Hemorrhagic Myocardial Infarction and Cardiac Rupture Risk: CMR Standard Risk Stratification

Background: Intramyocardial hemorrhage (IMH) is the mechanistic substrate for infarct expansion, microvascular obstruction (MVO), and contractile dysfunction after reperfused ST-elevation myocardial infarction (STEMI). Although these sequelae are well recognized, early identification of IMH burden before overt rupture has remained elusive. The Wall Strain Index (WSI), derived from strain heterogeneity between infarcted and remote myocardium, has been identified in preclinical and clinical studies as a marker of myocardial fragility. Importantly, in a large multicenter European Heart Journal analysis, a threshold of WSI > 2 was independently associated with cardiac rupture. Whether this rupture threshold translates into quantifiable IMH volume in human reperfused STEMI has not been systematically assessed.

Methods: We studied 259 patients with reperfused STEMI in the multicenter MIRON-RUPTURE cohort (clinicaltrials.gov NCT06450912). All patients underwent cardiac magnetic resonance (CMR) within one week of primary PCI. Infarct size, MVO, and IMH were quantified as a percentage of LV mass. WSI ratios (radial, circumferential, longitudinal) were derived from strain mapping. The primary analysis examined the relationship between radial WSI > 2 and IMH burden. Logistic regression adjusted for age, sex, body mass index, hypertension, diabetes, smoking, pain-to-balloon time, culprit LAD, infarct %LV, MVO %LV, and LVEF was used to assess predictors of WSI > 2.

Results: Among 259 patients (mean age 54 years, 82% men), 24 (9%) demonstrated WSI > 2. These patients exhibited a significantly greater hemorrhagic burden (mean IMH 8.6%LV vs. 5.0%LV, p = 0.02). A WSI threshold > 2 corresponded to an IMH burden exceeding 6.6%LV, thereby translating strain imbalance into quantifiable hemorrhagic volume. Larger infarct size, more extensive MVO, and reduced LVEF were observed in patients with WSI > 2, consistent with recognized consequences of IMH. In adjusted analyses, WSI ratio > 2 was strongly associated with IMH volume, with an adjusted risk ratio of 2.4 per 0.5-unit increase in WSI (95% CI 1.8–3.1, p < 0.001). The multivariable model integrating WSI with infarct and MVO achieved an AUC of 0.83 for prediction of severe IMH. Traditional clinical risk factors were not independently associated with WSI > 2.

Conclusion: In reperfused STEMI, WSI > 2 corresponds to an IMH burden > 8.6% of LV mass, defining a pre-rupture phenotype of myocardial fragility. While infarct size, MVO, and LVEF reflect downstream consequences of hemorrhagic injury, WSI provides an upstream, noninvasive biomarker that translates strain heterogeneity into hemorrhagic volume. These findings support WSI as a clinically actionable metric for early detection of patients at imminent risk of rupture.

Temporal Evolution of Hemorrhagic MI and Association of Wall Strain Index Ratio With Cardiac Rupture Risk. Temporal sequence of clinical and imaging manifestations following reperfused inferior wall myocardial infarction (IWMI) and relationship of wall strain index (WSI) ratio with intramyocardial hemorrhage (hMI). The top panel illustrates the progression from acute ischemia (ECG at presentation) to reperfusion (primary PCI), with subsequent hemodynamic monitoring in the coronary care unit (1 hour), pericardial effusion detected on echocardiography (2 hours), and late findings of infarct with microvascular obstruction (MVO) and intramyocardial hemorrhage identified by cardiac MRI (48 hours). The bottom panel shows box-and-whisker plots of WSI ratio across strain dimensions (longitudinal, circumferential, and radial) in patients (n=259) with hMI (red) and non-hMI (orange). Higher WSI ratios were consistently observed in hMI compared with non-hMI, most prominently in circumferential and radial strain (***P <0.001; *P <0.05). These findings highlight WSI as a marker of post-reperfusion myocardial injury burden and hemorrhagic transformation.