COMPARATIVE STUDY
JOURNAL ARTICLE

Pancoronary plaque vulnerability in patients with acute coronary syndrome and ruptured culprit plaque: a 3-vessel optical coherence tomography study

Rocco Vergallo, Xuefeng Ren, Taishi Yonetsu, Koji Kato, Shiro Uemura, Bo Yu, Haibo Jia, Farhad Abtahian, Aaron D Aguirre, Jinwei Tian, Sining Hu, Tsunenari Soeda, Hang Lee, Iris McNulty, Seung-Jung Park, Yangsoo Jang, Abhiram Prasad, Stephen Lee, Shaosong Zhang, Italo Porto, Luigi M Biasucci, Filippo Crea, Ik-Kyung Jang
American Heart Journal 2014, 167 (1): 59-67
24332143

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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