冠状动脉分叉病变的血管内超声研究
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摘要
目的：通过对分叉部位主支和分支血管行IVUS检查,观测动脉粥样硬化斑块及支架内新生内膜的环形分布情况；探讨斑块分布与管壁剪切力的关系；比较冠状动脉分叉部位动脉粥样硬化斑块分布与支架植入术后新生内膜分布的特点。研究支架对于分叉部位斑块及分叉脊重新分布的影响,探讨主支单支架植入后分支血管开口受累的机制及影响因素。
背景：冠状动脉分叉病变的介入治疗约占全部经皮冠状动脉介入治疗(percutaneous coronary intervention, PCI)的15-20%,是目前冠心病介入治疗领域的热点问题之一。即使是药物涂层支架已广泛应用,其靶病变重建率也仍然较高,特别是应用双支架术处理的分叉病变。目前对于冠状动脉分叉病变的治疗越来越倾向于应用由单支架术起始的必要性分支支架术(provisional SB stenting)。但是,主支支架植入后往往会使分支血管开口的狭窄加重,甚至导致分支血管开口完全闭塞,这是分叉病变介入治疗操作过程中最严重的并发症。近期的研究提示分叉脊移位或许是分支血管开口受累的主要机制。但是目前分叉脊移位在分支血管开口狭窄加重中的影响程度尚不清楚,特别是对分支血管开口术后变化的IVUS研究还很少见。
方法：将冠状动脉分叉部位分成3个长度为5mm的节段,即主支血管分叉近端(proximal main vessel, MVp),主支血管分叉远端(distal main vessel, MVd)和分支血管开口(side branch ostium, SBo),分别进行体积学IVUS分析。测量各个节段的血管、管腔和斑块的体积,并将横断面环形等分成4个象限进行分析,分别为分叉脊象限、心肌侧象限,分叉脊对侧象限和心包侧象限,比较各个象限中斑块或者新生内膜的体积及分布的对称情况。比较主支血管单支架植入后主支血管和分支血管的血管、管腔和斑块体积的变化情况,并进行相关及回归分析。
结果：共有102个病变入选纳入斑块分布研究；51处分叉病变纳入新生内膜分布研究,(单支架植入术亚组：27例,双支架植入术亚组：24例；共计82个靶血管节段：MVp22处,MVd41处和SBo19处)；54处分叉病变纳入分支血管开口受累的机制研究。无论在MVp, MVd还是SBo中,都是分叉脊对侧象限的斑块体积最大,其次是心肌侧象限,再次是心包侧象限,分叉脊象限的斑块体积最小(总体P值<0.001,两两比较P值<0.008)。在主支血管中,新生内膜的分布情况存在明显差异(MVp:P=0.007;MVd：P<0.001)；分叉脊象限明显小于分叉脊对侧象限(MVp：P=0.002；MVd:P=0.004)但是,在SBo中,并没有发现这种差异(P=0.422)。进一步研究发现,这种新生内膜分布的差异主要存在于单支架组中(MVp:P=0.042；MVd:P<0.001),而双支架组中,无论在主支还是分支血管中,新生内膜的分布不存在显著性差异(MVp：P=0.106；MVd；P=0.747；SBo：P=0.472)。斑块与新生内膜分布对称性在MVp中未见差别(2.0[1.2,3.7]vs.2.1[1,2,5.6],P=1.0),而在MVd和SBo中,新生内膜分布更加对称(MVd:1.6[0.8,2.8]vs.4.7[2.1,8.7.],P<0.001；SBo：1.0[0.7,3.1]vs.3.1[1.9,4.6],P=0.001)。在主支支架植入后,MVp和MVd的血管体积和管腔体积均明显增大,伴有斑块体积的轻度减少(P<0.001)。同时,SBo的血管体积和管腔体积均明显减少,伴有斑块体积的轻度增加(P<0.001)。在主支支架植入后,分叉脊移位占分支受累程度减少的84±22%,而斑块移位只占16±22%。分支受累程度与分叉脊移位呈显著的正相关(r=0.939,P<0.001),而与斑块移位无关(r=-0.034,P=0.809)。分叉脊移位与MVd的管腔体积增加(r=0.465,P<0.001)相关,斑块移位与MVp的斑块体积减少(r=0.495,P<0.001)相关。术前SBo的血管体积以及SEI(主支血管MVd支架扩张程度)是植入术后分支血管受累的预测因素,得到以下方程：分支血管受累程度=0.049×术前SBo的血管体积+0.827×SEI-1.518(R2=0.369)
结论：冠状动脉分叉部位的斑块分布存在一定的规律,分叉脊对侧象限的斑块最多,其次是心肌侧象限,再次是心包侧象限,分叉脊象限最小。新生内膜的分布与动脉粥样硬化斑块的分布模式相似,即均是在分叉脊对侧象限分布更多,但这只存在于主支血管之中,且这种趋势更不明显。不同的支架植入策略对于新生内膜的分布也是存在明显影响的,这种影响主要表现在分支血管中,而对于分叉近端的主支血管影响有限。分叉脊移位是导致分支开口受累的主要原因,占到其全部受累程度的84±22%,分支受累程度主要受分叉脊移位影响；分叉脊移位主要由于主支血管分叉远端管腔扩张导致,其主要机制是支架植入导致的管腔扩张,而斑块移位主要来自主支血管分叉近端；主支血管分叉远端支架扩张程度是术后分支血管受累的预测因素。
