Intravascular Ultrasound In Coronary Bifurcation Lesions

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.