TY - JOUR
T1 - Pancoronary plaque vulnerability in patients with acute coronary syndrome and ruptured culprit plaque
T2 - A 3-vessel optical coherence tomography study
AU - Vergallo, Rocco
AU - Ren, Xuefeng
AU - Yonetsu, Taishi
AU - Kato, Koji
AU - Uemura, Shiro
AU - Yu, Bo
AU - Jia, Haibo
AU - Abtahian, Farhad
AU - Aguirre, Aaron D.
AU - Tian, Jinwei
AU - Hu, Sining
AU - Soeda, Tsunenari
AU - Lee, Hang
AU - McNulty, Iris
AU - Park, Seung Jung
AU - Jang, Yangsoo
AU - Prasad, Abhiram
AU - Lee, Stephen
AU - Zhang, Shaosong
AU - Porto, Italo
AU - Biasucci, Luigi M.
AU - Crea, Filippo
AU - Jang, Ik Kyung
N1 - Funding Information:
This study was supported by grants from LightLab Imaging/St Jude Medical (I.K.J.), the “Enrico ed Enrica Sovena” Foundation, Rome, Italy (R.V.), the Japan Heart Foundation/Bayer Yakuhin Research Grant Abroad and the Mitsukoshi Health and Welfare Foundation (K.K.), the National Natural Science Foundation of China (B.Y. and H.J.), the National Institutes of Health (T32HL094301) (A.A.), and the Dr John Nam Research Fellowship grant. The authors are solely responsible for the design and conduct of this study, all study analyses, and drafting and editing of the manuscript.
PY - 2014/1
Y1 - 2014/1
N2 - 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.
AB - 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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U2 - 10.1016/j.ahj.2013.10.011
DO - 10.1016/j.ahj.2013.10.011
M3 - Article
C2 - 24332143
AN - SCOPUS:84890130307
SN - 0002-8703
VL - 167
SP - 59
EP - 67
JO - American heart journal
JF - American heart journal
IS - 1
ER -