Aim:We performed volumetric IVUS analysis of both the main vessel (MV) and side branch (SB) at the bifurcation site to study the circumferential distribution of atherosclerotic plaques in native coronary bifurcations and neointima in the stented bifurcation lesions with in-stent neointimal proliferation, to discuss the relationship of plaque distribution and wall shear stress distribution, and to compare the pattern of plaque distribution and neointimal distribution. We also aimed to study the contribution of plaque shift and carina shift in SB compromise, to discuss the mechanism and predict factors of side branch compromise after main vessel stenting.
Background:Approximately15%to20%of percutaneous coronary interventions (PCIs) are performed to treat coronary bifurcations, which is one of the hottest issue in PCI. Although drug-eluting stents (DES) have reduced restenosis rates in bifurcation lesions, the late target lesion revascularization is still a problem, especially for2-stent strategy. Nowadays, more and more provisional SB stenting are performed for coronary bifurcation lesions. During the provisional approach, MV stent implantation often aggravates an SB ostial stenosis, inducing SB ostial compromise, or even occlusion, which is the most important procedural complication during bifurcation lesion PCI. Some recent studies have suggested that carina shift may be a more important mechanism of SB compromise. Unfortunately, there has been no systemic study on relative contribution of carina shift and plaque shift using direct evaluation of SB.
Methods:IVUS examinations were performed in three5-mm long coronary segments of interest:the proximal MV (MVp), distal MV (MVd) and SB ostium (SBo). In each segment, the vessel volume, lumen volume, and plaque/neointimal volume were calculated. And every segment was divided into4quedrants:carina, epicardial, abcarinal, and myocardial. In each segment, the plaque/neointimal volume and eccentricity index were compared. We also compared the volumetric changes of vessel, lumen, and plaque of each segment for correlation and regression analysis.
