Post-mortem diagnosis of lymphocytic myocarditis revealed a 32% prevalence of recent myocardial infarction, coinciding with increased coronary plaque inflammation, hemorrhage, and instability.
Observational
Is lymphocytic myocarditis associated with increased inflammation and instability in coronary atherosclerotic plaques?
Lymphocytic myocarditis frequently co-occurs with recent myocardial infarction and is associated with coronary plaque inflammation and destabilization.
ObjectiveAlthough 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.MethodsThe 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.ResultsIn 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.ConclusionsThis 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.
Woudstra et al. (Sat,) conducted a observational in Lymphocytic myocarditis and myocardial infarction. Lymphocytic myocarditis vs. Controls was evaluated on Inflammatory infiltration, plaque stability, intraplaque hemorrhage and thrombi in coronary atherosclerotic lesions. Post-mortem diagnosis of lymphocytic myocarditis revealed a 32% prevalence of recent myocardial infarction, coinciding with increased coronary plaque inflammation, hemorrhage, and instability.
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