Mast cells are increased in the media of coronary lesions in patients with myocardial infarction and may favor atherosclerotic plaque instability.
Mast cells (MCs) may play an important role in plaque destabilization and atherosclerotic coronary complications. Here, we have studied the presence of MCs in the intima and media of unstable and stable coronary lesions at different time points after myocardial infarction (MI).



Coronary arteries were obtained at autopsy from patients with acute MI (up to 5 days old; n=27) and with chronic MI (5-14 days old; n=18), as well as sections from controls without cardiac disease (n=10). Herein, tryptase-positive MCs were quantified in the intima and media of both unstable and stable atherosclerotic plaques in infarct-related and non-infarct-related coronary arteries.



In the media of both acute and chronic MI patients, the number of MCs was significantly higher than in controls. This was also found when evaluating unstable and stable plaques separately. In patients with chronic MI, the number of MCs in unstable lesions was significantly higher than in stable lesions. This coincided with a significant increase in the relative number of unstable plaques in patients with chronic MI compared with control and acute MI. No differences in MC density were found between infarct-related and non-infarct-related coronary arteries in patients with MI.



The presence of MCs in the media of both stable and unstable atherosclerotic coronary lesions after MI suggests that MCs may be involved in the onset of MI and, on the other hand, that MI triggers intra-plaque infiltration of MCs especially in unstable plaques, possibly increasing the risk of re-infarction.
Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands; Institute for Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, The Netherlands.
Koba
K
Kupreishvili
Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands; Institute for Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, The Netherlands; Department of Internal Medicine, VU University Medical Center, Amsterdam, The Netherlands.
Wessel W
WW
Fuijkschot
Department of Cardiac Surgery, VU University Medical Center, Amsterdam, The Netherlands.
Alexander B A
AB
Vonk
Institute for Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, The Netherlands; Department of Internal Medicine, VU University Medical Center, Amsterdam, The Netherlands.
Yvo M
YM
Smulders
Institute for Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, The Netherlands; Department of Cardiac Surgery, OLVG, Amsterdam, The Netherlands.
Wim
W
Stooker
Institute for Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, The Netherlands; Department of Physiology, VU University Medical Center, Amsterdam, The Netherlands.
Victor W M
VW
Van Hinsbergh
Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands; Institute for Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, The Netherlands; Department of Internal Medicine, VU University Medical Center, Amsterdam, The Netherlands.
Hans W M
HW
Niessen
Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands; Institute for Cardiovascular Research (ICaR-VU), VU University Medical Center, Amsterdam, The Netherlands. Electronic address: paj.krijnen@vumc.nl.
Paul A J
PA
Krijnen
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D003331:Coronary Vessels / Q000473:pathology*; D005260:Female; D006801:Humans; D008297:Male; D008407:Mast Cells / Q000473:pathology*; D008875:Middle Aged; D009203:Myocardial Infarction / Q000473:pathology*; D058226:Plaque, Atherosclerotic / Q000473:pathology*; D017539:Tunica Intima / Q000473:pathology; D017540:Tunica Media / Q000473:pathology; D055815:Young Adult
Atherosclerosis; Mast cells; Myocardial infarction; Plaque stability