Inflammatory Differences in Plaque Erosion and Rupture in Patients With ST‐Segment Elevation Myocardial Infarction
BackgroundPlaque erosion causes 30% of ST‐segment elevation myocardial infarctions, but the underlying cause is unknown. Inflammatory infiltrates are less abundant in erosion compared with rupture in autopsy studies. We hypothesized that erosion and rupture are associated with significant difference...
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Format: | Article |
Language: | English |
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Wiley
2017-05-01
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Series: | Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease |
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Online Access: | https://www.ahajournals.org/doi/10.1161/JAHA.117.005868 |
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author | Sujay Chandran Johnathan Watkins Amina Abdul‐Aziz Manar Shafat Patrick A. Calvert Kristian M. Bowles Marcus D. Flather Stuart A. Rushworth Alisdair D. Ryding |
author_facet | Sujay Chandran Johnathan Watkins Amina Abdul‐Aziz Manar Shafat Patrick A. Calvert Kristian M. Bowles Marcus D. Flather Stuart A. Rushworth Alisdair D. Ryding |
author_sort | Sujay Chandran |
collection | DOAJ |
description | BackgroundPlaque erosion causes 30% of ST‐segment elevation myocardial infarctions, but the underlying cause is unknown. Inflammatory infiltrates are less abundant in erosion compared with rupture in autopsy studies. We hypothesized that erosion and rupture are associated with significant differences in intracoronary cytokines in vivo. Methods and ResultsForty ST‐segment elevation myocardial infarction patients with <6 hours of chest pain were classified as ruptured fibrous cap (RFC) or intact fibrous cap (IFC) using optical coherence tomography. Plasma samples from the infarct‐related artery and a peripheral artery were analyzed for expression of 102 cytokines using arrays; results were confirmed with ELISA. Thrombectomy samples were analyzed for differential mRNA expression using quantitative real‐time polymerase chain reaction. Twenty‐three lesions were classified as RFC (58%), 15 as IFC (38%), and 2 were undefined (4%). In addition, 12% (12 of 102) of cytokines were differentially expressed in both coronary and peripheral plasma. I‐TAC was preferentially expressed in RFC (significance analysis of microarrays adjusted P<0.001; ELISA IFC 10.2 versus RFC 10.8 log2 pg/mL; P=0.042). IFC was associated with preferential expression of epidermal growth factor (significance analysis of microarrays adjusted P<0.001; ELISA IFC 7.42 versus RFC 6.63 log2 pg/mL, P=0.036) and thrombospondin 1 (significance analysis of microarrays adjusted P=0.03; ELISA IFC 10.4 versus RFC 8.65 log2 ng/mL, P=0.0041). Thrombectomy mRNA showed elevated I‐TAC in RFC (P=0.0007) epidermal growth factor expression in IFC (P=0.0264) but no differences in expression of thrombospondin 1. ConclusionsThese results demonstrate differential intracoronary cytokine expression in RFC and IFC. Elevated thrombospondin 1 and epidermal growth factor may play an etiological role in erosion. |
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institution | Directory Open Access Journal |
issn | 2047-9980 |
language | English |
last_indexed | 2024-04-13T15:36:01Z |
publishDate | 2017-05-01 |
publisher | Wiley |
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series | Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease |
