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Updated: Jun 5, 2026

Myocardial Infarction and Functional Outcome Assessment in Pigs
Published on: April 25, 2014
Prolonged Inflammation Associates With Greater Infarct Size and Poor Outcome After ST-Segment Elevation Myocardial
Christian Graesser1, Johannes Krefting2, Marius Schwab3
1German Heart Centre Munich, Department of Cardiology, TUM University Hospital, Technical University of Munich, Munich, Germany; German Centre for Cardiovascular Research, Partner Site Munich Heart Alliance, Munich, Germany; Department of Internal Medicine III - Cardiology and Angiology, Saarland University Medical Center, Homburg/Saar, Germany.
Insights
Persistent high white blood cell counts after ST-elevation myocardial infarction (STEMI) indicate ongoing inflammation. This sustained leukocytosis is linked to larger infarct size, poorer heart function, and increased mortality risk.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Biomarkers
Background:
- Acute myocardial infarction (MI) triggers a systemic inflammatory response.
- The prognostic significance of persistent inflammation post-MI remains unclear.
- Leukocyte counts typically normalize within days, but sustained elevation warrants investigation.
Purpose of the Study:
- To investigate the relationship between sustained leukocytosis and clinical outcomes after ST-elevation myocardial infarction (STEMI).
- To determine if elevated leukocyte counts correlate with infarct size and left ventricular function.
- To identify persistent inflammation as a potential negative prognostic marker.
Main Methods:
- Analysis of over 1,700 STEMI patients treated with primary percutaneous coronary intervention.
- Stratification of patients based on leukocyte counts at admission and day 3.
- Assessment of infarct size, left ventricular function, and mortality rates.
- Monocyte RNA sequencing and murine MI models to study immune response.
Main Results:
- High leukocyte counts on day 3 post-STEMI were associated with larger infarct size.
- Persistent leukocytosis correlated with worse left ventricular function and increased 1- and 5-year mortality.
- Declining leukocyte counts indicated better recovery, while persistent elevation predicted poorer outcomes.
Conclusions:
- Persistent inflammation, indicated by elevated day 3 leukocyte counts, is linked to adverse cardiac remodeling and higher mortality post-STEMI.
- Unresolved inflammation serves as a negative prognostic indicator.
- Targeting persistent inflammation may offer a therapeutic strategy for STEMI patients.
Aims:
Acute myocardial infarction (MI) induces a systemic inflammatory response that usually resolves within days, but the prognostic impact of persistent inflammation is uncertain. We assessed whether sustained leukocytosis after ST-segment elevation myocardial infarction (STEMI) relates to infarct size, left ventricular function, and clinical outcomes.
Methods And Results:
In >1,700 STEMI patients treated with primary percutaneous coronary intervention, leukocytes peaked on admission and typically normalized by day 3. Patients were stratified by leukocyte tertiles at admission and day 3. High day 3 leukocyte counts were associated with larger infarct size (scintigraphy; peak creatine kinase-myocardial band and troponin T), worse left ventricular function in hospital and at 6 months, and higher 1- and 5-year mortality. Patients whose leukocyte counts declined had better recovery, whereas persistent leukocytosis marked the poorest outcomes. Monocyte RNA sequencing showed post-MI transcriptomic reprogramming, and murine MI models recapitulated a similar systemic immune response.
Conclusions:
Persistent inflammation, particularly elevated leukocyte counts at day 3 post-MI, is associated with adverse remodeling and increased mortality after STEMI, identifying unresolved inflammation as a negative prognostic marker and potential therapeutic target.
Related Concept Videos
Myocarditis I: Introduction
Chronic Inflammation: Introduction
Acute Coronary Syndrome I: Introduction
Ischemic Stroke ll: Pathophysiology
Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations
Acute Inflammation III: Local and Systemic Effects
