Baseline patient characteristics, angiographical and CMR findings
Of 250 initially enrolled patients, the final analysis was conducted on 235 patients (Fig. 1). Patients underwent pre-PCI CMR within a median of 4 (2–7) days before PCI and post-PCI CMR within a median of 12 (7–18) days after PCI completion. No significant CMR-related complications were observed and stent implantation was performed successfully in all patients for the final analysis. Baseline patient characteristics, angiographic and CMR findings of 235 patients are summarized in Table 1, and the detailed data set according to the presence or absence of UMI and PPL are shown in Supplemental Table 1. The mean age of the study population was 67 years, 15.3% were women, and the median left ventricular ejection fraction (LVEF) was 62 (54–68) %. A total of 40 (17.0%) patients had a prior history of MI. Compared to patients without UMI, those with UMI were less likely to have a history of MI (P = 0.017, respectively), whereas there was no significant difference in the prevalence of prior history of MI between the patients with and without PPL (P = 0.14, respectively).
UMI detected by CMR
Examples are shown in Fig. 2a. Median UMI volume was 8.7 (4.0–19.5) g in patients with UMI. The UMIs were predominantly located in the target vessel territories of PCI, accounting for 58.1% of cases. The presence of UMI was significantly associated with FFR and angiographic stenosis severity in the target vessels (UMI (+) vs UMI (−); FFR: 0.59 vs 0.66, P = 0.020; diameter stenosis: 76.7 vs 73.6%, P = 0.033, respectively). Patients with UMI were more likely to be male and have a higher body surface area (BSA), high-sensitivity cardiac troponin (hs-cTnI) levels at baseline, SYNTAX Scores, and prevalence of diabetes mellitus (P = 0.002, P < 0.001, P = 0.045, P < 0.001, P = 0.006, respectively).
Representative cardiac magnetic resonance images and angiographies (a) of a patient with unrecognized myocardial infarction; (b) of a patient with periprocedural new occurrence of LGE after PCI.
Incidence of PPL and cardiac biomarker elevation
The present study assessed PMI by PPL and cardiac biomarker elevation. In a total of 235 patients in a final analysis, 45 (19.1%) patients presented PPL on post-PCI CMR. Examples are shown in Fig. 2b. The median PPL mass was 3.9 g. Patients with PPL had greater biomarkers release than those without (hs-cTnI: 932 (207–7806) ng L−1 vs 285 (110–770) ng L−1, P < 0.001; CK-MB: 17 (10–34) U L−1 vs 11 (8–13), P < 0.001) in blood samples obtained at an average of 21.0 ± 1.5 h after PCI completion. Post-PCI hs-cTnI elevation ≥ 5 × URL occurred in 169 patients (71.9%), post-PCI hs-cTnI elevation ≥ 70 × URL in 37 patients (15.7%), and post-PCI CK-MB elevation ≥ 10 × URL in 1 patient (0.4%). There was a significant correlation between cardiac biomarker elevation and PPL (hs-cTnI: r = 0.67, P < 0.001, CK-MB: r = 0.55, P < 0.001, respectively), whereas 21.9% of patients with hs-cTnI elevation ≥ 5 × URL and 48.6% with hs-cTnI elevation ≥ 70 × URL showed PPL (Cohen’s kappa = 0.322). Compared to patients without PPL, those with PPL had higher NT-proBNP levels at presentation and were more likely to have UMI in the target vessel territories of PCI (24.4% vs 7.4%, P = 0.002) and multiple stent implantation (P = 0.036).
Determinants of the presence of UMI and the occurrence of PPL
In univariable and multivariable logistic regression analyses, BSA, the history of DM, SYNTAX Score, LVMI, and lesion stenosis severity were independent predictors of the presence of UMI (OR 11.5, 95% CI 2.53–82.6, P = 0.005; OR 2.28, 95% CI 1.09–4.79, P = 0.030; OR 1.12, 95% CI 1.06–1.20, P < 0.001; OR 1.02, 95% CI 1.00–1.04, P = 0.026, OR 1.03, 95% CI 1.00–1.07, P = 0.039, respectively) (Table 2). Meanwhile, UMI in the target vessel territories and log (NT-proBNP) before the index PCI were independent predictors of the occurrence of PPL (OR 3.77, 95% CI 1.52–9.36, P = 0.004; OR 1.32, 95% CI 1.05–1.65, P = 0.016, respectively), whereas the presence of recognized myocardial infarction in the target area was not significant (OR 1.06, 95% CI 0.38–3.00, P = 0.91) (Table 3).
Prognostic value of UMI and PPL
During the follow-up period of 2.2 (1.4–3.0) years, 31 of 235 patients (13.2%) reached the composite endpoint, including 1 cardiovascular death (0.4%), 6 nonfatal MI (2.6%), 3 hospitalization for congestive heart failure (1.3%), 2 stroke (0.9%), and 19 (8.1%) unplanned late revascularization.
Cox proportional hazard analysis revealed that the presence of UMI and the occurrence of PPL were independent predictors of MACE (Model 1 (adjusted by age and male sex): HR 4.62, 95% CI 2.24–9.54, P < 0.001; HR 2.33, 95% CI 1.11–4.91, P = 0.026; Model 2 (adjusted by EF and Syntax score): HR 4.62, 95% CI 2.23–9.57, P < 0.001; HR 2.33, 95% CI 1.11–4.93, P = 0.026) (Table 4). In contrast, post-PCI hs-cTnI elevation ≥ 5 × URL, hs-cTnI elevation ≥ 70 × URL, and CK-MB elevation ≥ 10 × URL were not significantly associated with MACE (P = 0.10, P = 0.070, P = 0.77, respectively). Kaplan–Meier analysis demonstrated a significantly increased risk of MACE in patients with UMI compared to those without, and the patients with PPL compared to those without (P < 0.001, P < 0.001, respectively) (Fig. 3). When stratified into four groups according to UMI presence and PPL occurrence, the patients with UMI and PPL had a significantly higher incidence of MACE (P < 0.001, Fig. 4).
Kaplan–Meier analysis for the incidence of MACE stratified by (a) the presence of UMI; (b) the occurrence of PPL. Event-free survival was significantly worse in patients with UMI and PPL.
Frequency of MACE stratified into four groups by the presence or occurrence of UMI and PPL. Blue: UMI (+), PPL (+); green: UMI (+), PPL (−); yellow: UMI (−), PPL (+); red: UMI (−), PPL (−). The patients with UMI and PPL showed significantly higher frequency of MACE.