; ^e ; Victor W.M. Van Hinsbergh ; MD ; PhD^b ; ^f ; Hans W.M. Niessen ; MD ; PhD^a ; ^b ; ^c ; Paul A.J. Krijnen ; PhD^a ; ^b ; ^{paj.krijnen@vumc.nl}
• 关键词：Myocardial infarction ; Mast cells ; Atherosclerosis ; Plaque stability
• 刊名：Journal of Cardiology
• 出版年：2017
• 出版时间：March 2017
• 年：2017
• 卷：69
• 期：3
• 页码：548-554
• 全文大小：1061 K
• 卷排序：69

文摘

Mast cells (MCs) may play an important role in plaque destabilization and atherosclerotic coronary complications. Here, we have studied the presence of MCs in the intima and media of unstable and stable coronary lesions at different time points after myocardial infarction (MI).MethodsCoronary arteries were obtained at autopsy from patients with acute MI (up to 5 days old; n = 27) and with chronic MI (5–14 days old; n = 18), as well as sections from controls without cardiac disease (n = 10). Herein, tryptase-positive MCs were quantified in the intima and media of both unstable and stable atherosclerotic plaques in infarct-related and non-infarct-related coronary arteries.ResultsIn the media of both acute and chronic MI patients, the number of MCs was significantly higher than in controls. This was also found when evaluating unstable and stable plaques separately. In patients with chronic MI, the number of MCs in unstable lesions was significantly higher than in stable lesions. This coincided with a significant increase in the relative number of unstable plaques in patients with chronic MI compared with control and acute MI. No differences in MC density were found between infarct-related and non-infarct-related coronary arteries in patients with MI.ConclusionThe presence of MCs in the media of both stable and unstable atherosclerotic coronary lesions after MI suggests that MCs may be involved in the onset of MI and, on the other hand, that MI triggers intra-plaque infiltration of MCs especially in unstable plaques, possibly increasing the risk of re-infarction.