van der Wal A C, Becker A E, Koch K T, Piek J J, Teeling P, van der Loos C M, David G K
Department of Cardiovascular Pathology, University of Amsterdam, Netherlands.
Heart. 1996 Oct;76(4):312-6. doi: 10.1136/hrt.76.4.312.
To investigate the extent of plaque inflammation in culprit lesions of patients with chronic stable angina.
Retrospective study.
Amsterdam reference centre.
89 consecutive patients who underwent directional coronary atherectomy, 58 of whom met the following inclusion criteria: chronic stable angina (Canadian Cardiovascular Society classification 1-3 (group 1, n = 28)); unstable angina (Braunwald class II (group 2, n = 18)); unstable angina (Braunwald class III (group 3, n = 12)).
Directional atherectomy in patients with angina pectoris.
Tissue areas of culprit lesions occupied by inflammatory cells and smooth muscle cells related to clinically defined ischaemic syndrome.
Areas (% of total surface area (mean (SEM)) rich in smooth muscle cells were larger in patients with chronic stable angina (group 1, 51.2 (20.9)) than in those with unstable angina (group 2, 42.1 (20.5); group 3, 29.5 (19.4)) (1 v 2 and 2 v 3, NS; 1 v 3, P < 0.004). Macrophage rich areas were significantly smaller in patients with stable angina (group 1, 21.8 (11.9)) than in those with unstable angina (group 2, 31.5 (14.6); group 3, 46.4 (16.7)) (1 v 2, P < 0.02; 2 v 3, P < 0.02; 1 v 3, P < 0.001). Mean numbers of T cells per mm2 were as follows: group 1, 17 (9.4); group 2, 25 (15.9); group 3, 41 (30.6) (1 v 2, P 0.04; 2 v 3, P 0.07; 1 v 3, P < 0.001). Areas with HLA-DR positive cells showed the same pattern as macrophages and T cells and were smaller in stable (29.9 (12.4)) than in unstable angina (group 2, 40.4 (17.6); group 3, 52.4 (12.0)) (1 v 2, P < 0.02; 2 v 3, P < 0.05; 1 v 3, P < 0.001).
The inverse relation between the extent of inflammatory activity in plaque tissues of culprit lesions and the clinical stability of the ischaemic syndrome supports the concept that reduction of inflammation favours plaque stabilisation. At the same time, the considerable overlap between groups indicates that patients with clinically stable angina do not all have histologically stable plaques.
研究慢性稳定型心绞痛患者罪犯病变中斑块炎症的程度。
回顾性研究。
阿姆斯特丹参考中心。
89例连续接受定向冠状动脉斑块旋切术的患者，其中58例符合以下纳入标准：慢性稳定型心绞痛（加拿大心血管学会分级1 - 3级（第1组，n = 28））；不稳定型心绞痛（Braunwald II级（第2组，n = 18））；不稳定型心绞痛（Braunwald III级（第3组，n = 12））。
对心绞痛患者进行定向斑块旋切术。
与临床定义的缺血综合征相关的罪犯病变中炎症细胞和平滑肌细胞所占的组织面积。
慢性稳定型心绞痛患者（第1组）富含平滑肌细胞的面积（占总表面积的百分比（均值（标准误））为51.2（20.9））大于不稳定型心绞痛患者（第2组，42.1（20.5）；第3组，29.5（19.4））（第1组与第2组以及第2组与第3组比较，无显著性差异；第1组与第3组比较，P < 0.004）。稳定型心绞痛患者富含巨噬细胞的面积（第1组，21.8（11.9））显著小于不稳定型心绞痛患者（第2组，31.5（14.6）；第3组，46.4（16.7））（第1组与第2组比较，P < 0.02；第2组与第3组比较，P < 0.02；第1组与第3组比较，P < 0.001）。每平方毫米T细胞的平均数量如下：第1组，17（9.4）；第2组，25（15.9）；第3组，41（30.6）（第1组与第2组比较，P = 0.04；第2组与第3组比较，P = 0.07；第1组与第3组比较，P < 0.001）。HLA - DR阳性细胞区域呈现与巨噬细胞和T细胞相同的模式，稳定型心绞痛患者该区域面积（29.9（12.4））小于不稳定型心绞痛患者（第2组，40.4（17.6）；第3组，52.4（12.0））（第1组与第2组比较，P < 0.02；第2组与第3组比较，P < 0.05；第1组与第3组比较，P < 0.001）。
罪犯病变斑块组织中炎症活动程度与缺血综合征临床稳定性之间的负相关关系支持了炎症减轻有利于斑块稳定的概念。同时，各组之间存在相当大的重叠，表明临床稳定型心绞痛患者并非都具有组织学上稳定的斑块。