Results:In total,102lesions were included in the plaque distribution study. Fifty-one lesions (27in1-stent subgroup, and24in2-stent subgroup) were enrolled in the neointima distribution study, including82segments (22in MVp,41in MVd and19in SBo). And54lesions in54patients were included in side branch compromise analysis. In the plaque group, the plaque volume differed significantly between the four quadrants (P﹤0.001). In all3segments (MVp, MVd and SBo), the plaque burden was largest in the abcarinal quadrant, followed by the myocardial, epicardial, and carinal quadrants, respectively. In the neointima group, the neointimal burden differed significantly in the MVp and MVd (P=0.007, P﹤0.001, separately), while the four quadrants did not differ in the SB (p=0.422). In the MVp and MVd, the neointimal volume was larger in the abcarinal than the carinal quadrant (in MVp, P=0.002; in MVd, P=0.004). Further analysis indicated that these difference derived from the1-stent subgroup (in MVp,P=0.042; in MVd, P﹤0.001). While in2-stent subgroup, we couldn't find any difference, whatever in MV or SB (in MVp, P=0.106; in MVd, P=0.747; in SBo, P=0.472). When comparing the eccentricity indices between plaque and neointima groups, there was no difference in the MVp (2.0[1.2,3.7] vs.2.1[1.2,5.6], P=1.0), while the neointima group was significantly smaller than plaque group in the MVd (1.6[0.8,2.8] vs.4.7[2.1,8.7], P﹤0.001) and SBo (1.0[0.7,3.1] vs.3.1[1.9,4.6], P=0.001). After MV stenting, the vessel and lumen volume increased significantly in both the MVp and MVd, while the plaque volumes decreased slightly (P﹤0.001). With regard to the SBo, both the lumen and vessel volume decreased, while the plaque volume slightly increased (P﹤0.001). SB compromise was significantly correlated with carina shift (r=0.939, P﹤0.001), but not with plaque shift (r=-0.034, P=0.809). Carina shift was significantly correlated with MVd lumen volume increase (r=0.495, P﹤0.001), and plaque shift was significantly correlated with MVp plaque volume decrease (r=0.495, P﹤0.001). Pre-intervention SBo vessel volume and MVd stent expansion index (SEI) were the predictive factors for SB compromise:
SB compromise=0.049X pre-intervention SBo vessel volume+0.827X SEI-1.518(R2=0.369)
Conelus i ons:Volumetric IVUS examination for coronary bifurcation lesions shows that the circumferential plaque distribution has some regular pattern; it is the largest in the abcarinal quadrant, followed by the myocardial, epicardial, and carinal quadrants, respectively. In neointimal proliferation lesions, the neointima distribution follows a similar pattern only in the MV, with larger neointima volume in the abcarinal quadrant than in the carinal quadrant, but the tendency is less prominent. The different stenting strategy also has different influence on neointima distribution, mainly in MVp, while not in MVd or SBo. Carina shift is the main mechanism of side branch compromise after MV stenting, which contributed84±22%. Carina shift derives from MVd vessel volume change, which is induced by MVd lumen expansion after stent implantation. Whereas plaque shift mainly comes from MVp. MVd stent expansion is the predictive factor for SB compromise after MV stent implantation.
