Woudstra Linde, Biesbroek P Stefan, Emmens Reindert W, Heymans Stephane, Juffermans Lynda J, van Rossum Albert C, Niessen Hans W M, Krijnen Paul A J
Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands; ICaR-VU, Institute for Cardiovascular Research, VU University Medical Center, The Netherlands.
ICaR-VU, Institute for Cardiovascular Research, VU University Medical Center, The Netherlands; Department of Cardiology, VU University Medical Center, The Netherlands; ICIN, Inter-university Cardiology Institute of the Netherlands, Utrecht, The Netherlands.
Int J Cardiol. 2017 Apr 1;232:53-62. doi: 10.1016/j.ijcard.2017.01.052. Epub 2017 Jan 7.
Although lymphocytic myocarditis (LM) clinically can mimic myocardial infarction (MI), they are regarded as distinct clinical entities. However, we observed a high prevalence (32%) of recent MI in patients diagnosed post-mortem with LM. To investigate if LM changes coronary atherosclerotic plaque, we analyzed in autopsied hearts the inflammatory infiltrate and stability in coronary atherosclerotic lesions in patients with LM and/or MI.
The three main coronary arteries were isolated at autopsy of patients with LM, with MI of 3-6h old, with LM and MI of 3-6h old (LM+MI) and controls. In tissue sections of atherosclerotic plaque-containing coronary segments inflammatory infiltration, plaque stability, intraplaque hemorrhage and thrombi were determined via (immuno)histological criteria.
In tissue sections of those coronary segments the inflammatory infiltrate was found to be significantly increased in patients with LM, LM+MI and MI compared with controls. This inflammatory infiltrate consisted predominantly of macrophages and neutrophils in patients with only LM or MI, of lymphocytes in LM+MI and MI patients and of mast cells in LM+MI patients. Moreover, in LM+MI and MI patients this coincided with an increase of unstable plaques and thrombi. Finally, LM and especially MI and LM+MI patients showed significantly increased intraplaque hemorrhage.
This study demonstrates prevalent co-occurrence of LM with a very recent MI at autopsy. Moreover, LM was associated with remodeling and inflammation of atherosclerotic plaques indicative of plaque destabilization pointing to coronary spasm, suggesting that preexistent LM, or its causes, may facilitate the development of MI.
虽然淋巴细胞性心肌炎(LM)在临床上可能类似于心肌梗死(MI),但它们被视为不同的临床实体。然而,我们观察到在尸检诊断为LM的患者中近期MI的患病率很高(32%)。为了研究LM是否会改变冠状动脉粥样硬化斑块,我们在尸检心脏中分析了LM和/或MI患者冠状动脉粥样硬化病变中的炎症浸润和稳定性。
在对LM患者、3 - 6小时龄MI患者、3 - 6小时龄LM合并MI(LM + MI)患者及对照组进行尸检时,分离出三条主要冠状动脉。通过(免疫)组织学标准,在含有动脉粥样硬化斑块的冠状动脉节段的组织切片中确定炎症浸润、斑块稳定性、斑块内出血和血栓情况。
与对照组相比,在那些冠状动脉节段的组织切片中,发现LM患者、LM + MI患者和MI患者的炎症浸润显著增加。仅LM或MI患者的这种炎症浸润主要由巨噬细胞和中性粒细胞组成,LM + MI和MI患者由淋巴细胞组成,LM + MI患者由肥大细胞组成。此外,在LM + MI和MI患者中,这与不稳定斑块和血栓的增加相吻合。最后,LM患者尤其是MI和LM + MI患者的斑块内出血显著增加。
本研究表明在尸检时LM与近期MI普遍共存。此外,LM与动脉粥样硬化斑块的重塑和炎症相关,提示斑块不稳定,指向冠状动脉痉挛,表明先前存在的LM或其病因可能促进MI的发生。