プロバイオティクスと健康に関するジャーナル
オープンアクセス

概要

Optical Coherence Tomography Analysis of Clinical and Subclinical Plaque Rupture

Takashi Kubo, Atsushi Tanaka, Hironori Kitabata, Yoshiki Matsuo, Takashi Tanimoto, Kohei Ishibashi, Makoto Orii, Yasutsugu Shiono, Kunihiro Shimamura, Yuichi Ozaki, Yasushi Ino, Toshio Imanishi and Takashi Akasaka

Background: Coronary plaque ruptures occur not only in acute coronary syndrome (ACS) patients but also in non-ACS patients. There is a great interest in the reason why some plaque ruptures lead to ACS but others do not. We used optical coherence tomography (OCT) to identify anatomic features that lead to the development of culprit lesions causing ACS after plaque rupture.

Methods: We assessed 102 plaque ruptures by using OCT and compared lesion morphologies between symptomatic plaque rupture in unstable angina pectoris (UAP; n=67) and silent plaque rupture in stable angina pectoris (SAP; n=35). Results: In the cross-sectional view, rupture was observed at plaque shoulder in 67% of UAP and 71% of SAP (p=0.660). In the longitudinal view, plaque rupture was located proximally to the minimal lumen area (MLA) site in 49% of UAP and 57% of SAP (p=0.449). Distance between the rupture site and the MLA site was similar in UAP and SAP (2.64 ± 1.45 mm vs. 2.99 ± 1.70 mm, p=0.280). Maximal ruptured cavity area was significantly greater in UAP compared with SAP (1.57 ± 0.54 mm2 vs.1.30 ± 0.72 mm2, p=0.032). Lumen area at rupture site (3.00 ± 0.86 mm2 vs. 3.45 ± 1.18 mm2, p=0.030) and MLA (2.69 ± 0.80 mm2 vs. 3.12 ± 1.14 mm2, p=0.029) was significantly smaller in UAP compared with SAP. The frequency of lipid-rich plaque (84% vs. 63%, p=0.019) and intracoronary thrombus (94% vs. 3%, p<0.001) was significantly higher in UAP compared with SAP.

Conclusions: The present OCT study found 4 risk factors linking ruptured plaques to acute coronary syndromes: greater degree of plaque rupture, smaller lumen, lipid-rich plaque, and evidence of thrombus. It is conceivable that the greater degree of plaque rupture in the lipid-rich plaque provokes more increased thrombus formation and the smaller lumen requires less thrombus to precipitate an acute coronary event.