Systemic inflammation after STEMI – impact on infarct size and outcome

https://doi.org/10.1007/s00392-024-02526-y

Christian Gräßer (München)1, J. Krefting (München)1, F. Voll (München)1, T. Trenkwalder (München)1, S. Kufner (München)1, E. Xhepa (München)1, M. Joner (München)1, S. Cassese (München)2, M. von Scheidt (München)1, H. Schunkert (München)1, G. Ndrepepa (München)1, A. Kastrati (München)1, T. Keßler (München)1, H. Sager (München)1

1Deutsches Herzzentrum München Klinik für Herz- und Kreislauferkrankungen München, Deutschland; 2Deutsches Herzzentrum München München, Deutschland

 

Background: Acute myocardial infarction (MI) causes systemic inflammation. This leads to leukocyte accumulation inside the cardiac tissue, promoting inflammation and removing dead cells. On day 3 after MI the reparative phase is initiated, where cardiac macrophages adopt anti-inflammatory phenotypes, which supports scar formation and cardiac healing. Resolution of inflammation needs to occur in a timely and coordinated fashion and overzealous inflammation leads to adverse cardiac remodeling after MI.

Objective: To correlate persistent inflammation and delayed resolution of inflammation (as indicated by sustained elevated leukocyte counts on day 3 after MI) with infarct size and clinical outcome in patients presenting with acute ST-elevation myocardial infarction (STEMI). 

Methods and Results: In this retrospective study, we analyzed data of STEMI patients treated with primary percutaneous coronary intervention (PPCI) from a historical cohort (1155 patients, 2002-2007) and a contemporary cohort (698 patients, 2014-2022). In both cohorts we grouped patients in tertiles according to leukocyte counts on day 3 after MI. Leukocyte count on day three was available in 976 (84,5%) and 468 (67%) respectively. In the historical cohort, groups were as follows: tertile 1 (T1, n=332; interquartile range [IQR] 0.81 – 7.70 [109/l]), tertile 2 (T2, n=319; IQR 7.71 – 9.70 [109/l]) and tertile 3 (T3, n=325; IQR 9.71 – 24.95 [109/l]). Serial single-photon emission computerized tomography imaging was available on admission and 7 to 14 days. Patients with elevated leukocyte counts after 72h (T3 group) showed greatest area at risk and infarct size: myocardial area at risk before PPCI (median) was 20.0% (IQR 11.0–36.0%) in T1, 25.0% (IQR 14.0–40.0%) in T2 and 27.4% (IQR, 15.0–51.0%) of the left ventricle in T3. The final infarct size in the 7 to 14 days scintigraphy (median) was 7.0% (IQR 1.0–17.0%) in T1, 12.0% (IQR 3.0–24.7%) in T2 and 13.0% (IQR 5.0–30.0%) of the left ventricle in T3. 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. One-year follow-up for all-cause mortality was available in 911 (78.9%) patients. 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, groups were as follows: T1 (n=157; IQR 1.00 – 8.12 [109/l]), T2 (n=156; IQR 8.13 – 10.41 [109/l] and T3 (n=157; IQR 10.43 – 29.2 [109/l]. As in the historical cohort, we found that patients with elevated leukocyte counts after 72h (T3 group) showed greatest enzymatic infarct size, estimated by peak CK-MB values and reduced LV-EF. One-year follow-up for all-cause mortality was available in 468 (100%) patients. 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: Persistent inflammation, estimated by elevated leukocyte counts 72h after STEMI, is associated with poorer outcomes at one year in both cohorts. These findings highlight the importance of a timely resolution of inflammation following MI. 

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