Key result
Acute infection was associated with increased mast cell densities in the intima and media of coronary arteries in patients with early acute myocardial infarction.
Why the study?
Systemic inflammation caused by infection increases the risk of acute myocardial infarction by potentially affecting atherosclerotic plaque stability, but the specific effects on coronary artery inflammation and cell types remain unclear.
Does acute infection increase intra-plaque inflammation and plaque instability in patients with acute myocardial infarction?
Observational (n=35)
No
Does acute infection increase intra-plaque inflammation and plaque instability in patients with acute myocardial infarction?
Answers are grounded in this paper and cite their sources.
Acute infection is associated with increased mast cell infiltration in coronary plaques during early AMI, potentially contributing to plaque destabilization and increased cardiovascular risk.
Systemic inflammation caused by infection peaks the risk of acute myocardial infarction (AMI), presumably by affecting atherosclerotic plaque (AP) stability. In this study, APs were examined in AMI patients with acute infection (AI). Four groups of AMI patients with or without AI were compared to determine the effects of infection on both early (<6 h) and late (6 h–14 days) AMI: Early AMI, early AMI + AI, late AMI and late AMI + AI. Changes in the AP were determined by measuring stenosis (Elastica von Gieson), plaque stability (thickness of fibrotic cap and leukocytes presence) and intraplaque haemorrhage (GLUT-1 and Perls). Inflammation was determined by measuring leukocytes, macrophages, mast cells and neutrophilic granulocytes in the different regions of the coronary arteries: intima, media and adventitia. AI did not affect coronary stenosis, plaque stability or intraplaque haemorrhage. Plaque instability increased in late AMI + AI compared to early AMI + AI ( p = 0.0056). AI did not affect leukocyte-, macrophage- or neutrophil numbers in the coronary artery wall. However, increased mast cell densities were found in the intima and media in early AMI + AI patients ( p = 0.022; p < 0.0001 respectively), while mast cells decreased significantly in the intima late AMI + AI patients ( p < 0.0001), and non-significantly in the media ( p = 0.0609). Therefore we conclude that, in contrast to other inflammatory cell types, mast cell influx into the coronary artery wall is increased in patients with AI with early AMI. As mast cells produce vasoconstricting compounds, this may contribute to the increased risk of AMI in patients with AI.
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Fiet et al. (2026) conducted an observational in Acute myocardial infarction (AMI) (n=35). Acute infection vs. No acute infection was evaluated on Mast cell density in the intima and media of coronary arteries (p=p=0.022; p<0.0001). Acute infection was associated with increased mast cell densities in the intima and media of coronary arteries in patients with early acute myocardial infarction.
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