Linde Woudstra1, P Stefan Biesbroek2, Reindert W Emmens3, Stephane Heymans4, Lynda J Juffermans5, Albert C van Rossum5, Hans W M Niessen6, Paul A J Krijnen7. 1. Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands; ICaR-VU, Institute for Cardiovascular Research, VU University Medical Center, The Netherlands. Electronic address: l.woudstra@vumc.nl. 2. 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. 3. ICaR-VU, Institute for Cardiovascular Research, VU University Medical Center, The Netherlands. 4. Center for Heart Failure Research, Cardiovascular Research Institute Maastricht (CARIM), University Hospital Maastricht, Maastricht, The Netherlands. 5. ICaR-VU, Institute for Cardiovascular Research, VU University Medical Center, The Netherlands; Department of Cardiology, VU University Medical Center, The Netherlands. 6. Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands; ICaR-VU, Institute for Cardiovascular Research, VU University Medical Center, The Netherlands; Department of Cardiothoracic Surgery, VU University Medical Center, The Netherlands. 7. Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands; ICaR-VU, Institute for Cardiovascular Research, VU University Medical Center, The Netherlands.
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 3-6h 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. 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. Copyright Â
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 3-6h 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. 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. Copyright Â
Authors: Linde Woudstra; Lynda J M Juffermans; Albert C van Rossum; Hans W M Niessen; Paul A J Krijnen Journal: Heart Fail Rev Date: 2018-07 Impact factor: 4.214
Authors: Patrick F Walker; Anthony D Foster; Philip A Rothberg; Thomas A Davis; Matthew J Bradley Journal: PLoS One Date: 2018-11-29 Impact factor: 3.240