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. 2025 Mar 18;151(11):760-772.
doi: 10.1161/CIRCULATIONAHA.124.070729. Epub 2025 Feb 19.

Prognostic Relevance of Type 4a Myocardial Infarction and Periprocedural Myocardial Injury in Patients With Non-ST-Segment-Elevation Myocardial Infarction

Affiliations

Prognostic Relevance of Type 4a Myocardial Infarction and Periprocedural Myocardial Injury in Patients With Non-ST-Segment-Elevation Myocardial Infarction

Matteo Armillotta et al. Circulation. .

Abstract

Background: Periprocedural myocardial injury (PMI) with or without type 4a myocardial infarction (MI) might occur in patients with non-ST-segment-elevation MI (NSTEMI) after percutaneous coronary intervention (PCI). This study investigated the incidence and prognostic relevance of these events, according to current definitions, in patients with NSTEMI undergoing PCI. The best cardiac troponin I (cTnI) threshold of PMI for prognostic stratification is also suggested.

Methods: Consecutive patients with NSTEMI from January 2017 to April 2022 undergoing PCI with stable or falling pre-PCI cTnI levels were enrolled. According to the Fourth Universal Definition of Myocardial Infarction, the study population was stratified into those experiencing (1) PMI with type 4a MI, (2) PMI without type 4a MI, or (3) no PMI. Post-PCI cTnI increase >20% with an absolute postprocedural value of ≥5 times the 99th percentile upper reference limit within 48 hours after PCI was used to define PMI. The primary end point was 1-year all-cause mortality, and the secondary end point consisted of major adverse cardiovascular events at 1 year, including all-cause mortality, nonfatal reinfarction, urgent revascularization, nonfatal ischemic stroke, and hospitalization for heart failure. Internal validation was performed in patients enrolled between May 2022 and April 2023.

Results: Among 1412 patients with NSTEMI undergoing PCI with stable or falling cTnI levels at baseline, 240 (17%) experienced PMI with type 4a MI, 288 (20.4%) experienced PMI without type 4a MI, and 884 (62.6%) experienced no PMI. PMI was associated with an increased risk of adverse clinical outcomes, with patients with type 4a MI demonstrating the highest rates of 1-year all-cause mortality and major adverse cardiovascular events. A post-PCI ΔcTnI >20% but ≤40% showed similar outcomes to patients without PMI, whereas >40% was identified as the optimal threshold for prognostically relevant PMI, confirmed in an internal validation cohort of 305 patients.

Conclusions: Periprocedural ischemic events were frequent in patients with NSTEMI undergoing PCI with prognostic implications. A post-PCI ΔcTnI >40%, combined with an absolute postprocedural value of ≥5 times the 99th percentile upper reference limit, was identified as the optimal threshold for diagnosing prognostically relevant PMI. Recognizing these events may improve risk stratification and management of patients with NSTEMI.

Keywords: myocardial infarction; non-ST elevated myocardial infarction; percutaneous coronary intervention; treatment outcomes; troponin.

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Conflict of interest statement

None.

Figures

Figure 1.
Figure 1.
Distributions of cTnI concentrations during hospitalization of the primary cohort study, stratified according to periprocedural ischemic events. Violin plots of initial cardiac troponin I (cTnI) value on hospital arrival (A), peak cTnI value of the non–ST-segment–elevation myocardial infarction (MI) before percutaneous coronary intervention (PCI); B), baseline cTnI values within 1 hour before PCI (C), and peak cTnI value after PCI (D). cTnI concentrations were expressed as a multiple of the upper reference limit (URL) on a log scale, considering differences between conventional and high-sensitivity troponin I assays, as well as between sexes. Between-group differences were evaluated by Mann-Whitney U test. Sample sizes: overall cohort, n=1412; periprocedural myocardial injury (PMI) with type 4a MI, n=240; PMI without type 4a MI, n=288; and no PMI, n=884. Type 4a MI was diagnosed in cases of PMI accompanied by ≥1 of the following criteria: (1) new ischemic electrocardiographic changes; (2) development of new pathological Q waves; (3) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality consistent with ischemic origin; or (4) angiographic evidence of a procedural flow-limiting complication such as coronary dissection, side-branch loss, slow flow, thrombus, or distal embolization. ns Indicates non-significant (P>0.05).
Figure 2.
Figure 2.
Cumulative incidence curves for the primary and secondary end points at 1-year follow-up in the primary cohort study, stratified by periprocedural ischemic events. A, Primary end point stratified by the presence of periprocedural myocardial injury (PMI). B, Further stratification of the primary end point in patients with PMI, comparing those with adjudicated type 4a myocardial infarction (MI) with those without type 4a MI. C, Secondary end point stratified by PMI. D, Further stratification of the secondary end point in patients with PMI, comparing those with adjudicated type 4a MI with those without type 4a MI. Type 4a MI was diagnosed in cases of PMI accompanied by ≥1 of the following criteria: (1) new ischemic electrocardiographic changes; (2) development of new pathological Q waves; (3) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality consistent with ischemic origin; or (4) angiographic evidence of a procedural flow-limiting complication such as coronary dissection, side-branch loss, slow flow, thrombus, or distal embolization. The primary end point was 1-year all-cause mortality. The secondary end point was a composite of major adverse cardiovascular events at 1 year, including all-cause mortality, nonfatal reinfarction, urgent revascularization, nonfatal ischemic stroke, and hospitalization for heart failure.
Figure 3.
Figure 3.
Cumulative incidence curves for the primary and secondary end points at 1-year follow-up in the primary cohort study, stratified by post-PCI ΔcTnI levels of ≤20%, >20% but ≤40%, and >40%. A, Primary end point stratified by post–percutaneous coronary intervention (PCI) change in cardiac troponin I (ΔcTnI) levels. B, Secondary end point stratified by post-PCI ΔcTnI levels. The primary end point was 1-year all-cause mortality. The secondary end point was a composite of major adverse cardiovascular events at 1 year, including all-cause mortality, non-fatal reinfarction, urgent revascularization, nonfatal ischemic stroke, and hospitalization for heart failure.

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