Kupreishvili Koba, Fuijkschot Wessel W, Vonk Alexander B A, Smulders Yvo M, Stooker Wim, Van Hinsbergh Victor W M, Niessen Hans W M, Krijnen Paul A J
Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands; Institute for Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, The Netherlands.
Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands; Institute for Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, The Netherlands; Department of Internal Medicine, VU University Medical Center, Amsterdam, The Netherlands.
J Cardiol. 2017 Mar;69(3):548-554. doi: 10.1016/j.jjcc.2016.04.018. Epub 2016 Jun 7.
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).
Coronary 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.
In 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.
The 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.
肥大细胞(MCs)可能在斑块不稳定和动脉粥样硬化性冠状动脉并发症中起重要作用。在此,我们研究了心肌梗死(MI)后不同时间点不稳定和稳定冠状动脉病变的内膜和中膜中MCs的存在情况。
从急性心肌梗死患者(发病至多5天;n = 27)、慢性心肌梗死患者(发病5 - 14天;n = 18)尸检获取冠状动脉,以及从无心脏病的对照者(n = 10)获取切片。在此,对梗死相关和非梗死相关冠状动脉中不稳定和稳定动脉粥样硬化斑块的内膜和中膜中的类胰蛋白酶阳性MCs进行定量。
在急性和慢性心肌梗死患者的中膜中,MCs数量均显著高于对照组。分别评估不稳定和稳定斑块时也发现了这一情况。在慢性心肌梗死患者中,不稳定病变中的MCs数量显著高于稳定病变。这与慢性心肌梗死患者中不稳定斑块的相对数量相比对照组和急性心肌梗死患者显著增加相一致。心肌梗死患者梗死相关和非梗死相关冠状动脉之间的MC密度无差异。
心肌梗死后稳定和不稳定动脉粥样硬化冠状动脉病变的中膜中存在MCs,这表明MCs可能参与心肌梗死的发病,另一方面,心肌梗死触发MCs向斑块内浸润,尤其是在不稳定斑块中,可能增加再梗死风险。