Nonculprit Lesion Plaque Morphology in Patients With ST-Segment–Elevation Myocardial Infarction: Results From the COMPLETE Trial Optical Coherence Tomography Substudys
Complete revascularization with routine percutaneous coronary intervention of nonculprit lesions after primary percutaneous coronary intervention improves outcomes in ST-segment-elevation myocardial infarction. Whether this benefit is associated with nonculprit lesion vulnerability is unknown. In a...
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| Published in | Circulation. Cardiovascular interventions Vol. 13; no. 7; p. e008768 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Heart Association, Inc
01.07.2020
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 1941-7632 1941-7640 1941-7632 |
| DOI | 10.1161/CIRCINTERVENTIONS.119.008768 |
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| Abstract | Complete revascularization with routine percutaneous coronary intervention of nonculprit lesions after primary percutaneous coronary intervention improves outcomes in ST-segment-elevation myocardial infarction. Whether this benefit is associated with nonculprit lesion vulnerability is unknown.
In a prospective substudy of the COMPLETEs trial (Complete vs Culprit-Only Revascularization to Treat Multi-Vessel Disease After Early PCI for STEMI), we performed optical coherence tomography of at least 2 coronary arteries before nonculprit lesion percutaneous coronary intervention in 93 patients with ST-segment-elevation myocardial infarction and multivessel disease; and the ST-segment-elevation myocardial infarction culprit vessel if there was unstented segment amenable to imaging. Nonculprit lesions were categorized as obstructive (≥70% stenosis by visual angiographic assessment) or nonobstructive, and as thin-cap fibroatheroma (TCFA) or non-TCFA by optical coherence tomography criteria. TCFA was defined as a lesion with mean fibrous cap thickness <65 μm overlying a lipid arc >90°.
On a patient level, at least one obstructive TCFA was observed in 44/93 (47%) of patients. On a lesion level, there were 58 TCFAs among 150 obstructive nonculprit lesions compared with 74 TCFAs among 275 nonculprit lesions (adjusted TCFA prevalence: 35.4% versus 23.2%,
=0.022). Compared with obstructive non-TCFAs, obstructive TCFAs had similar lesion length (23.1 versus 20.8 mm,
=0.16) but higher lipid quadrants (55.2 versus 19.2,
<0.001), greater mean lipid arc (203.8° versus 84.5°,
<0.001), and more macrophages (97.1% versus 54.4%,
<0.001) and cholesterol crystals (85.8% versus 44.3%,
<0.001). For nonobstructive lesions, TCFA lesions had similar lesion length (16.7 versus 14.6 mm,
=0.11), but more lipid quadrants (36.4 versus 13.5,
<0.001), and greater mean lipid arc (191.8° versus 84.2°,
<0.001) compared with non-TCFA.
Among patients who underwent optical coherence tomography imaging in the COMPLETE trial, nearly 50% had at least one obstructive nonculprit lesion containing complex vulnerable plaque. Obstructive lesions more commonly harbored vulnerable plaque morphology than nonobstructive lesions. This may help explain the benefit of routine percutaneous coronary intervention of obstructive nonculprit lesions in patients with ST-segment-elevation myocardial infarction and multivessel disease. Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01740479s. |
|---|---|
| AbstractList | Complete revascularization with routine percutaneous coronary intervention of nonculprit lesions after primary percutaneous coronary intervention improves outcomes in ST-segment-elevation myocardial infarction. Whether this benefit is associated with nonculprit lesion vulnerability is unknown.
In a prospective substudy of the COMPLETEs trial (Complete vs Culprit-Only Revascularization to Treat Multi-Vessel Disease After Early PCI for STEMI), we performed optical coherence tomography of at least 2 coronary arteries before nonculprit lesion percutaneous coronary intervention in 93 patients with ST-segment-elevation myocardial infarction and multivessel disease; and the ST-segment-elevation myocardial infarction culprit vessel if there was unstented segment amenable to imaging. Nonculprit lesions were categorized as obstructive (≥70% stenosis by visual angiographic assessment) or nonobstructive, and as thin-cap fibroatheroma (TCFA) or non-TCFA by optical coherence tomography criteria. TCFA was defined as a lesion with mean fibrous cap thickness <65 μm overlying a lipid arc >90°.
On a patient level, at least one obstructive TCFA was observed in 44/93 (47%) of patients. On a lesion level, there were 58 TCFAs among 150 obstructive nonculprit lesions compared with 74 TCFAs among 275 nonculprit lesions (adjusted TCFA prevalence: 35.4% versus 23.2%,
=0.022). Compared with obstructive non-TCFAs, obstructive TCFAs had similar lesion length (23.1 versus 20.8 mm,
=0.16) but higher lipid quadrants (55.2 versus 19.2,
<0.001), greater mean lipid arc (203.8° versus 84.5°,
<0.001), and more macrophages (97.1% versus 54.4%,
<0.001) and cholesterol crystals (85.8% versus 44.3%,
<0.001). For nonobstructive lesions, TCFA lesions had similar lesion length (16.7 versus 14.6 mm,
=0.11), but more lipid quadrants (36.4 versus 13.5,
<0.001), and greater mean lipid arc (191.8° versus 84.2°,
<0.001) compared with non-TCFA.
