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TCT-599 Not all plaque ruptures are born equal: an optical coherence tomography study
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, VOL. 68, NO. 18, SUPPL B, 2016
TCT-598 Plaque rupture in coronary atherosclerosis is associated with increased plaque structural stress Charis Costopoulos,1 Yuan Huang,2 Adam Brown,3 Patrick Calvert,4 Stephen Hoole,5 Nick West,6 Jonathan Gillard,7 Zhongzhao Teng,8 Martin Bennett9 1 University of Cambridge, LONDON, United Kingdom; 2University of Cambridge; 3Papworth Hospital, Cambridge, United Kingdom; 4United States; 5Papworth Hospital, Cambridge, United Kingdom; 6Papworth hospital, Cambridge, United Kingdom; 7University of Cambridge; 8 University of Cambridge; 9Cambridge University Hospitals, UK, Cambridge, United Kingdom BACKGROUND Plaque rupture is the commonest cause of myocardial infarction, occurring particularly in higher-risk lesions such as fibroatheromas. However, prospective virtual-histology intravascular ultrasound (VH-IVUS) studies indicate that <10% higher-risk plaques cause clinical events over 3-years, indicating that other factors also determine plaque rupture. Plaque rupture occurs when plaque structural stress (PSS) exceeds its mechanical strength; however, the determinants of PSS and its association with plaque rupture are not known. The objective of this study was to identify the determinants of PSS, and the relationship between PSS and plaque rupture. METHODS We analyzed plaque structure and composition in 4,053 VH-IVUS frames from 32 fibroatheromas with rupture from the VIVA study and 32 fibroatheromas without rupture on optical coherence tomography from a stable angina cohort. Mechanical loading in the peri-luminal region was estimated by calculating maximum principal plaque structural stress by finite element analysis. RESULTS PSS increased with increasing lumen area (r¼0.46; p¼0.001), lumen eccentricity (r¼0.32; p¼0.001), and necrotic core 10% (r ¼0.12; p¼0.001), but reduced when dense calcium 10% (r ¼-0.12; p¼0.001). Ruptured fibroatheromas showed higher PSS (133 [90-191] vs. 104kPa [75-142]; p¼0.002) and variation in PSS (55 [37-75] vs. 43kPa [34-59]; p¼0.002) than non-ruptured fibroatheromas. PSS was higher in segments proximal to the rupture site (143 [101-200] vs. 120kPa [78-180]; p¼0.001) vs. distal segments, associated with increased necrotic core (19.1 [11-29] vs. 14.3% [8-23]; p¼0.001) but reduced fibrous/fibrofatty tissue (63.6 [46-78] vs. 72.7% [54-86]; p¼0.001). PSS >135kPa was a good predictor of rupture in higher-risk regions.
B243
CONCLUSION PSS is determined by plaque composition, plaque architecture, and lumen geometry. PSS and PSS variability are increased in plaques with rupture, particularly at proximal segments. Incorporating PSS into plaque assessment may improve identification of rupture-prone plaques. CATEGORIES IMAGING: Vulnerable Plaque
TCT-599 Not all plaque ruptures are born equal: an optical coherence tomography study Hesham Refaat Moustafa Sherif,1 Giampaolo Niccoli,2 Giancarla Scalone3 1 Zagazig university, Zagazig, Egypt; 2Catholic University Clinical Hospital, Rome, Italy; 3Department of Cardiology, Hospital Clinic, Barcelona, Barcelona, Spain BACKGROUND Plaque rupture (PR) represents the most common substrate of coronary thrombosis, in at least 50% of cases. Chronic low grade inflammation is a coommon background for atherosclerosis development, however, increased plaque inflammation may predispose by itself to PR. In the last decade, studies performed by optical coherence tomography (OCT) have allowed to establish the severity of plaque inflammation by assessing macrophage infiltration (MØI). Our retrospective study aimed at assessing the role of plaque inflammation in PR among patients with acute coronary syndrome (ACS) using OCT. METHODS We enrolled fifty-six (56) patients with ACS exhibiting PR at the site of the culprit stenosis identified by OCT. Patients were divided in two cohorts according to the presence of MØI at OCT analysis, defined as signal-rich, distinct, or confluent punctate regions that exceed the intensity of background speckle noise. Serum highsensitivity C-reactive protein (CRP) was measured on admission by latex-enhanced immunophelometric assay. RESULTS Thirty-seven (66%) patients had MØI at the site of PR, while 19 (34%) patients had no evidence of MØI. Patients with MØI showed a higher rate of CRP values > 