spelling | doaj.art-e97e82911e704c39b49de12d5bfe72732022-12-22T02:41:16ZengWileyJournal of the American Heart Association: Cardiovascular and Cerebrovascular Disease2047-99802017-05-016510.1161/JAHA.117.005868Inflammatory Differences in Plaque Erosion and Rupture in Patients With ST‐Segment Elevation Myocardial InfarctionSujay Chandran0Johnathan Watkins1Amina Abdul‐Aziz2Manar Shafat3Patrick A. Calvert4Kristian M. Bowles5Marcus D. Flather6Stuart A. Rushworth7Alisdair D. Ryding8Norfolk and Norwich University Hospital, Norwich, United KingdomPILAR Research and Education, Cambridge, United KingdomNorwich Medical School, University of East Anglia, Norwich, United KingdomNorwich Medical School, University of East Anglia, Norwich, United KingdomPapworth Hospital NHS Foundation Trust, Papworth Everard Cambridge, United KingdomNorfolk and Norwich University Hospital, Norwich, United KingdomNorfolk and Norwich University Hospital, Norwich, United KingdomNorwich Medical School, University of East Anglia, Norwich, United KingdomNorfolk and Norwich University Hospital, Norwich, United KingdomBackgroundPlaque erosion causes 30% of ST‐segment elevation myocardial infarctions, but the underlying cause is unknown. Inflammatory infiltrates are less abundant in erosion compared with rupture in autopsy studies. We hypothesized that erosion and rupture are associated with significant differences in intracoronary cytokines in vivo. Methods and ResultsForty ST‐segment elevation myocardial infarction patients with <6 hours of chest pain were classified as ruptured fibrous cap (RFC) or intact fibrous cap (IFC) using optical coherence tomography. Plasma samples from the infarct‐related artery and a peripheral artery were analyzed for expression of 102 cytokines using arrays; results were confirmed with ELISA. Thrombectomy samples were analyzed for differential mRNA expression using quantitative real‐time polymerase chain reaction. Twenty‐three lesions were classified as RFC (58%), 15 as IFC (38%), and 2 were undefined (4%). In addition, 12% (12 of 102) of cytokines were differentially expressed in both coronary and peripheral plasma. I‐TAC was preferentially expressed in RFC (significance analysis of microarrays adjusted P<0.001; ELISA IFC 10.2 versus RFC 10.8 log2 pg/mL; P=0.042). IFC was associated with preferential expression of epidermal growth factor (significance analysis of microarrays adjusted P<0.001; ELISA IFC 7.42 versus RFC 6.63 log2 pg/mL, P=0.036) and thrombospondin 1 (significance analysis of microarrays adjusted P=0.03; ELISA IFC 10.4 versus RFC 8.65 log2 ng/mL, P=0.0041). Thrombectomy mRNA showed elevated I‐TAC in RFC (P=0.0007) epidermal growth factor expression in IFC (P=0.0264) but no differences in expression of thrombospondin 1. ConclusionsThese results demonstrate differential intracoronary cytokine expression in RFC and IFC. Elevated thrombospondin 1 and epidermal growth factor may play an etiological role in erosion.https://www.ahajournals.org/doi/10.1161/JAHA.117.005868coronary artery diseaseerosioninflammationmyocardial infarctionoptical coherence tomographythrombospondin 1 |
spellingShingle | Sujay Chandran Johnathan Watkins Amina Abdul‐Aziz Manar Shafat Patrick A. Calvert Kristian M. Bowles Marcus D. Flather Stuart A. Rushworth Alisdair D. Ryding Inflammatory Differences in Plaque Erosion and Rupture in Patients With ST‐Segment Elevation Myocardial Infarction Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease coronary artery disease erosion inflammation myocardial infarction optical coherence tomography thrombospondin 1 |
title | Inflammatory Differences in Plaque Erosion and Rupture in Patients With ST‐Segment Elevation Myocardial Infarction |
title_full | Inflammatory Differences in Plaque Erosion and Rupture in Patients With ST‐Segment Elevation Myocardial Infarction |
title_fullStr | Inflammatory Differences in Plaque Erosion and Rupture in Patients With ST‐Segment Elevation Myocardial Infarction |
title_full_unstemmed | Inflammatory Differences in Plaque Erosion and Rupture in Patients With ST‐Segment Elevation Myocardial Infarction |
title_short | Inflammatory Differences in Plaque Erosion and Rupture in Patients With ST‐Segment Elevation Myocardial Infarction |
title_sort | inflammatory differences in plaque erosion and rupture in patients with st segment elevation myocardial infarction |
topic | coronary artery disease erosion inflammation myocardial infarction optical coherence tomography thrombospondin 1 |
url | https://www.ahajournals.org/doi/10.1161/JAHA.117.005868 |
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