血管内超声在急性心肌梗死中的作用

作者:王江友[1] 鄢华[1] 
单位:武汉亚洲心脏病医院[1]

摘要:
   易损斑块破裂及继发血栓形成是导致急性心肌梗死(Acute Myocardial Infarction,AMI)发生的最重要机制。AMI的典型血管内超声(intravascular ultrasound,IVUS)特征包括斑块破裂、血栓、正性重构、衰减斑块、点状钙化、透亮斑块及薄帽的纤维粥样斑块。无复流现象主要由经皮冠状动脉介入治疗(percutaneous coronary intervention,PCI)过程中斑块破裂碎片及继发的血栓栓塞所导致。灰阶IVUS的一些特征是AMI患者发生无复流现象的独立预测因子,这些特征包括斑块破裂、血栓形成、正性重构、斑块负荷重、PCI术后斑块容积的减少、组织脱垂、大的坏死核心及薄帽的纤维粥样斑块。易引发心血管事件的非罪犯血管病变更倾向于拥有斑块负荷≥70%,更小的管腔面积≤4.0mm2,或称为薄帽的纤维粥样斑块。
关键词:心肌梗死;冠状动脉粥样硬化;血管内超声;冠脉介入治疗
   急性心肌梗死(AMI)主要由自发斑块破裂或侵蚀及继发血栓形成所致[1] 。血管内超声(IVUS)在检测斑块特点、围术期并发症及评估药物治疗后斑块演变方面起到重要的角色。经皮冠状动脉介入治疗(PCI)前,通过IVUS检测能够提供血管管腔大小、斑块及斑块长度,评估斑块形态、钙化程度及血管重构类型;发现易损斑块(包括斑块破裂、血栓形成、斑块衰减、透亮斑块、点状钙化斑块及薄帽的纤维粥样斑块);检测是否存在血管夹层及动脉瘤;决定支架选择的尺寸及长度[2] 。IVUS亦能预测支架植入后远端栓塞及无复流的发生。越来越多研究证实,IVUS的一些特征能够预测围术期心肌梗死的发生,这些特征包括血栓形成[3-4] 、斑块负荷重[3-4] 、正性重构[5-6] 、PCI术后斑块容积的减少[4,7]及薄帽的纤维粥样斑块[8] 。IVUS能够非常有效评估斑块形态变化,并且亦能够预测患者长期临床预后[9-11] 。近期Singh等[12]研究发现,与传统冠脉造影指导PCI相比,IVUS指导AMI患者PCI,能够降低院内死亡率,但增加住院费用及血管并发症,并没有减少住院时间。本文将从AMI患者PCI术前及术后IUVS的发现及预测围术期心肌梗死的能力做一综述。
AMI患者PCI术前血管IVUS特征
斑块破裂

