Structural myocardial injury and microvascular damage independently determine severe reperfusion phenotypes after STEMI: results from a large contemporary CMR cohort

Background

Microvascular obstruction (MVO) and intramyocardial hemorrhage (IMH) represent the most severe phenotypes of reperfusion injury following primary PCI in ST-elevation myocardial infarction (STEMI). Their structural and clinical determinants, as well as the incremental prognostic contribution of cardiac magnetic resonance (CMR), remain incompletely defined in contemporary practice.

Purpose

To identify independent predictors of MVO and IMH and quantify the incremental predictive value of CMR-derived parameters beyond clinical and angiographic assessment.

Methods

In consecutive STEMI patients from the multicenter SINERGY-ACUTE cohort undergoing early CMR (n=268), MVO was assessed by late gadolinium enhancement and IMH by T2* imaging. Penalized multivariable logistic regression was applied to account for collinearity. Hierarchical models were constructed: (1) clinical, (2) clinical + angiographic, and (3) clinical + angiographic + CMR (infarct size, LV volumes, MVO/IMH). Discrimination was evaluated using AUC with 95% CI and DeLong testing. Incremental value was assessed by ΔAUC, Net Reclassification Improvement (NRI), and Integrated Discrimination Improvement (IDI). Internal validation was performed using bootstrap resampling.

Results

A total of 268 STEMI patients with CMR was included in the study with the median age of 60 years. MVO was detected in 40.8%, while IMH was detected in 19% of patients. Independent predictors of MVO were infarct size (per 5% increase: OR 1.26, 95% CI 1.17–1.36; p<0.001), LVESV (per 10 mL: OR 1.18, 95% CI 1.10–1.27; p<0.001), angiographic no-reflow (OR 1.94, 95% CI 1.42–2.66; p<0.001), and log peak troponin (OR 1.41, 95% CI 1.22–1.63; p<0.001). Clinical AUC was 0.63 versus 0.86 for the CMR-integrated model (ΔAUC +0.23; p<0.001; NRI 0.38; IDI 0.14).

Independent predictors of IMH were infarct size (OR 1.31 per 5%; p<0.001), LVESV (OR 1.22 per 10 mL; p<0.001), presence of MVO (OR 2.48; p<0.001), and log NT-proBNP (OR 1.47; p<0.001). Clinical AUC improved from 0.67 to 0.91 with CMR integration (ΔAUC +0.24; p<0.001; NRI 0.44; IDI 0.18). Bootstrap-corrected AUC values remained robust with preserved calibration.

Conclusions

Infarct size is the dominant structural determinant of both MVO and IMH after STEMI. Notably, MVO was independently associated with peak troponin, reflecting the magnitude of acute myocardial necrosis, whereas IMH was independently linked to NT-proBNP, consistent with greater hemodynamic stress and early ventricular dysfunction. CMR-derived parameters provide substantial and statistically robust incremental discrimination beyond clinical and angiographic assessment, supporting systematic early imaging-based phenotyping of reperfusion injury in contemporary STEMI care.