Rapid fall in circulating non‐classical monocytes in ST elevation myocardial infarction patients correlates with cardiac injury

Myocardial infarction leads to a rapid innate immune response that is ultimately required for repair of damaged heart tissue. We therefore examined circulating monocyte dynamics immediately after reperfusion of the culprit coronary vessel in STEMI patients to determine whether this correlated with l...

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Bibliographic Details
Published in:The FASEB journal 2021-05, Vol.35 (5), p.e21604-n/a
Main Authors: Marsh, Sarah A., Park, Catherine, Redgrave, Rachael E., Singh, Esha, Draganova, Lilia, Boag, Stephen E., Spray, Luke, Ali, Simi, Spyridopoulos, Ioakim, Arthur, Helen M.
Format: Article
Language:English
Subjects:
animal models
Animals
coronary circulation
Female
Heart Injuries - blood
Heart Injuries - etiology
Heart Injuries - pathology
Humans
Male
Mice
Middle Aged
monocytes
Monocytes - pathology
myocardial infarction
Prospective Studies
Retrospective Studies
ST Elevation Myocardial Infarction - complications
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Summary:Myocardial infarction leads to a rapid innate immune response that is ultimately required for repair of damaged heart tissue. We therefore examined circulating monocyte dynamics immediately after reperfusion of the culprit coronary vessel in STEMI patients to determine whether this correlated with level of cardiac injury. A mouse model of cardiac ischemia/reperfusion injury was subsequently used to establish the degree of monocyte margination to the coronary vasculature that could potentially contribute to the drop in circulating monocytes. We retrospectively analyzed blood samples from 51 STEMI patients to assess the number of non‐classical (NC), classical, and intermediate monocytes immediately following primary percutaneous coronary intervention. Classical and intermediate monocytes showed minimal change. On the other hand, circulating numbers of NC monocytes fell by approximately 50% at 90 minutes post‐reperfusion. This rapid decrease in NC monocytes was greatest in patients with the largest infarct size (P 
ISSN:0892-6638
1530-6860
DOI:10.1096/fj.202100240R