Moreno P R, Falk E, Palacios I F, Newell J B, Fuster V, Fallon J T
Cardiovascular Pathology Research Laboratory, Massachusetts General Hospital, Boston.
Circulation. 1994 Aug;90(2):775-8. doi: 10.1161/01.cir.90.2.775.
Rupture of atherosclerotic plaques is probably the most important mechanism underlying the sudden onset of acute coronary syndromes. Macrophages may release lytic enzymes that degrade the fibrous cap and therefore produce rupture of the atherosclerotic plaque. This study was designed to quantify macrophage content in coronary plaque tissue from patients with stable and unstable coronary syndromes.
Hematoxylin and eosin and immunostaining with anti-human macrophage monoclonal antibody (PG-M1) were performed. Computerized planimetry was used to analyze 26 atherectomy specimens comprising 524 pieces of tissue from 8 patients with chronic stable angina, 8 patients with unstable angina, and 10 patients with non-Q-wave myocardial infarction. Total plaque area was 417 +/- 87 mm2 x 10(-2) in patients with stable angina, 601 +/- 157 mm2 x 10(-2) in patients with unstable angina, and 499 +/- 87 mm2 x 10(-2) in patients with non-Q-wave myocardial infarction (P = NS). The macrophage-rich area was larger in plaques from patients with unstable angina (61 +/- 18 mm2 x 10(-2)) and non-Q-wave myocardial infarction (87 +/- 32 mm2 x 10(-2)) than in plaques from patients with stable angina (14 +/- 5 mm2 x 10(-2)) (P = .024). The percentage of the total plaque area occupied by macrophages was also larger in patients with unstable angina (13.3 +/- 5.6%) and non-Q-wave myocardial infarction (14.6 +/- 4.6%) than in patients with stable angina (3.14 +/- 1%) (P = .018). Macrophage-rich sclerotic tissue was largest in patients with non-Q-wave myocardial infarction (67 +/- 30 mm2 x 10(-2)) and unstable angina (55 +/- 19 mm2 x 10(-2)) than in patients with stable angina (11.5 +/- 4.1 mm2 x 10(-2)) (P = .046). Macrophage-rich atheromatous gruel was also largest in patients with non-Q-wave myocardial infarction (15 +/- 4 mm2 x 10(-2)) than in patients with unstable angina (3.3 +/- 1.7 mm2 x 10(-2)) or stable angina (2.4 +/- 1.2 mm2 x 10(-2)) (P = .026).
Macrophage-rich areas are more frequently found in patients with unstable angina and non-Q-wave myocardial infarction. This suggests that macrophages are a marker of unstable atherosclerotic plaques and may play a significant role in the pathophysiology of acute coronary syndromes.
动脉粥样硬化斑块破裂可能是急性冠状动脉综合征突然发作的最重要机制。巨噬细胞可能释放溶解酶，降解纤维帽，从而导致动脉粥样硬化斑块破裂。本研究旨在量化稳定型和不稳定型冠状动脉综合征患者冠状动脉斑块组织中的巨噬细胞含量。
进行苏木精-伊红染色及抗人巨噬细胞单克隆抗体（PG-M1）免疫染色。采用计算机图像分析技术对26例旋切标本进行分析，这些标本包括来自8例慢性稳定型心绞痛患者、8例不稳定型心绞痛患者和10例非Q波心肌梗死患者的524块组织。稳定型心绞痛患者的总斑块面积为417±87mm²×10⁻²，不稳定型心绞痛患者为601±157mm²×10⁻²，非Q波心肌梗死患者为499±87mm²×10⁻²（P=无显著性差异）。不稳定型心绞痛患者（61±18mm²×10⁻²）和非Q波心肌梗死患者（87±32mm²×10⁻²）斑块中富含巨噬细胞的区域大于稳定型心绞痛患者（14±5mm²×10⁻²）（P=0.024）。不稳定型心绞痛患者（13.3±5.6%）和非Q波心肌梗死患者（14.6±4.6%）巨噬细胞占总斑块面积的百分比也高于稳定型心绞痛患者（3.14±1%）（P=0.018）。非Q波心肌梗死患者（67±30mm²×10⁻²）和不稳定型心绞痛患者（55±19mm²×10⁻²）富含巨噬细胞的硬化组织大于稳定型心绞痛患者（11.5±4.1mm²×10⁻²）（P=0.046）。非Q波心肌梗死患者（15±4mm²×10⁻²）富含巨噬细胞的粥样物质也多于不稳定型心绞痛患者（3.3±1.7mm²×10⁻²）或稳定型心绞痛患者（2.4±1.2mm²×10⁻²）（P=0.026）。
不稳定型心绞痛和非Q波心肌梗死患者中更常见富含巨噬细胞的区域。这表明巨噬细胞是不稳定动脉粥样硬化斑块的标志物，可能在急性冠状动脉综合征的病理生理学中起重要作用。