  易损斑块破裂和/或侵蚀及继发血栓形成是急性心肌梗死发生的主要病理机制。图1A提示斑块破裂形成空腔,并且空腔与血管腔相通,靠近管腔面覆盖有残留的薄纤维膜碎片[13] 。斑块破裂典型的IVUS征象为纤维帽出现破口,斑块内部见到血流灌注,并且斑块中的脂质外渗,留下纤维帽而形成空腔。斑块破裂部位通过具有完整管腔轮廓的血管分割,往往提示多发斑块破裂。Hong等[14]研究发现,46%STEMI患者中存在斑块破裂,而NSTEMI为29%;进一步发现,与NSTEMI相比,STEMI患者更倾向于发生多发斑块破裂(19% vs.13%, p=0.14)。然而,斑块空腔横截面积和破裂斑块长度在STEMI与NSTEMI患者中并无差异(2.34±1.16 mm2vs.2.33±1.58 mm2, p=0.9, and 2.69±1.11 mm vs. 2.67±1.67mm, p=0.9)。Kusama等[15]研究报道,斑块破裂与易损病变形态学特征相关,多存在软斑块及正性重构。Yamagishi等[16]研究发现,破裂的斑块常常为软纤维脂质类型,破裂的斑块有较大的斑块容积并较重的斑块负荷,斑块的脂质特性加上斑块的容积,使斑块趋于不稳定,易于破裂。斑块破裂与阻塞性血栓形成存在密切相关,并且斑块破裂的纵向形态亦影响冠脉血流。血栓存在也能够影响IVUS对斑块破裂的检测效能。
血栓
   IVUS识别血栓至少需要满足以下两个特征:独特的低回声团块,透亮的斑点状斑块,斑块内存在通道,斑块内空腔,或存在分离的移动团块(图1B)。血栓典型的IVUS征象为管腔内团状物,分层、分叶,相对为低回声区域。通过IVUS检测血栓的比率相对较低,在于IVUS分辨率受到一定限制。通过注射造影剂或生理盐水冲散瘀滞的血流,清理血管腔,从而能够使得IVUS更好识别血栓。然而,以上提到的特征均未能作为确定诊断血栓的必备条件,并且通过IVUS诊断血栓应当作为怀疑或假设的结论[2] 。Hong等[14]研究发现,在STEMI患者中IVUS检测血栓比率为34%,而在NSTEMI为21%。
正性重构
   冠状动脉血管重构主要通过评估病变处血管外弹力膜横截面积(EEM CSA)来实现。血管重构指数(remodeling index, RI)为斑块处血管外横截面积与临近无斑块处的参考管腔外横截面积的比值。血管正性重构定义为RI>1.05(图1C),RI范围在0.95-1.05定义为中间性重构,而RI<0.95为负性重构[17]。但是目前一般认为RI>1为正性重构,RI<1为负性重构。Hasegawa等[18]研究发现,在AMI患者中,IVUS检测到55%患者存在血管正性重构;另外,与负性重构患者相比,血管正性重构的患者年龄偏大,并且钙化和含微钙化的软斑块更为多见。
衰减斑块
   最近多项临床研究证实[19-21] ,衰减斑块与急性心肌梗死、围术期心肌坏死及介入治疗过程中无复流的发生均存在明显相关。新近的临床研究表明,IVUS回声衰减斑块与冠心病经皮介入治疗患者围手术期心梗或无复流相关。既往IVUS回声衰减斑块的机制曾被推测与微钙化、纤维透明变性、胆固醇结晶、或机化的血栓有关。新的研究发现,IVUS回声衰减斑块背后的机制是含有大的坏死核心的纤维粥样斑块(FA)或含有大的脂质池的病理性内膜增厚(PIT) [22] (图1D)。随着坏死核心或脂质池的增大,IVUS回声衰减发生率增加。脂质/坏死核心的大小与斑块破裂显著相关。Davies等[23]研究发现,当斑块中脂质/坏死核心占斑块面积<40%时,动脉粥样硬化斑块破裂处于高风险状态。