Lymphocytic myocarditis occurs with myocardial infarction and coincides with increased inflammation, hemorrhage and instability in coronary artery atherosclerotic plaques. (1st April 2017)

• Record Type: Journal Article
• Authors: 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.
• Is Part Of: International journal of cardiology. Volume 232(2017)
• Page Start: 53
• Page End: 62
• Publication Date: 2017-04-01
• Subjects: Lymphocytic myocarditis -- Myocardial infarction -- Coronary arteries -- Inflammation -- Plaque instability; Cardiology -- Periodicals; Electronic journals; 616.12
• DOI: 10.1016/j.ijcard.2017.01.052
• Languages: English
• ISSNs: 0167-5273

Abstract

Abstract: Objective: 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. Methods: The three main coronary arteries were isolated at autopsy of patients with LM, with MI of 3–6 h old, with LM and MI of 3–6 h 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. Results: 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. Conclusions: 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.