Key result
Increased mean CT lung density is linked to ~75% higher in-hospital MACE risk in STEMI.
Why the study?
Subclinical pulmonary congestion may occur after STEMI before overt HF develops, but its clinical significance remains unclear.
Does higher mean lung density on CT predict in-hospital MACEs in acute STEMI patients without overt heart failure?
Cohort (n=276)
No
Does higher mean lung density on CT predict in-hospital MACEs in acute STEMI patients without overt heart failure?
CT-detected subclinical pulmonary congestion in acute STEMI patients without overt heart failure is independently associated with an increased risk of in-hospital major adverse cardiovascular events.
Background Subclinical pulmonary congestion may occur after ST-segment elevation myocardial infarction (STEMI) before overt heart failure (HF) develops. However, its clinical significance remains unclear. This study aimed to investigate the clinical correlates and in-hospital prognostic significance of computed tomography (CT)-detected subclinical pulmonary congestion in acute STEMI patients without overt HF. Methods We retrospectively enrolled 276 consecutive patients with acute STEMI classified as Killip class I who underwent chest CT at admission. Quantitative CT-derived mean lung density was used to assess subclinical pulmonary congestion. Patients were stratified into subgroups using K-means clustering based on mean lung density. A logistic regression model was constructed to discriminate the two subgroups, and the importance of clinical features was ranked accordingly. For prognostic analysis, univariable and multivariable logistic regression analyses were performed to evaluate the independent association between mean lung density and in-hospital major adverse cardiovascular events (MACEs). Results Two distinct subgroups were identified. The median (IQR) mean lung density was −806 [−826 to −785] HU in subgroup 1 and −727 [−747 to −704] HU in subgroup 2 ( P < 0.001). Compared with subgroup 1, patients in the higher mean lung density phenotype (subgroup 2) exhibited significantly higher levels of cardiac enzymes, increased neutrophil and monocyte counts, and worse left ventricular function. Feature importance analysis identified markers of myocardial injury as the strongest correlates of increased mean lung density, followed by inflammatory cell counts and cardiac functional parameters. During hospitalization, 56 patients (20.3%) experienced MACEs, with a higher incidence in subgroup 2 than in subgroup 1 (30.4% vs. 14.4%). Increased mean lung density was associated with in-hospital MACEs in univariable analysis (OR per 1-SD increment, 1.92; 95% CI, 1.41–2.62; P < 0.001) and remained independently associated after adjustment for CK, LVEF, and neutrophil count (adjusted OR, 1.75; 95% CI, 1.24–2.47; P = 0.002). Conclusion The higher mean lung density phenotype on CT, suggestive of subclinical pulmonary congestion, is associated with greater myocardial injury, heightened inflammatory activation, and impaired left ventricular function in patients with acute STEMI without overt HF. Multivariable analysis showed an independent association between increased mean lung density and in-hospital MACEs, supporting its potential role in early risk stratification among Killip class I patients.
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Hua et al. (2026) conducted a cohort in Acute STEMI without overt heart failure (Killip class I) (n=276). Increased mean lung density on CT vs. Lower mean lung density was evaluated on In-hospital major adverse cardiovascular events (MACEs) (adjusted OR 1.75, 95% CI 1.24-2.47, p=0.002). Increased mean lung density on CT, indicative of subclinical pulmonary congestion, was independently associated with a higher risk of in-hospital major adverse cardiovascular events (adjusted OR 1.75) in patients with acute STEMI without overt heart failure.
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