而当脂质/坏死核心占斑块面积40%以上时,IVUS回声衰减的发生率最高。此外,表浅的、靠近血管腔面的回声衰减几乎仅见于含坏死核心的FA,并且越靠近管腔,回声衰减越提示为成熟的坏死核心。相反,含有相对年轻的脂质池的PIT,其回声衰减常出现在靠近外膜处,特别是在靠近内膜/中侧边界。 虽然斑块内的胆固醇结晶或微钙化形成对于IVUS回声衰减的形成并非必须,但是,越成熟的动脉粥样硬化斑块,其斑块成分更为复杂和更多异质性,将导致IVUS回声衰减越接近管腔。Wu等[19]研究报道,78%AMI患者存在衰减斑块。Lee等[20]研究发现,在STEMI患者中衰减斑块占39.6%,NSTEMI为17.6%。进一步研究发现,与不存在衰减斑块患者相比,存在衰减斑块患者炎性指标(C-反应蛋白)更高,造影可视的血栓及TIMI血流<2级更为常见,IVUS检测到斑块负荷及血管重构指数更显著,病变处管腔面积更小,并且血栓、正性重构及斑块破裂更为常见。
透亮斑块
  一项随访期为2年的前瞻性临床研究发现,冠脉斑块中存在回声透亮斑块能够增加急性冠脉事件的风险,尤其当这种无回声区位于IVUS斑块表浅部位时[16] 。Thim等[24]研究发现,与回声衰减斑块相比,回声透亮区意味着存在相对较小的坏死核心或脂质池。此外,越靠近血管腔面的无回声区提示越成熟的坏死核心,而斑块深部的无回声区则意味着相对年轻的脂质池。既往对于灰阶IVUS无回声区的确切机制仍然有争议。一些学者推测,无回声应该是均匀组织成分(如脂质池)的标志,而坏死核心是伴有多个组织反射界面的异质性组织,因此应为强回声,而不是低回声。然而,最近由Pu等[22]研究结果发现,实际上无论是脂质池或坏死核心均可以造成IVUS回声透亮斑块。显然,既往单用IVUS回声透亮斑块来识别富含脂质的冠脉斑块是错误的,因为与IVUS回声透亮斑块相比,IVUS回声衰减斑块提示更大的脂质/坏死核心(图1E,F)。当脂质/坏死核心占斑块面积的20-40%时,IVUS回声透亮斑块发生率最高;当脂质/坏死核心占斑块面积>40%以上时,回声衰减斑块出现率最高。
点状钙化
   钙化病变在临床上一直被认为是稳定的病变,但是点状钙化与缺血性心血管事件的发生率增加存在明显有关[25-26] 。既往临床研究表明,与稳定型心绞痛相比,AMI患者钙化类型不同,AMI患者的罪犯病变处存在更多的点状钙化,破裂的冠状动脉斑块往往伴随着点状钙化[27-28] 。最近的研究证实,IVUS点状钙化与不稳定斑块相关。纤维粥样斑块出现IVUS点状钙化比纤维钙化斑块出现的几率更大。其次,与纤维钙化斑块相比,纤维粥样斑块出现更小的IVUS钙化沉积。病理研究表明,点状钙化是心源性猝死的斑块破裂的常见特征,小的钙盐沉积经常出现在FA的纤维帽中(图1G)。这种点状钙化斑块所导致的斑块脆弱增加可能与非钙化斑块成分交界的钙沉积引起的机械不稳定性有关。
薄帽的纤维粥样斑块
   斑块成分在斑块破裂及血栓形成中一直扮演重要的角色,并且后两者是急性冠脉事件发生的罪魁祸首[29] 。含有大的脂质核的纤维粥样斑块相较硬化斑块具有更高的破裂风险[30]。通过虚拟组织学血管内超声(VH-IVUS)将薄帽的纤维粥样斑块定义为坏死核心占斑块面积10%以上,并且至少在连续3帧无纤维组织覆盖的图像中证实,而且斑块负荷至少超过40%(图像1H) [31] 。在绝大部分冠脉血栓及冠脉猝死患者中,薄帽的纤维粥样斑块作为斑块破裂的前体状态[20] 。既往研究发现,与稳定性心绞痛患者相比,VH-IVUS证实的薄帽的纤维粥样斑块更易在AMI患者中发现[32]
AMI患者PCI术后血管IVUS特征
组织脱垂

