Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
Biostatistics Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
JAMA Cardiol. 2018 Mar 1;3(3):207-214. doi: 10.1001/jamacardio.2017.5234.
Patients with culprit plaque rupture are known to have pancoronary plaque vulnerability. However, the characteristics of nonculprit plaques in patients with acute coronary syndromes caused by plaque erosion are unknown.
To investigate the nonculprit plaque phenotype in patients with acute coronary syndrome according to culprit plaque pathology (erosion vs rupture) by 3-vessel optical coherence tomography imaging.
DESIGN, SETTING, AND PARTICIPANTS: In this observational cohort study, between August 2010 and May 2014, 82 patients with acute coronary syndrome who underwent preintervention optical coherence tomography imaging of all 3 major epicardial coronary arteries were enrolled at the Massachusetts General Hospital Optical Coherence Tomography Registry database. Analysis of the data was conducted between November 2016 and July 2017. Patients were classified into 2 groups based on the culprit lesion pathology: 17 patients with culprit plaque erosion and 34 patients with culprit plaque rupture. Thirty-one patients with the absence of culprit rupture or erosion were excluded from further analysis.
Preintervention 3-vessel optical coherence tomography imaging.
Plaque characteristics at the culprit and nonculprit lesions evaluated by optical coherence tomography.
In 51 patients (37 men; mean age, 58.7 years), the characteristics of 51 culprit plaques and 216 nonculprit plaques were analyzed. In patients with culprit erosion, the mean (SD) number of nonculprit plaques per patient was smaller (3.4 [1.9] in erosion vs 4.7 [2.1] in rupture, P = .05). Patient-based analysis showed that none of 17 patients with culprit plaque erosion had nonculprit plaque rupture, whereas 26% of the patients (9 of 34) with culprit plaque rupture had nonculprit plaque rupture (P = .02). Plaque-based analysis showed that, compared with the culprit rupture group (n = 158), the culprit erosion group (n = 58) had lower prevalence of plaque rupture (0% vs 8%; P < .001), macrophage accumulation (29% vs 53%; P = .01), microvessels (21% vs 42%; P = .003), and spotty calcium (5% vs 22%; P = .006) in the nonculprit lesions. The prevalence of lipid-rich plaque, thin-cap fibroatheroma, and thrombus did not differ between the groups.
Compared with those with culprit plaque rupture, patients with acute coronary syndrome caused by culprit plaque erosion had a smaller number of nonculprit plaques and the lower levels of panvascular instability, affirming that distinct pathophysiologic mechanisms operate in plaque erosion and plaque rupture.
已知破裂的罪犯斑块患者具有全冠状动脉斑块易损性。然而,斑块侵蚀引起的急性冠状动脉综合征患者的非罪犯斑块的特征尚不清楚。
通过 3 血管光学相干断层成像术研究根据罪犯斑块病理学(侵蚀与破裂)的急性冠状动脉综合征患者的非罪犯斑块表型。
设计、设置和参与者:在这项观察性队列研究中,2010 年 8 月至 2014 年 5 月间,在马萨诸塞州综合医院光学相干断层扫描登记处数据库中,对所有 3 大心外膜冠状动脉进行了预介入光学相干断层扫描成像的 82 名急性冠状动脉综合征患者入组。数据分析于 2016 年 11 月至 2017 年 7 月进行。根据罪犯病变病理学将患者分为 2 组:17 名罪犯斑块侵蚀患者和 34 名罪犯斑块破裂患者。31 名无罪犯破裂或侵蚀的患者被排除在进一步分析之外。
预介入 3 血管光学相干断层扫描成像。
光学相干断层扫描评估罪犯和非罪犯病变的斑块特征。
在 51 名患者(37 名男性;平均年龄 58.7 岁)中,分析了 51 个罪犯斑块和 216 个非罪犯斑块。在有罪犯侵蚀的患者中,每位患者的平均(SD)非罪犯斑块数量较小(侵蚀为 3.4 [1.9],破裂为 4.7 [2.1],P =.05)。基于患者的分析显示,17 名罪犯斑块侵蚀患者中没有非罪犯斑块破裂,而 34 名罪犯斑块破裂患者中有 26%(9 名)有非罪犯斑块破裂(P =.02)。基于斑块的分析显示,与罪犯破裂组(n = 158)相比,罪犯侵蚀组(n = 58)的非罪犯斑块破裂发生率较低(0% vs 8%;P <.001),斑块内巨噬细胞聚集(29% vs 53%;P =.01),微血管(21% vs 42%;P =.003)和点状钙(5% vs 22%;P =.006)。两组之间富含脂质的斑块、薄帽纤维粥样瘤和血栓的发生率无差异。
与罪犯斑块破裂患者相比,由罪犯斑块侵蚀引起的急性冠状动脉综合征患者的非罪犯斑块数量较少,全血管不稳定程度较低,这证实了斑块侵蚀和斑块破裂的病理生理机制明显不同。