3 mg/dl as compared to those without MØI (92% vs. 47%, p¼0.004). In contrast, patients without MØI had a higher prevalence of hypertension compared to those with MØI (89% vs. 59%, p¼0.021). Furthermore, the group with MØI exhibited a significantly higher rate of lipid-rich plaques (86% vs. 50%, p¼0.008), a higher rate of multifocal disease (59% vs. 10%, p<0.001) and a MØI in both culprit and remote lesions (97% vs. 0%, p<0.001) compared to those without MØI. At multivariate analysis, CRP value >3 mg/dl was the only independent predictor of MØI in the culprit plaque (OR 8.72, 95% CI 1.78 - 41.67, p¼ 0.007). CONCLUSION In conclusion, PR can be caused by predominant inflammatory or non-inflammatory mechanisms, over a common low grade chronic inflammatory background well known from pathology observations. Keywords. acute coronary syndrome; plaque rupture; optical coherence tomography; systemic inflammation; local inflammation. CATEGORIES IMAGING: Vulnerable Plaque
TCT-600 Impact of myocardial bridging on atherosclerotic plaque vulnerability assessed by OCT Ryotaro Yamada,1 Teruyoshi Kume,2 Yutaka Goryo,3 Terumasa Koyama,4 Kenzo Fukuhara,5 Yasuhiko Kamata,6 Yusuke Kobayashi,7 Hiroshi Okamoto,8 Yoji Neishi,9 Shiro Uemura10 1 Kawasaki Medical School, Kurashiki, Japan; 2Kurashiki, Japan; 3 Kawasaki Medical School; 4Kawasaki Medical School; 5Kawasaki Medical School, Kurashiki, Japan; 6Kawasaki Medical School; 7 Kawasaki Medical School; 8Kawasaki Medical School; 9Kawasaki Medical School, Kurashiki, Japan; 10Kawasaki Medical School, Kurashiki, Japan BACKGROUND A myocardial bridge (MB) that partially covers the left anterior descending coronary artery (LAD) sometimes leads to atherosclerotic plaque formation proximal to the MB because of low shear stress with hemodynamic disturbance. However, it is not clear if the MB is actually related to the atherosclerotic plaque vulnerability. We assessed the hypothesis that a MB detected by angiography potentially impacts atherosclerotic vulnerability assessed by optical coherence tomography (OCT) among angina patients.
TCT-598 Plaque rupture in coronary atherosclerosis is associated with increased plaque structural stress Charis Costopoulos,1 Yuan Huang,2 Adam Brown,3 Patrick Calvert,4 Stephen Hoole,5 Nick West,6 Jonathan Gillard,7 Zhongzhao Teng,8 Martin Bennett9 1 University of Cambridge, LONDON, United Kingdom; 2University of Cambridge; 3Papworth Hospital, Cambridge, United Kingdom; 4United States; 5Papworth Hospital, Cambridge, United Kingdom; 6Papworth hospital, Cambridge, United Kingdom; 7University of Cambridge; 8 University of Cambridge; 9Cambridge University Hospitals, UK, Cambridge, United Kingdom BACKGROUND Plaque rupture is the commonest cause of myocardial infarction, occurring particularly in higher-risk lesions such as fibroatheromas. However, prospective virtual-histology intravascular ultrasound (VH-IVUS) studies indicate that <10% higher-risk plaques cause clinical events over 3-years, indicating that other factors also determine plaque rupture. Plaque rupture occurs when plaque structural stress (PSS) exceeds its mechanical strength; however, the determinants of PSS and its association with plaque rupture are not known. The objective of this study was to identify the determinants of PSS, and the relationship between PSS and plaque rupture. METHODS We analyzed plaque structure and composition in 4,053 VH-IVUS frames from 32 fibroatheromas with rupture from the VIVA study and 32 fibroatheromas without rupture on optical coherence tomography from a stable angina cohort. Mechanical loading in the peri-luminal region was estimated by calculating maximum principal plaque structural stress by finite element analysis. RESULTS PSS increased with increasing lumen area (r¼0.46; p¼0.001), lumen eccentricity (r¼0.32; p¼0.001), and necrotic core 10% (r ¼0.12; p¼0.001), but reduced when dense calcium 10% (r ¼-0.12; p¼0.001). Ruptured fibroatheromas showed higher PSS (133 [90-191] vs. 104kPa [75-142]; p¼0.002) and variation in PSS (55 [37-75] vs. 43kPa [34-59]; p¼0.002) than non-ruptured fibroatheromas. PSS was higher in segments proximal to the rupture site (143 [101-200] vs. 120kPa [78-180]; p¼0.001) vs. distal segments, associated with increased necrotic core (19.1 [11-29] vs. 14.3% [8-23]; p¼0.001) but reduced fibrous/fibrofatty tissue (63.6 [46-78] vs. 72.7% [54-86]; p¼0.001). PSS >135kPa was a good predictor of rupture in higher-risk regions.