   在支架植入过程中,支架挤压血管腔内组织导致组织脱垂并不是一个少见临床现象,并且易通过IVUS检测发现(图1I)。PCI术前IVUS发现血管内特征与PCI术组织脱垂的发生存在明显相关,这些特征包括软斑块(非纤维或钙化斑块)、小的血管管腔及斑块负荷重。研究表明,直接PCI发生组织脱垂风险相对较高[33-34] 。既往研究表明,在AMI患者支架植入过程中,发生组织脱垂占27%,并且支架长度、斑块破裂及血管正性重构是组织脱垂发生的独立预测因子;进一步研究发现,组织脱垂、斑块破裂及血栓形成均与支架植入后CK-MB升高独立相关[35]
支架贴壁不良
   支架贴壁不良可被认为是血管内膜延迟愈合的征象或非最优化支架植入的后果。支架贴壁不良也许能够增加支架内血栓形成的风险,主要与支架挤压血管腔内组织有关。Hoeven等[36]对比研究在STEMI患者中使用金属裸支架(BMS)和雷帕霉素药物洗脱支架(SES)发生急性和晚期支架贴壁不良的情况,结果发现SES中发生急性支架贴壁不良占38.5%,BMS为33.8%,两组无统计学差异;然而,晚期支架贴壁不良发生方面,SES(37.5%)明显高于BMS(12.5%);获得性支架贴壁不良,SES患者中被发现存在25.0%,明显高于BMS患者(5.0%);预测急性支架贴壁不良发生风险因素包括血管参考直径大小(SES: OR 3.49, 95% CI 1.29 to 9.43; BMS: OR 28.8, 95% CI 4.25 to 94.5)和球囊压力(BMS: OR 0.74, 95% CI 0.58 to 0.94);预测晚期支架贴壁不良发生风险因素包括糖尿病(SES: OR 0.16, 95% CI 0.02 to 1.35),血管参考直径(BMS: OR 19.2, 95% CI 2.64 to 139.7)及最大球囊扩张压力(BMS: OR 0.74, 95% CI 0.55to 1.00);植入SES支架后,发生获得性支架贴壁不良的患者中, 84%患者发现存在血管正性重构和16%患者存在斑块容量减少。
IVUS预测围术期心肌梗死的角色
   围术期MI或无复流现象常常能够在AMI患者介入治疗期间发生,一旦发生远期预后不佳,目前并无有效药物及治疗手段改善其预后,因此早期识别发生围术期MI或无复流病变至关重要。无复流现象主要由PCI过程中斑块破裂碎片及继发的血栓栓塞所导致。Tanaka等[5]研究报道,脂质池样影像特征和血管外弹力膜横截面积是AMI患者介入手术期间发生无复流现象的独立预测因子。Kusama等[15]研究发现,AMI患者中存在斑块破裂,PCI术后发生无复流现象风险明显增高,并且心肌呈色分级更低。Endo等[37]研究报道,IVUS超声衰减斑块长度≥5mm和斑块破裂与STEMI患者介入治疗后发生无复流现象存在密切相关。既往研究证实,血管正性重构、斑块破裂、IVUS检测到血栓及组织脱垂均与PCI围术期肌钙蛋白升高独立相关[38] 。另有研究证实,组织脱垂、HsCRP及病变处多发斑块破裂与AMI患者PCI术后发生无复流相关[39] 。Ohshima等[40]研究发现,斑块破裂空腔体积是STEMI患者PCI术后发生无复流现象的独立预测因子。然而,虚拟组织学IVUS检测斑块成分与AMI患者PCI术后发生无复流或慢血流现象的相关程度,一直存在争议[41-44] 。最近一项大样本研究关于斑块成分与无复流发生的相关性,结果发现,虚拟组织学IVUS检测到富含坏死核心斑块与无复流发生存在独立相关[8]
总结
   IVUS在PCI术前评估血管几何结构及形态,并且能够提供动脉粥样硬化斑块的定量成分信息方面将是一项非常重要的检测工具。IVUS亦能够额外的用于PCI术后发现组织脱垂及支架贴壁不良等支架植入期间发生的不良事件。另外,IVUS能够检测靶血管病变处斑块性质,预防围术期心肌梗死或无复流现象发生起到重要的作用。虽然,IVUS检测能力受限于其分辨能力较低,但是作为指导临床决策方面(如评估血管尺寸、血管重构及选择支架尺寸及大小)并不逊色于分辨力较高的光学相干断层扫描(OCT)。在AMI患者中,相比于传统造影指导PCI,IVUS指导PCI能够减少死亡率及血管并发症。最近发展的结合IVUS与近红外光谱技术检测斑块性质及成分,想必将来在AMI患者中使用IVUS评估靶血管病变特点,减少支架植入后相关并发症发生将会越来越普遍。

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图1提示:IVUS发现急性心肌梗死患者病变处特征。(A)斑块破裂形成空腔,并且空腔与血管腔相通,靠近管腔面覆盖有残留的薄纤维膜碎片(箭头所示);(B)管腔内团状物,分层、分叶,相对为低回声区域(箭头所示);(C)血管正性重构,重构指数为1.21;(D)衰减斑块即含有大的坏死核心的纤维粥样斑块(FA)或含有大的脂质池的病理性内膜增厚(PIT),IVUS显示低回声区,无钙化及高密度纤维斑块;(E)透亮斑块为纤维粥样斑块内富含成熟的坏死核心,IVUS回声透亮出现在表浅的、靠近血管腔面(箭头所示);(F)透亮斑块为含有大的脂质池的病理性内膜增厚(PIT),IVUS回声透亮出现在靠近血管外膜处(箭头所示);(H)薄帽的纤维粥样斑块,IVUS提示坏死核心占斑块面积35.4%,斑块负荷为83.3%;(I)在支架植入过程中,支架挤压血管腔内组织导致组织脱垂(箭头所示)。

 

 

 

 


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