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Nonculprit Vulnerable Plaques and Prognosis in Myocardial Infarction With Versus Without ST-Segment Elevation: A PROSPECT II Substudy
Department of Cardiology, Aarhus University Hospital, Denmark; Department of Clinical Medicine, Aarhus University, Denmark.
Department of Cardiology, Aarhus University Hospital, Denmark; Department of Clinical Medicine, Aarhus University, Denmark.
New York-Presbyterian Hospital and Division of Cardiology, Columbia University Irving Medical Center, New York, NY, USA; Clinical Trials Center, Cardiovascular Research Foundation, New York, NY, USA.
Department of Cardiology, Aarhus University Hospital, Denmark; Department of Clinical Medicine, Aarhus University, Denmark .
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2025 (English)In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 151, no 25, p. 1767-1779Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Clinical guidelines recommend different revascularization strategies for nonculprit lesions in patients with ST-segment-elevation myocardial infarction (STEMI) versus non-STEMI (NSTEMI). Whether the prevalence of untreated high-risk vulnerable plaques differs in STEMI and NSTEMI and affects their outcomes is unknown.

METHODS: In PROSPECT II (Providing Regional Observations to Study Predictors of Events in the Coronary Tree II), a multicenter, prospective natural history study, patients with recent myocardial infarction underwent 3-vessel coronary angiography with coregistered near-infrared spectroscopy and intravascular ultrasound after successful percutaneous coronary intervention of obstructive lesions from 2014 through 2017. Two-feature high-risk plaques were defined as those with both plaque burden ≥70% and maximum lipid core burden index over any 4-mm segment ≥324.7. The primary end point was major adverse cardiovascular events arising from untreated nonculprit lesions during a median 3.7-year follow-up.

RESULTS: Of 898 patients, 199 (22.2%) with 849 nonculprit lesions had STEMI and 699 (77.8%) with 2784 nonculprit lesions had NSTEMI. By intravascular ultrasound, the median nonculprit lesion length was 17.4 mm (interquartile range, 16.3-18.5) in STEMI and 17.7 mm (interquartile range, 17.1-18.4) in NSTEMI (P=0.63), and the median minimal lumen area was 5.5 mm2 (interquartile range, 5.3-5.7 mm2) in STEMI and 5.5 mm2 (interquartile range, 5.3-5.6 mm2) in NSTEMI (P=0.99). At the lesion level, the prevalence of 2-feature high-risk nonobstructive nonculprit plaques was slightly higher in patients with STEMI than in patients with NSTEMI (12.8% versus 10.1%; P=0.03). At the patient level, however, the prevalence of 2-feature high-risk plaques was similar in STEMI versus NSTEMI (38.8% versus 32.7%; P=0.11). The prevalence of patients with 1 or more lesions meeting at least 1 high-risk plaque criterion was also similar (plaque burden ≥70%, 63.3% versus 57.8% [P=0.16]; maximum lipid core burden index over any 4-mm segment ≥324.7, 63.3% versus 57.6% [P=0.15]). The 4-year rates of nonculprit lesion-related major adverse cardiovascular events were similar in STEMI versus NSTEMI (8.6% versus 7.8%; hazard ratio, 1.02 [95% CI, 0.57-1.81]; P=0.95), as were the rates of all major adverse cardiovascular events (14.2% versus 13.0%; hazard ratio, 1.06 [95% CI, 0.68-1.64]; P=0.80).

CONCLUSIONS: In the PROSPECT II study, the per-patient prevalence of high-risk vulnerable plaques was comparable in STEMI versus NSTEMI, as was the overall long-term incidence of nonculprit lesion-related and all major adverse cardiovascular events. These results support a similar revascularization strategy for nonculprit lesions in patients with STEMI or NSTEMI after culprit lesion management.

REGISTRATION: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02171065.

Place, publisher, year, edition, pages
Lippincott Williams & Wilkins, 2025. Vol. 151, no 25, p. 1767-1779
Keywords [en]
ST elevation myocardial infarction, coronary artery disease, non-ST elevation myocardial infarction, spectroscopy, near-infrared
National Category
Cardiology and Cardiovascular Disease
Identifiers
URN: urn:nbn:se:oru:diva-121850DOI: 10.1161/CIRCULATIONAHA.124.071980ISI: 001511457300005PubMedID: 40549845OAI: oai:DiVA.org:oru-121850DiVA, id: diva2:1976536
Funder
Novo Nordisk Foundation, NNF22OC0074083
Note

Funding Agencies:

This PROSPECT II substudy was supported by a grant from the Novo Nordisk Foundation (grant NNF22OC0074083). The PROSPECT II trial was supported by grant funding from Abbott Vascular, Santa Clara, CA; Infraredx Inc, Bedford, MA; and The Medicines Company, Basel, Switzerland.

Available from: 2025-06-25 Created: 2025-06-25 Last updated: 2025-06-25Bibliographically approved

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