背景：冠状动脉分叉病变的介入治疗约占全部经皮冠状动脉介入治疗(percutaneous coronary intervention, PCI)的15-20%,是目前冠心病介入治疗领域的热点问题之一。即使是药物涂层支架已广泛应用,其靶病变重建率也仍然较高,特别是应用双支架术处理的分叉病变。目前对于冠状动脉分叉病变的治疗越来越倾向于应用由单支架术起始的必要性分支支架术(provisional SB stenting)。但是,主支支架植入后往往会使分支血管开口的狭窄加重,甚至导致分支血管开口完全闭塞,这是分叉病变介入治疗操作过程中最严重的并发症。近期的研究提示分叉脊移位或许是分支血管开口受累的主要机制。但是目前分叉脊移位在分支血管开口狭窄加重中的影响程度尚不清楚,特别是对分支血管开口术后变化的IVUS研究还很少见。
方法：将冠状动脉分叉部位分成3个长度为5mm的节段,即主支血管分叉近端(proximal main vessel, MVp),主支血管分叉远端(distal main vessel, MVd)和分支血管开口(side branch ostium, SBo),分别进行体积学IVUS分析。测量各个节段的血管、管腔和斑块的体积,并将横断面环形等分成4个象限进行分析,分别为分叉脊象限、心肌侧象限,分叉脊对侧象限和心包侧象限,比较各个象限中斑块或者新生内膜的体积及分布的对称情况。比较主支血管单支架植入后主支血管和分支血管的血管、管腔和斑块体积的变化情况,并进行相关及回归分析。
结果：共有102个病变入选纳入斑块分布研究；51处分叉病变纳入新生内膜分布研究,(单支架植入术亚组：27例,双支架植入术亚组：24例；共计82个靶血管节段：MVp22处,MVd41处和SBo19处)；54处分叉病变纳入分支血管开口受累的机制研究。无论在MVp, MVd还是SBo中,都是分叉脊对侧象限的斑块体积最大,其次是心肌侧象限,再次是心包侧象限,分叉脊象限的斑块体积最小(总体P值<0.001,两两比较P值<0.008)。在主支血管中,新生内膜的分布情况存在明显差异(MVp:P=0.007;MVd：P<0.001)；分叉脊象限明显小于分叉脊对侧象限(MVp：P=0.002；MVd:P=0.004)但是,在SBo中,并没有发现这种差异(P=0.422)。进一步研究发现,这种新生内膜分布的差异主要存在于单支架组中(MVp:P=0.042；MVd:P<0.001),而双支架组中,无论在主支还是分支血管中,新生内膜的分布不存在显著性差异(MVp：P=0.106；MVd；P=0.747；SBo：P=0.472)。斑块与新生内膜分布对称性在MVp中未见差别(2.0[1.2,3.7]vs.2.1[1,2,5.6],P=1.0),而在MVd和SBo中,新生内膜分布更加对称(MVd:1.6[0.8,2.8]vs.4.7[2.1,8.7.],P<0.001；SBo：1.0[0.7,3.1]vs.3.1[1.9,4.6],P=0.001)。在主支支架植入后,MVp和MVd的血管体积和管腔体积均明显增大,伴有斑块体积的轻度减少(P<0.001)。同时,SBo的血管体积和管腔体积均明显减少,伴有斑块体积的轻度增加(P<0.001)。在主支支架植入后,分叉脊移位占分支受累程度减少的84±22%,而斑块移位只占16±22%。分支受累程度与分叉脊移位呈显著的正相关(r=0.939,P<0.001),而与斑块移位无关(r=-0.034,P=0.809)。分叉脊移位与MVd的管腔体积增加(r=0.465,P<0.001)相关,斑块移位与MVp的斑块体积减少(r=0.495,P<0.001)相关。术前SBo的血管体积以及SEI(主支血管MVd支架扩张程度)是植入术后分支血管受累的预测因素,得到以下方程：分支血管受累程度=0.049×术前SBo的血管体积+0.827×SEI-1.518(R2=0.369)
结论：冠状动脉分叉部位的斑块分布存在一定的规律,分叉脊对侧象限的斑块最多,其次是心肌侧象限,再次是心包侧象限,分叉脊象限最小。新生内膜的分布与动脉粥样硬化斑块的分布模式相似,即均是在分叉脊对侧象限分布更多,但这只存在于主支血管之中,且这种趋势更不明显。不同的支架植入策略对于新生内膜的分布也是存在明显影响的,这种影响主要表现在分支血管中,而对于分叉近端的主支血管影响有限。分叉脊移位是导致分支开口受累的主要原因,占到其全部受累程度的84±22%,分支受累程度主要受分叉脊移位影响；分叉脊移位主要由于主支血管分叉远端管腔扩张导致,其主要机制是支架植入导致的管腔扩张,而斑块移位主要来自主支血管分叉近端；主支血管分叉远端支架扩张程度是术后分支血管受累的预测因素。
Aim:We performed volumetric IVUS analysis of both the main vessel (MV) and side branch (SB) at the bifurcation site to study the circumferential distribution of atherosclerotic plaques in native coronary bifurcations and neointima in the stented bifurcation lesions with in-stent neointimal proliferation, to discuss the relationship of plaque distribution and wall shear stress distribution, and to compare the pattern of plaque distribution and neointimal distribution. We also aimed to study the contribution of plaque shift and carina shift in SB compromise, to discuss the mechanism and predict factors of side branch compromise after main vessel stenting.
