Abstract 4147282: Systemic inflammation after STEMI – impact on infarct size and outcome –

Background: Systemic inflammation due to acute myocardial infarction (MI) leads to leukocyte accumulation inside cardiac tissue. Three days after MI the reparative phase is initiated, where cardiac macrophages adopt anti-inflammatory phenotypes and support scar formation and cardiac healing. Delayed resolution of inflammation leads to adverse cardiac remodeling after MI. Objective: To correlate persistent inflammation and delayed resolution of inflammation with infarct size and mortality in patients with ST-elevation myocardial infarction (STEMI). Methods and Results: This retrospective study, included data of STEMI patients treated with primary percutaneous coronary intervention (PPCI) from a historical (n=1155, 2002-2007) and contemporary (n=698, 2014-2022) cohort. Patients were grouped in tertiles according to leukocyte counts on day 3 after MI, as a surrogate parameter for delayed resolution of inflammation. In the historical cohort Serial single-photon emission computerized tomography imaging was available on admission and 7 to 14 days. Patients with elevated leukocyte counts after 72 h (T3 group) showed greatest area at risk (AAR) before PPCI (T1, AAR (median): 20.0% (IQR 11.0–36.0%); T2, AAR (median): 25.0% (IQR 14.0–40.0%), T3, AAR (median): 27.4% (IQR, 15.0–51.0%) and final infarct size (FIS) after 7 to 14 days after MI (T1, FIS (median): 7.0% (IQR 1.0–17.0%); T2, FIS (median): 12.0% (IQR 3.0–24.7%); T3, FIS (median): 13.0% (IQR 5.0–30.0%)) of the left ventricle. In line with these scintigraphic findings, peak creatine kinase myocardial band (CK-MB) values, as an enzymatic estimate of the infarct size, were also highest in T3. Additionally left ventricular ejection fraction (LV-EF) was lowest in the T3. At one year, 8 patients in T1, 7 patients in T2, and 22 patients in T3 had died (Kaplan–Meier estimates of 1-year mortality: 2.6%, 2.3%, and 7.3%, respectively (log-rank test: T1 vs. T3: p=0.01; T2 vs. T3: p=0.03). In the contemporary cohort we also found that patients with elevated leukocyte counts after 72 h (T3 group) showed greatest enzymatic infarct size, estimated by peak CK-MB values and reduced LV-EF. At one year, 6 patients in T1, 13 patients in T2 and 25 patients in T3 had died (Kaplan–Meier estimates of 1-year mortality: 3.8%, 8.3%, and 15.9%, respectively (log-rank test: T1 vs. T3: p<0.005, T2 vs. T3: p=0.004). Conclusion: Delayed resolution of inflammation following MI, is associated with poorer outcomes at one year in STEMI patients.

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Journal
Circulation
Published
2024-11-12
DOI
https://doi.org/10.1161/circ.150.suppl_1.4147282
Primary Topic
Cardiovascular Disease and Adiposity
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article
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article

Abstract 4147282: Systemic inflammation after STEMI – impact on infarct size and outcome –

Hendrik B. Sager, Johannes Krefting, Thorsten Kessler, Sebastian Kufner et al.
Circulation
Cardiovascular Disease and Adiposity
article

Abstract 4147282: Systemic inflammation after STEMI – impact on infarct size and outcome –

Hendrik B. Sager, Johannes Krefting, Thorsten Kessler, Sebastian Kufner, A. Kastrati, Teresa Trenkwalder, Gjin Ndrepepa, Salvatore Cassese, Erion Xhepa, Felix Voll, Moritz von Scheidt, Heribert Schunkert, Michael Joner, Christian Graesser
article en

Abstract

Background: Systemic inflammation due to acute myocardial infarction (MI) leads to leukocyte accumulation inside cardiac tissue. Three days after MI the reparative phase is initiated, where cardiac macrophages adopt anti-inflammatory phenotypes and support scar formation and cardiac healing. Delayed resolution of inflammation leads to adverse cardiac remodeling after MI. Objective: To correlate persistent inflammation and delayed resolution of inflammation with infarct size and mortality in patients with ST-elevation myocardial infarction (STEMI). Methods and Results: This retrospective study, included data of STEMI patients treated with primary percutaneous coronary intervention (PPCI) from a historical (n=1155, 2002-2007) and contemporary (n=698, 2014-2022) cohort. Patients were grouped in tertiles according to leukocyte counts on day 3 after MI, as a surrogate parameter for delayed resolution of inflammation. In the historical cohort Serial single-photon emission computerized tomography imaging was available on admission and 7 to 14 days. Patients with elevated leukocyte counts after 72 h (T3 group) showed greatest area at risk (AAR) before PPCI (T1, AAR (median): 20.0% (IQR 11.0–36.0%); T2, AAR (median): 25.0% (IQR 14.0–40.0%), T3, AAR (median): 27.4% (IQR, 15.0–51.0%) and final infarct size (FIS) after 7 to 14 days after MI (T1, FIS (median): 7.0% (IQR 1.0–17.0%); T2, FIS (median): 12.0% (IQR 3.0–24.7%); T3, FIS (median): 13.0% (IQR 5.0–30.0%)) of the left ventricle. In line with these scintigraphic findings, peak creatine kinase myocardial band (CK-MB) values, as an enzymatic estimate of the infarct size, were also highest in T3. Additionally left ventricular ejection fraction (LV-EF) was lowest in the T3. At one year, 8 patients in T1, 7 patients in T2, and 22 patients in T3 had died (Kaplan–Meier estimates of 1-year mortality: 2.6%, 2.3%, and 7.3%, respectively (log-rank test: T1 vs. T3: p=0.01; T2 vs. T3: p=0.03). In the contemporary cohort we also found that patients with elevated leukocyte counts after 72 h (T3 group) showed greatest enzymatic infarct size, estimated by peak CK-MB values and reduced LV-EF. At one year, 6 patients in T1, 13 patients in T2 and 25 patients in T3 had died (Kaplan–Meier estimates of 1-year mortality: 3.8%, 8.3%, and 15.9%, respectively (log-rank test: T1 vs. T3: p<0.005, T2 vs. T3: p=0.004). Conclusion: Delayed resolution of inflammation following MI, is associated with poorer outcomes at one year in STEMI patients.

CirculationVol. 150(Suppl_1)
Deutsches Herzzentrum der Charité (DE), Deutsches Herzzentrum München (DE)
Good health and well-being
Openalex Percentile: Top 61%
Cardiovascular Disease and Adiposity
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