Among patients who underwent optical coherence tomography imaging in the COMPLETE trial, nearly 50% had at least one obstructive nonculprit lesion containing complex vulnerable plaque. Obstructive lesions more commonly harbored vulnerable plaque morphology than nonobstructive lesions. This may help explain the benefit of routine percutaneous coronary intervention of obstructive nonculprit lesions in patients with ST-segment-elevation myocardial infarction and multivessel disease. Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01740479s. Complete revascularization with routine percutaneous coronary intervention of nonculprit lesions after primary percutaneous coronary intervention improves outcomes in ST-segment-elevation myocardial infarction. Whether this benefit is associated with nonculprit lesion vulnerability is unknown.BACKGROUNDComplete revascularization with routine percutaneous coronary intervention of nonculprit lesions after primary percutaneous coronary intervention improves outcomes in ST-segment-elevation myocardial infarction. Whether this benefit is associated with nonculprit lesion vulnerability is unknown.In a prospective substudy of the COMPLETEs trial (Complete vs Culprit-Only Revascularization to Treat Multi-Vessel Disease After Early PCI for STEMI), we performed optical coherence tomography of at least 2 coronary arteries before nonculprit lesion percutaneous coronary intervention in 93 patients with ST-segment-elevation myocardial infarction and multivessel disease; and the ST-segment-elevation myocardial infarction culprit vessel if there was unstented segment amenable to imaging. Nonculprit lesions were categorized as obstructive (≥70% stenosis by visual angiographic assessment) or nonobstructive, and as thin-cap fibroatheroma (TCFA) or non-TCFA by optical coherence tomography criteria. TCFA was defined as a lesion with mean fibrous cap thickness <65 μm overlying a lipid arc >90°.METHODSIn a prospective substudy of the COMPLETEs trial (Complete vs Culprit-Only Revascularization to Treat Multi-Vessel Disease After Early PCI for STEMI), we performed optical coherence tomography of at least 2 coronary arteries before nonculprit lesion percutaneous coronary intervention in 93 patients with ST-segment-elevation myocardial infarction and multivessel disease; and the ST-segment-elevation myocardial infarction culprit vessel if there was unstented segment amenable to imaging. Nonculprit lesions were categorized as obstructive (≥70% stenosis by visual angiographic assessment) or nonobstructive, and as thin-cap fibroatheroma (TCFA) or non-TCFA by optical coherence tomography criteria. TCFA was defined as a lesion with mean fibrous cap thickness <65 μm overlying a lipid arc >90°.On a patient level, at least one obstructive TCFA was observed in 44/93 (47%) of patients. On a lesion level, there were 58 TCFAs among 150 obstructive nonculprit lesions compared with 74 TCFAs among 275 nonculprit lesions (adjusted TCFA prevalence: 35.4% versus 23.2%, P=0.022). Compared with obstructive non-TCFAs, obstructive TCFAs had similar lesion length (23.1 versus 20.8 mm, P=0.16) but higher lipid quadrants (55.2 versus 19.2, P<0.001), greater mean lipid arc (203.8° versus 84.5°, P<0.001), and more macrophages (97.1% versus 54.4%, P<0.001) and cholesterol crystals (85.8% versus 44.3%, P<0.001). For nonobstructive lesions, TCFA lesions had similar lesion length (16.7 versus 14.6 mm, P=0.11), but more lipid quadrants (36.4 versus 13.5, P<0.001), and greater mean lipid arc (191.8° versus 84.2°, P<0.001) compared with non-TCFA.RESULTSOn a patient level, at least one obstructive TCFA was observed in 44/93 (47%) of patients. On a lesion level, there were 58 TCFAs among 150 obstructive nonculprit lesions compared with 74 TCFAs among 275 nonculprit lesions (adjusted TCFA prevalence: 35.4% versus 23.2%, P=0.022). Compared with obstructive non-TCFAs, obstructive TCFAs had similar lesion length (23.1 versus 20.8 mm, P=0.16) but higher lipid quadrants (55.2 versus 19.2, P<0.001), greater mean lipid arc (203.8° versus 84.5°, P<0.001), and more macrophages (97.1% versus 54.4%, P<0.001) and cholesterol crystals (85.8% versus 44.3%, P<0.001). For nonobstructive lesions, TCFA lesions had similar lesion length (16.7 versus 14.6 mm, P=0.11), but more lipid quadrants (36.4 versus 13.5, P<0.001), and greater mean lipid arc (191.8° versus 84.2°, P<0.001) compared with non-TCFA.Among patients who underwent optical coherence tomography imaging in the COMPLETE trial, nearly 50% had at least one obstructive nonculprit lesion containing complex vulnerable plaque. Obstructive lesions more commonly harbored vulnerable plaque morphology than nonobstructive lesions. This may help explain the benefit of routine percutaneous coronary intervention of obstructive nonculprit lesions in patients with ST-segment-elevation myocardial infarction and multivessel disease. Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01740479s.CONCLUSIONSAmong patients who underwent optical coherence tomography imaging in the COMPLETE trial, nearly 50% had at least one obstructive nonculprit lesion containing complex vulnerable plaque. Obstructive lesions more commonly harbored vulnerable plaque morphology than nonobstructive lesions. This may help explain the benefit of routine percutaneous coronary intervention of obstructive nonculprit lesions in patients with ST-segment-elevation myocardial infarction and multivessel disease. Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01740479s. |
