Systemic progression of atherosclerosis after STEMI: a prospective cohort analysis

Background ST- elevation myocardial infarction (STEMI) typically reflects an acute event within chronic systemic atherosclerosis. (1) It remains unclear whether STEMI is associated with accelerated progression of atherosclerosis in extracoronary vascular beds, whether such progression carries prognostic relevance, and whether it is related to infarct severity at the tissue level. (2) We therefore investigated 1-year extracoronary plaque progression in patients with STEMI compared with chronic coronary syndrome (CCS), examined its association with long-term outcomes, and evaluated the relationship between infarct severity and subsequent plaque progression. Methods In this prospective cohort study, 173 patients (CCS n=84, STEMI n=98) underwent three-dimensional ultrasound quantification of carotid and femoral plaque volume at baseline and 12 months. Plaque progression was defined as absolute change in cumulative plaque volume. Determinants of progression were assessed using multivariable linear regression. In STEMI patients, myocardial infarct severity was assessed by cardiac magnetic resonance (CMR) and tested for association with plaque progression. Major adverse cardiovascular and cerebrovascular events (MACCE) and its association with plaque progression were evaluated using Cox proportional hazards models. Results Baseline cumulative plaque volume was higher in CCS (mean age: 65.0 years, 26.2% female) than STEMI patients (mean age: 58.6 years, 21.11% female) (161.00 ±325.75 mm3 vs 66.50 ±114.75 mm3, respectively, p < 0.001). Over 12 months, cumulative plaque volume increased more in STEMI than in CCS (median 61.5 (±90.25) vs 37.5 (±76.25) mm³, p = 0.001 (Figure 1)). In multivariable regression, STEMI presentation was independently associated with greater plaque progression (β 54.6 mm³, 95% CI 27.9 to 81.2, p < 0.001.) During a median follow up of 6.6 years, high plaque progression was independently associated with MACCE (hazard ratio 5.50, 95% CI 1.59 to 19.05, p = 0.007) with good model discrimination (C- index 0.758). Unsupervised clustering revealed three distinct systemic progression phenotypes within the STEMI cohort, showing markedly different plaque progression levels, p = 0.003, and characterized by divergent metabolic and inflammatory risk constellations. CMR-derived Infarct size and presence of microvascular obstruction was not associated with plaque progression (p = 0.713). Conclusions STEMI is associated with accelerated extracoronary atherosclerotic plaque progression compared with CCS. Extracoronary plaque progression independently predicts long-term adverse cardiovascular outcomes and exhibits marked heterogeneity across biologically distinct phenotypes, whereas no association with tissue-level infarct severity was observed.