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Published on: September 3, 2020
Unchanged cellular inflammatory response following recurrent ST-elevation myocardial infarction
Joyce Lim1, James King2, Trent Williams3
1Heart and Stroke Research Program, Hunter Medical Research Institute, New Lambton Heights, NSW, Australia; College of Health, Medicine and Wellbeing, University of Newcastle, Callaghan, NSW, Australia.
Insights
Recurrent ST-elevation myocardial infarctions (STEMIs) do not show a dampened inflammatory response. Leukocyte counts and subtypes remain similar after a second STEMI, indicating no long-term cellular memory effect.
Area of Science:
- Cardiology
- Immunology
- Hematology
Background:
- Recurrent ST-elevation myocardial infarctions (STEMIs) are linked to worse patient outcomes.
- A blunted hematopoietic response is hypothesized as the cause, but human data is lacking.
- Investigating leukocyte response after first vs. second STEMI is crucial.
Purpose of the Study:
- To determine if the inflammatory response, specifically leukocyte subtypes, is altered after recurrent STEMIs.
- To validate the hypothesis of a diminished hematopoietic response in patients with repeated myocardial infarctions.
Main Methods:
- Retrospective cohort study design.
- Analysis of full blood counts (leukocyte response and subtypes) within 24 hours and daily post-percutaneous coronary intervention (PCI) for first and second STEMI.
- Comparison of qualitative and quantitative differences in leukocyte response between the two events.
Main Results:
- Thirty-one patients with recurrent STEMI were analyzed.
- No significant differences were found in mean or peak leukocyte response (including subtypes) between the first and second STEMI, even after adjusting for infarct size.
- Leukocyte response remained consistent from admission to day three post-PCI.
Conclusions:
- The cellular inflammatory response, measured by circulating leukocytes and their subtypes, does not exhibit a long-term memory effect after recurrent STEMIs.
- The hypothesis of a dampened hematopoietic response contributing to poorer prognosis in recurrent STEMI is not supported by this study's findings on leukocyte dynamics.
Background:
Recurrent ST-elevation myocardial infarctions (STEMIs) are associated with poorer prognosis. A diminished haematopoietic response has been proposed as the mechanism responsible for this, but has yet to be validated in human studies. We therefore aim to map out the leukocyte response, and its subtypes, following the first and second STEMI to identify if the inflammatory response is dampened after recurrent myocardial infarctions.
Methods:
Retrospective cohort study of patients presenting with recurrent STEMI undergoing percutaneous coronary intervention. Full blood counts were taken within 24 h of each admission, and daily thereafter. The primary outcome was whether there were any qualitative or quantitative difference in leukocyte cell response (and its subtypes) between first and second STEMI.
Results:
Thirty-one patients (mean age 59 years [SD 14.9], 26 males [83.9%]) with an average of 3.1 years between infarcts were included in the study. Overall, between first and second STEMI, similar mean leukocyte response (and its subtypes) was observed from admission to day three post PCI. Similarly, the peak leukocyte response (and its subtypes) was similar between the two STEMIs, even after adjusting for infarct size.
Conclusions:
In recurrent STEMIs, there is no long-term memory effect on the cellular inflammatory response leading to diminished peripherally circulating leucocytes, and its subtypes.
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