Key result
In STEMI patients, plaque rupture with high plasma PTX3 was associated with a higher risk of MACE compared to plaque erosion with low PTX3 (24.1% vs 5.3%; HR 5.63, 95% CI 1.57-20.16, P=0.008).
Why the study?
Culprit-plaque morphology and pentraxin-3 influence coronary disease outcomes, but the prognostic value of combining culprit-plaque morphology and plasma PTX3 in STEMI patients was unclear.
Do culprit-plaque morphology and plasma PTX3 levels predict major adverse cardiovascular events in patients with STEMI?
Cohort (n=236)
Do culprit-plaque morphology and plasma PTX3 levels predict major adverse cardiovascular events in patients with STEMI?
Hazard Ratio: 5.63 (95% CI 1.57–20.16)
Absolute Event Rate: 24.1% vs 5.3%
p-value: p=0.008
Combining culprit-plaque morphology assessed by OCT with plasma PTX3 levels enhances the prediction of major adverse cardiovascular events in patients with STEMI.
High PTX3 with PR or PE flags elevated MACE risk post-STEMI; supports combining OCT morphology and biomarkers to refine stratification in prospective studies.
BACKGROUND: Culprit‑plaque morphology [plaque rupture (PR) and plaque erosion (PE) identified by optical coherence tomography (OCT)] and biomarker of vascular inflammation, pentraxin-3 (PTX3), have been reported to influence clinical outcomes in coronary diseases. We aimed to investigate the prognostic implication of culprit-plaque morphology and plasma PTX3 for major adverse cardiovascular events (MACE) in patients with ST-segment elevation myocardial infarction (STEMI). METHODS: A total of 236 patients were enrolled and divided into four groups: PE/low-PTX3 (n = 57), PE/high-PTX3 (n = 47), PR/low-PTX3 (n = 78) and PR/high-PTX3 (n = 54). MACE was defined as the composite of all-cause death, recurrence of myocardial infarction, stroke and unplanned revascularization of any coronary artery. RESULTS: During the follow-up of 1.9 years, a total of 40 (16.9%) MACE were observed: 5.3% (3 patients) among patients with PE/low-PTX3, 21.3% (10 patients) among patients with PE/high-PTX3, 17.9% (14 patients) among patients with PR/low-PTX3 and 24.1% (13 patients) among patients with PR/high-PTX3 (Log rank P = 0.013). In fully adjusted analyses, patients with high-PTX3 were associated with higher MACE risk (HR: 2.40, 95% CI: 1.26-4.57, P = 0.008). Patients with PR/high-PTX3 (HR: 5.63, 95% CI: 1.57-20.16, P = 0.008) and PE/high-PTX3 (HR: 5.44, 95% CI: 1.46-20.29, P = 0.012) presented higher MACE risk than those with PE/low-PTX3. Adding plasma PTX3 levels and PR to the risk prediction model increased the area under curves to 76.1% (95% CI: 67.6-84.5%) and the NRI (28.1%, 95% CI: 0.3-48.3%, P=0.040) and IDI (2.4%, 95% CI: 0.1-12.9%, P = 0.040). CONCLUSION: Patients with PR/high-PTX3 and PE/high-PTX3 presented a poorer prognosis than those with PE/low-PTX3. Combining the culprit-plaque morphology with PTX3 enhanced the predictive ability for MACE and contributed to better identification of high-risk patients. TRIAL REGISTRATION NUMBER: This study is registered at clinical trials.gov as NCT03593928.
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Wang et al. (2021) conducted a cohort in ST-segment elevation myocardial infarction (STEMI) (n=236). Plaque rupture with high plasma PTX3 vs. Plaque erosion with low plasma PTX3 was evaluated on Major adverse cardiovascular events (MACE), defined as the composite of all-cause death, recurrence of myocardial infarction, stroke and unplanned revascularization of any coronary artery (HR 5.63, 95% CI 1.57-20.16, p=0.008). In STEMI patients, plaque rupture with high plasma PTX3 was associated with a higher risk of MACE compared to plaque erosion with low PTX3 (24.1% vs 5.3%; HR 5.63, 95% CI 1.57-20.16, P=0.008).
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