| Author | Schampaert, Erick Kassam, Saleem Bainey, Kevin R. Storey, Robert F. Nguyen, Helen Wang, Jia Wood, David A. Meeks, Brandi Mehta, Shamir R. Cantor, Warren J. Sheth, Tej Lavi, Shahar Welsh, Robert C. Mehran, Roxana Pinilla-Echeverri, Natalia Cairns, John A. |
| AuthorAffiliation | Population Health Research Institute, McMaster University and Hamilton Health Sciences, ON, Canada (N.P.-E., S.R.M., J.W., H.N., B.M., T.S.). London Health Sciences Centre, Western University, ON, Canada (S.L.). Hôpital du Sacré-Cœur de Montréal, Université de Montréal, QC, Canada (E.S.). Southlake Regional Health Centre, University of Toronto, ON, Canada (W.J.C.). Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, AB, Canada (K.R.B., R.C.W.). Scarborough Health Network–Centenary site, ON, Canada (S.K.). The Zena A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, NY (R.M.). Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, United Kingdom (R.F.S.). Centre for Cardiovascular Innovation, St Paul’s and Vancouver General Hospitals, University of British Columbia, Vancouver, Canada (D.A.W., J.A.C.) |
| AuthorAffiliation_xml | – name: Population Health Research Institute, McMaster University and Hamilton Health Sciences, ON, Canada (N.P.-E., S.R.M., J.W., H.N., B.M., T.S.). London Health Sciences Centre, Western University, ON, Canada (S.L.). Hôpital du Sacré-Cœur de Montréal, Université de Montréal, QC, Canada (E.S.). Southlake Regional Health Centre, University of Toronto, ON, Canada (W.J.C.). Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, AB, Canada (K.R.B., R.C.W.). Scarborough Health Network–Centenary site, ON, Canada (S.K.). The Zena A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, NY (R.M.). Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, United Kingdom (R.F.S.). Centre for Cardiovascular Innovation, St Paul’s and Vancouver General Hospitals, University of British Columbia, Vancouver, Canada (D.A.W., J.A.C.) |
| Author_xml | – sequence: 1 givenname: Natalia surname: Pinilla-Echeverri fullname: Pinilla-Echeverri, Natalia organization: Population Health Research Institute, McMaster University and Hamilton Health Sciences, ON, Canada (N.P.-E., S.R.M., J.W., H.N., B.M., T.S.). London Health Sciences Centre, Western University, ON, Canada (S.L.). Hôpital du Sacré-Cœur de Montréal, Université de Montréal, QC, Canada (E.S.). Southlake Regional Health Centre, University of Toronto, ON, Canada (W.J.C.). Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, AB, Canada (K.R.B., R.C.W.). Scarborough Health Network–Centenary site, ON, Canada (S.K.). The Zena A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, NY (R.M.). Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, United Kingdom (R.F.S.). Centre for Cardiovascular Innovation, St Paul’s and Vancouver General Hospitals, University of British Columbia, Vancouver, Canada (D.A.W., J.A.C.) – sequence: 2 givenname: Shamir surname: Mehta middlename: R. fullname: Mehta, Shamir R. – sequence: 3 givenname: Jia surname: Wang fullname: Wang, Jia – sequence: 4 givenname: Shahar surname: Lavi fullname: Lavi, Shahar – sequence: 5 givenname: Erick surname: Schampaert fullname: Schampaert, Erick – sequence: 6 givenname: Warren surname: Cantor middlename: J. fullname: Cantor, Warren J. – sequence: 7 givenname: Kevin surname: Bainey middlename: R. fullname: Bainey, Kevin R. – sequence: 8 givenname: Robert surname: Welsh middlename: C. fullname: Welsh, Robert C. – sequence: 9 givenname: Saleem surname: Kassam fullname: Kassam, Saleem – sequence: 10 givenname: Roxana surname: Mehran fullname: Mehran, Roxana – sequence: 11 givenname: Robert surname: Storey middlename: F. fullname: Storey, Robert F. – sequence: 12 givenname: Helen surname: Nguyen fullname: Nguyen, Helen – sequence: 13 givenname: Brandi surname: Meeks fullname: Meeks, Brandi – sequence: 14 givenname: David surname: Wood middlename: A. fullname: Wood, David A. – sequence: 15 givenname: John surname: Cairns middlename: A. fullname: Cairns, John A. – sequence: 16 givenname: Tej surname: Sheth fullname: Sheth, Tej |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32646305$$D View this record in MEDLINE/PubMed |
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