Systemic inflammation increases mast cell numbers in coronary arteries in patients who died from myocardial infarction

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.