Key result
OCT-derived culprit thin-cap fibroatheroma had a 43.8% vs 14.3% 3-month MACE rate (14.3%-60.0% across rSS strata, P=0.23) in STEMI patients after PCI.
Why the study?
While residual SYNTAX score quantifies untreated macroscopic coronary artery disease and OCT resolves microscopic plaque architecture such as thin-cap fibroatheroma, the descriptive characteristics and short-term outcomes of combining both measures in STEMI patients undergoing primary PCI required exploration.
Does combining post-PCI residual SYNTAX score with OCT-derived culprit lesion thin-cap fibroatheroma predict 3-month major adverse cardiac events in patients with STEMI undergoing primary PCI?
Observational (n=30)
Blinded outcome and imaging assessment
No
Does combining post-PCI residual SYNTAX score with OCT-derived culprit lesion thin-cap fibroatheroma predict 3-month major adverse cardiac events in patients with STEMI undergoing primary PCI?
Answers are grounded in this paper and cite their sources.
In this exploratory pilot study of 30 STEMI patients undergoing primary PCI, the presence of OCT-derived culprit lesion thin-cap fibroatheroma was descriptively associated with a higher rate of 3-month MACE (43.8% vs. 14.3% without TCFA), though differences across combined rSS and TCFA strata were not statistically significant.
Background ST-elevation myocardial infarction (STEMI) remains a leading cause of global morbidity and mortality. While percutaneous coronary intervention (PCI) is the definitive reperfusion strategy, residual disease burden and plaque vulnerability both influence clinical recovery. The residual SYNTAX score (rSS) quantifies untreated macroscopic coronary artery disease, whereas optical coherence tomography (OCT) resolves microscopic plaque architecture, notably thin-cap fibroatheroma (TCFA). This pilot study explored the descriptive characteristics and short-term outcomes associated with combining rSS and OCT-derived TCFA in a highly selected STEMI cohort. Methods This retrospective observational pilot study included 30 patients with STEMI who underwent primary PCI and culprit lesion OCT evaluation at a tertiary care center. Patients were stratified into four groups according to the presence of culprit TCFA and the post-PCI rSS threshold ( ≤ ≤ 4 vs. > 4): group 0 (TCFA absent, rSS > 4), group 1 (TCFA absent, rSS ≤ ≤ 4), group 2 (TCFA present, rSS > 4), and group 3 (TCFA present, rSS ≤ ≤ 4). The primary clinical endpoint was major adverse cardiac events (MACE)—a composite of all-cause death, recurrent myocardial infarction, target lesion revascularization, heart failure hospitalisation, and ischemic stroke—assessed over 3 months. Results The cohort (mean age, 54.5 ± 10.1 years; 83.3% male, 40% with diabetes mellitus) had a 53.3% prevalence (16 of 30) of culprit lesion TCFA. Complete or reasonable revascularization (rSS ≤ 4) was achieved in 12 patients (40.0%). The overall cumulative 3-month MACE rate was 30.0% (9 of 30). MACE occurred in 1 of 7 patients (14.3%) in group 0, 1 of 7 (14.3%) in group 1, 4 of 11 (36.4%) in group 2, and 3 of 5 (60.0%) in group 3 (Fisher exact test, P = 0.23; log-rank P = 0.38). Patients with TCFA accounted for 7 of 9 clinical events (77.8%). Given the small subgroup sizes ( n < 12), multivariable predictive risk modeling was not performed. Conclusions In this exploratory pilot cohort of STEMI patients undergoing PCI, the presence of OCT-derived TCFA was descriptively associated with higher short-term adverse event rates across both complete and incomplete revascularization strata. Given the small sample size and clear indication bias, these findings are strictly hypothesis-generating and support the need for adequately powered prospective registries to evaluate dual anatomical-biological risk stratification.
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Syed et al. (2026) conducted an observational in ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI) (n=30). Culprit lesion thin-cap fibroatheroma (TCFA) on OCT combined with post-PCI residual SYNTAX score (rSS ≤ 4 vs. > 4) vs. Absence of culprit lesion TCFA stratified by post-PCI residual SYNTAX score (rSS ≤ 4 vs. > 4) was evaluated on Major adverse cardiac events (MACE: composite of all-cause death, recurrent myocardial infarction, target lesion revascularization, heart failure hospitalization, and ischemic stroke) at 3 months (p=0.23). OCT-derived culprit thin-cap fibroatheroma had a 43.8% vs 14.3% 3-month MACE rate (14.3%-60.0% across rSS strata, P=0.23) in STEMI patients after PCI.
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