Rocco Vergallo1, Xuefeng Ren2, Taishi Yonetsu1, Koji Kato1, Shiro Uemura3, Bo Yu2, Haibo Jia4, Farhad Abtahian1, Aaron D Aguirre5, Jinwei Tian4, Sining Hu4, Tsunenari Soeda1, Hang Lee6, Iris McNulty1, Seung-Jung Park7, Yangsoo Jang8, Abhiram Prasad9, Stephen Lee10, Shaosong Zhang11, Italo Porto12, Luigi M Biasucci13, Filippo Crea13, Ik-Kyung Jang14. 1. Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA. 2. Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, The Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin, China. 3. First Department of Medicine, Nara Medical University, Nara, Japan. 4. Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA; Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, The Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education, Harbin, China. 5. Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA. 6. Biostatistics Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA. 7. Asan Medical Center, Seoul, Republic of Korea. 8. Severance Cardiovascular Hospital, Yonsei University, Seoul, Republic of Korea. 9. Department of Internal Medicine, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN. 10. Department of Medicine, Queen Mary Hospital, Hong Kong University, Hong Kong, China. 11. LightLab Imaging, Inc/St Jude Medical, Westford, MA. 12. Cardiovascular and Neurological Department, San Donato Hospital, Arezzo Italy. 13. Department of Cardiovascular Medicine, Catholic University of the Sacred Heart, Rome, Italy. 14. Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA. Electronic address: ijang@partners.org.
Abstract
BACKGROUND: Recent studies described different clinical and underlying plaque characteristics between patients with and without plaque rupture presenting with acute coronary syndrome (ACS). In light of the systemic nature of atherosclerosis, we hypothesized that nonculprit plaques might also express different morphological features in these 2 groups of patients. METHODS: Thirty-eight patients with ACS who underwent 3-vessel optical coherence tomography imaging were identified from the Massachusetts General Hospital Optical Coherence Tomography Registry. Based on culprit plaque morphology, the study population was divided into 2 groups: patients with plaque rupture at the culprit lesion (group 1) and patients with nonruptured plaque at the culprit lesion (group 2). Prevalence and features of nonculprit plaques were compared between the 2 groups. RESULTS: A total of 118 nonculprit plaques were analyzed. Patients in group 1 (n = 17) had nonculprit plaques with higher prevalence of thin-cap fibroatheroma (52.9% vs 19.0%, P = .029) and disruption (35.3% vs 4.8%, P = .016) compared with patients in group 2 (n = 21). Nonculprit plaques in group 1 showed wider maximum lipid arc (198.9° ± 41.7° vs 170.2° ± 41.9°, P = .003), greater lipid length (7.8 ± 4.4 mm vs 5.1 ± 2.4 mm, P = .003), higher lipid index (1196.9 ± 700.5 vs 747.7 ± 377.3, P = .001), and thinner fibrous cap (107.0 ± 56.5 μm vs 137.3 ± 69.8 μm, P = .035) compared with those in group 2. CONCLUSIONS: The present study showed distinctive features of nonculprit plaques between patients with ACS caused by plaque rupture and patients with ACS caused by nonruptured plaques. Patients with plaque rupture had increased pancoronary vulnerability in nonculprit plaques, suggesting that a more aggressive treatment paradigm aiming at the stabilization of vulnerable plaques may offer additional benefit to these patients.
BACKGROUND: Recent studies described different clinical and underlying plaque characteristics between patients with and without plaque rupture presenting with acute coronary syndrome (ACS). In light of the systemic nature of atherosclerosis, we hypothesized that nonculprit plaques might also express different morphological features in these 2 groups of patients. METHODS: Thirty-eight patients with ACS who underwent 3-vessel optical coherence tomography imaging were identified from the Massachusetts General Hospital Optical Coherence Tomography Registry. Based on culprit plaque morphology, the study population was divided into 2 groups: patients with plaque rupture at the culprit lesion (group 1) and patients with nonruptured plaque at the culprit lesion (group 2). Prevalence and features of nonculprit plaques were compared between the 2 groups. RESULTS: A total of 118 nonculprit plaques were analyzed. Patients in group 1 (n = 17) had nonculprit plaques with higher prevalence of thin-cap fibroatheroma (52.9% vs 19.0%, P = .029) and disruption (35.3% vs 4.8%, P = .016) compared with patients in group 2 (n = 21). Nonculprit plaques in group 1 showed wider maximum lipid arc (198.9° ± 41.7° vs 170.2° ± 41.9°, P = .003), greater lipid length (7.8 ± 4.4 mm vs 5.1 ± 2.4 mm, P = .003), higher lipid index (1196.9 ± 700.5 vs 747.7 ± 377.3, P = .001), and thinner fibrous cap (107.0 ± 56.5 μm vs 137.3 ± 69.8 μm, P = .035) compared with those in group 2. CONCLUSIONS: The present study showed distinctive features of nonculprit plaques between patients with ACS caused by plaque rupture and patients with ACS caused by nonruptured plaques. Patients with plaque rupture had increased pancoronary vulnerability in nonculprit plaques, suggesting that a more aggressive treatment paradigm aiming at the stabilization of vulnerable plaques may offer additional benefit to these patients.
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