B243
CONCLUSION PSS is determined by plaque composition, plaque architecture, and lumen geometry. PSS and PSS variability are increased in plaques with rupture, particularly at proximal segments. Incorporating PSS into plaque assessment may improve identification of rupture-prone plaques. CATEGORIES IMAGING: Vulnerable Plaque
TCT-599 Not all plaque ruptures are born equal: an optical coherence tomography study Hesham Refaat Moustafa Sherif,1 Giampaolo Niccoli,2 Giancarla Scalone3 1 Zagazig university, Zagazig, Egypt; 2Catholic University Clinical Hospital, Rome, Italy; 3Department of Cardiology, Hospital Clinic, Barcelona, Barcelona, Spain BACKGROUND Plaque rupture (PR) represents the most common substrate of coronary thrombosis, in at least 50% of cases. Chronic low grade inflammation is a coommon background for atherosclerosis development, however, increased plaque inflammation may predispose by itself to PR. In the last decade, studies performed by optical coherence tomography (OCT) have allowed to establish the severity of plaque inflammation by assessing macrophage infiltration (MØI). Our retrospective study aimed at assessing the role of plaque inflammation in PR among patients with acute coronary syndrome (ACS) using OCT. METHODS We enrolled fifty-six (56) patients with ACS exhibiting PR at the site of the culprit stenosis identified by OCT. Patients were divided in two cohorts according to the presence of MØI at OCT analysis, defined as signal-rich, distinct, or confluent punctate regions that exceed the intensity of background speckle noise. Serum highsensitivity C-reactive protein (CRP) was measured on admission by latex-enhanced immunophelometric assay. RESULTS Thirty-seven (66%) patients had MØI at the site of PR, while 19 (34%) patients had no evidence of MØI. Patients with MØI showed a higher rate of CRP values > 3 mg/dl as compared to those without MØI (92% vs. 47%, p¼0.004). In contrast, patients without MØI had a higher prevalence of hypertension compared to those with MØI (89% vs. 59%, p¼0.021). Furthermore, the group with MØI exhibited a significantly higher rate of lipid-rich plaques (86% vs. 50%, p¼0.008), a higher rate of multifocal disease (59% vs. 10%, p<0.001) and a MØI in both culprit and remote lesions (97% vs. 0%, p<0.001) compared to those without MØI. At multivariate analysis, CRP value >3 mg/dl was the only independent predictor of MØI in the culprit plaque (OR 8.72, 95% CI 1.78 - 41.67, p¼ 0.007). CONCLUSION In conclusion, PR can be caused by predominant inflammatory or non-inflammatory mechanisms, over a common low grade chronic inflammatory background well known from pathology observations. Keywords. acute coronary syndrome; plaque rupture; optical coherence tomography; systemic inflammation; local inflammation. CATEGORIES IMAGING: Vulnerable Plaque
TCT-600 Impact of myocardial bridging on atherosclerotic plaque vulnerability assessed by OCT Ryotaro Yamada,1 Teruyoshi Kume,2 Yutaka Goryo,3 Terumasa Koyama,4 Kenzo Fukuhara,5 Yasuhiko Kamata,6 Yusuke Kobayashi,7 Hiroshi Okamoto,8 Yoji Neishi,9 Shiro Uemura10 1 Kawasaki Medical School, Kurashiki, Japan; 2Kurashiki, Japan; 3 Kawasaki Medical School; 4Kawasaki Medical School; 5Kawasaki Medical School, Kurashiki, Japan; 6Kawasaki Medical School; 7 Kawasaki Medical School; 8Kawasaki Medical School; 9Kawasaki Medical School, Kurashiki, Japan; 10Kawasaki Medical School, Kurashiki, Japan BACKGROUND A myocardial bridge (MB) that partially covers the left anterior descending coronary artery (LAD) sometimes leads to atherosclerotic plaque formation proximal to the MB because of low shear stress with hemodynamic disturbance. However, it is not clear if the MB is actually related to the atherosclerotic plaque vulnerability. We assessed the hypothesis that a MB detected by angiography potentially impacts atherosclerotic vulnerability assessed by optical coherence tomography (OCT) among angina patients.