Background:Approximately15%to20%of percutaneous coronary interventions (PCIs) are performed to treat coronary bifurcations, which is one of the hottest issue in PCI. Although drug-eluting stents (DES) have reduced restenosis rates in bifurcation lesions, the late target lesion revascularization is still a problem, especially for2-stent strategy. Nowadays, more and more provisional SB stenting are performed for coronary bifurcation lesions. During the provisional approach, MV stent implantation often aggravates an SB ostial stenosis, inducing SB ostial compromise, or even occlusion, which is the most important procedural complication during bifurcation lesion PCI. Some recent studies have suggested that carina shift may be a more important mechanism of SB compromise. Unfortunately, there has been no systemic study on relative contribution of carina shift and plaque shift using direct evaluation of SB.
Methods:IVUS examinations were performed in three5-mm long coronary segments of interest:the proximal MV (MVp), distal MV (MVd) and SB ostium (SBo). In each segment, the vessel volume, lumen volume, and plaque/neointimal volume were calculated. And every segment was divided into4quedrants:carina, epicardial, abcarinal, and myocardial. In each segment, the plaque/neointimal volume and eccentricity index were compared. We also compared the volumetric changes of vessel, lumen, and plaque of each segment for correlation and regression analysis.
Results:In total,102lesions were included in the plaque distribution study. Fifty-one lesions (27in1-stent subgroup, and24in2-stent subgroup) were enrolled in the neointima distribution study, including82segments (22in MVp,41in MVd and19in SBo). And54lesions in54patients were included in side branch compromise analysis. In the plaque group, the plaque volume differed significantly between the four quadrants (P﹤0.001). In all3segments (MVp, MVd and SBo), the plaque burden was largest in the abcarinal quadrant, followed by the myocardial, epicardial, and carinal quadrants, respectively. In the neointima group, the neointimal burden differed significantly in the MVp and MVd (P=0.007, P﹤0.001, separately), while the four quadrants did not differ in the SB (p=0.422). In the MVp and MVd, the neointimal volume was larger in the abcarinal than the carinal quadrant (in MVp, P=0.002; in MVd, P=0.004). Further analysis indicated that these difference derived from the1-stent subgroup (in MVp,P=0.042; in MVd, P﹤0.001). While in2-stent subgroup, we couldn't find any difference, whatever in MV or SB (in MVp, P=0.106; in MVd, P=0.747; in SBo, P=0.472). When comparing the eccentricity indices between plaque and neointima groups, there was no difference in the MVp (2.0[1.2,3.7] vs.2.1[1.2,5.6], P=1.0), while the neointima group was significantly smaller than plaque group in the MVd (1.6[0.8,2.8] vs.4.7[2.1,8.7], P﹤0.001) and SBo (1.0[0.7,3.1] vs.3.1[1.9,4.6], P=0.001). After MV stenting, the vessel and lumen volume increased significantly in both the MVp and MVd, while the plaque volumes decreased slightly (P﹤0.001). With regard to the SBo, both the lumen and vessel volume decreased, while the plaque volume slightly increased (P﹤0.001). SB compromise was significantly correlated with carina shift (r=0.939, P﹤0.001), but not with plaque shift (r=-0.034, P=0.809). Carina shift was significantly correlated with MVd lumen volume increase (r=0.495, P﹤0.001), and plaque shift was significantly correlated with MVp plaque volume decrease (r=0.495, P﹤0.001). Pre-intervention SBo vessel volume and MVd stent expansion index (SEI) were the predictive factors for SB compromise:
SB compromise=0.049X pre-intervention SBo vessel volume+0.827X SEI-1.518(R2=0.369)
Conelus i ons:Volumetric IVUS examination for coronary bifurcation lesions shows that the circumferential plaque distribution has some regular pattern; it is the largest in the abcarinal quadrant, followed by the myocardial, epicardial, and carinal quadrants, respectively. In neointimal proliferation lesions, the neointima distribution follows a similar pattern only in the MV, with larger neointima volume in the abcarinal quadrant than in the carinal quadrant, but the tendency is less prominent. The different stenting strategy also has different influence on neointima distribution, mainly in MVp, while not in MVd or SBo. Carina shift is the main mechanism of side branch compromise after MV stenting, which contributed84±22%. Carina shift derives from MVd vessel volume change, which is induced by MVd lumen expansion after stent implantation. Whereas plaque shift mainly comes from MVp. MVd stent expansion is the predictive factor for SB compromise after MV stent implantation.
