Key result
STEMI presentation was a significant predictor of plaque rupture compared to UA/NSTEMI (76.0% vs 29.4%; OR 9.35; 95% CI 1.66-52.61; P=0.01) in patients with acute coronary syndrome.
Why the study?
Contemporary optical coherence tomography findings in patients with acute coronary syndromes remain controversial.
Do optical coherence tomography (OCT) findings of culprit lesion plaque morphology differ between patients presenting with STEMI versus UA/NSTEMI?
Observational (n=110)
No
Do optical coherence tomography (OCT) findings of culprit lesion plaque morphology differ between patients presenting with STEMI versus UA/NSTEMI?
Effect estimate: OR 9.35 (95% CI 1.66-52.61)
Absolute Event Rate: 76% vs 29.4%
p-value: p=0.01
OCT imaging reveals that culprit lesions in STEMI are more frequently characterized by plaque rupture, lipid-rich plaques, and thrombus compared to UA/NSTEMI, suggesting distinct pathophysiologic mechanisms drive different ACS presentations.
Observational OCT data suggest distinct ACS morphologies by presentation; hypothesis-generating and should not yet alter practice.
BACKGROUND: Contemporary optical coherence tomography (OCT) findings in patients with acute coronary syndromes (ACS) are still subject of controversy. We sought to use OCT to evaluate plaque morphology and phenotype classification in patients with ACS. METHODS: Using optical coherence tomography, culprit lesions were morphologically classified as plaque rupture, plaque erosion, calcified nodule, thin-cap fibroatheroma, thick-cap fibroatheroma (TCFA) or fibrotic, fibrocalcific or fibrolipidic plaque. Quantitative and qualitative analyses also included cholesterol crystals, neovascularization, spotty calcification and thrombus. RESULTS: Of the 110 lesions imaged from June 2012 to April 2016, 54 (49%) were in patients with unstable angina (UA), 31 (28%) were in non-ST-elevation myocardial infarction (STEMI) patients and 25 (23%) were in STEMI patients. Compared with STEMI patients, patients with UA/non-STEMI were older and had more hypertension, hypercholesterolemia, known coronary artery disease, prior myocardial infarction and higher use of antiplatelet therapy. More patients with STEMI had lipidic arc >90% (36.6 versus 70.8%, P = 0.003), red and mixed thrombus (12.9 versus 28.0% and 7.1 versus 44.0%, respectively, all P < 0.001), plaque rupture (29.4 versus 76.0%, P < 0.001) and TCFA (57.1 versus 84.0%; P = 0.01). Predictors of plaque rupture were STEMI at presentation (odds ratio: 9.35, 95% confidence interval: 1.66-52.61, P = 0.01) and diabetes mellitus (odds ratio: 6.16, 95% confidence interval: 1.33-28.58, P = 0.02). CONCLUSIONS: In this single-center study, the culprit lesion of patients with STEMI had more lipid, red and mixed thrombus, plaque rupture and TCFA versus patients with UA/non-STEMI. Clinical presentation may be driven by distinct pathophysiologic mechanisms in patients with ACS.
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Gomes et al. (2021) conducted an observational in Acute coronary syndrome (n=110). STEMI presentation vs. UA/NSTEMI presentation was evaluated on Plaque rupture (OR 9.35, 95% CI 1.66-52.61, p=0.01). STEMI presentation was a significant predictor of plaque rupture compared to UA/NSTEMI (76.0% vs 29.4%; OR 9.35; 95% CI 1.66-52.61; P=0.01) in patients with acute coronary syndrome.
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