引文
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2. Sharma SK, Kini AS. Coronary Bifurcation Lesions[J]. Cardiology Clinics, 2006,24(2):233-246.
3. Louvard Y, Thomas M, Dzavik V, et al. Classification of coronary artery bifurcation lesions and treatments:time for a consensus![J]. Catheterization and Cardiovascular Interventions,2008,71(2):175-183.
4. Latib A, Colombo A. Bifurcation Disease What Do We Know, What Should We Do?[J]. JACC:Cardiovascular Interventions,2008,1(3):218-226.
5. Tsuchida K, Colombo A, Lefevre T, et al. The clinical outcome of percutaneous treatment of bifurcation lesions in multivessel coronary artery disease with the sirolimus-eluting stent:insights from the Arterial Revascularization Therapies Study part Ⅱ (ARTS Ⅱ)[J]. European Heart Journal,2007,28(4):433-442.
6. Latib A, Moussa Ⅰ, Sheiban Ⅰ, et al. When are two stents needed? Which technique is the best? How to perform?[J]. Eurolntervention 2010,6(Supplement J):J81-J87.
7. Iakovou Ⅰ, Foin N, Andreou A, et al. New strategies in the treatment of coronary bifurcations[J], Herz,2011,36:198-213.
8. Chatzizisis YS, Coskun AU, Jonas M, et al. Role of Endothelial Shear Stress in the Natural History of Coronary Atherosclerosis and Vascular RemodelingMolecular, Cellular, and Vascular Behavior[J]. Journal of the American College of Cardiology,2007,49(25):2379-2393.
9. Cecchi E, Giglioli C, Valente S, et al. Role of hemodynamic shear stress in cardiovascular disease[J]. Atherosclerosis,2011,214(2):249-256.
10. Traub O, Berk BC. Laminar shear stress:mechanisms by which endothelial cells transduce an atheroprotective force[J]. Arterioscler Thromb Vase Biol, 1998,18(5):677-685.
11. Kimura BJ, Russo RJ, Bhargava V, et al. Atheroma morphology and distribution in proximal left anterior descending coronary artery:in vivo observations[J]. J Am Coll Cardiol,1996,27(4):825-831.
12. Badak O, Schoenhagen P, Tsunoda T, et al. Characteristics of atherosclerotic plaque distribution in coronary artery bifurcations:an intravascular ultrasound analysis[J]. Coronary Artery Disease,2003,14(4):309-316.
13. Tsutsui H, Yamagishi M, Uematsu M, et al. Intravascular Ultrasound Evaluation of Plaque Distribution at Curved Coronary Segments[J]. The American Journal of Cardiology,1998,81 (8):977-981.
14. Jeremias A, Huegel H, Lee DP, et al. Spatial orientation of atherosclerotic plaque in non-branching coronary artery segments [J]. Atherosclerosis, 2000,152(1):209-215.
15. van der Giessen AG, Wentzel JJ, Meijboom WB, et al. Plaque and shear stress distribution in human coronary bifurcations:a multislice computed tomography study[J]. EuroIntervention,2009,4(5):654-661.
16. Nakagawa Y, Kimura T, Morimoto T, et al. Incidence and risk factors of late target lesion revascularization after sirolimus-eluting stent implantation (3-year follow-up of the j-Cypher Registry)[J]. The American Journal of Cardiology,2010,106(3):329-336.
17. Richter Y, Groothuis A, Seifert P, et al. Dynamic flow alterations dictate leukocyte adhesion and response to endovascular interventions [J]. The Journal of Clinical Investigation,2004,113(11):1607-1614.
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