Author + information
- Annapoorna S. Kini, MD∗ (, )
- Takahiro Yoshimura, MD,
- Yuliya Vengrenyuk, PhD,
- Jossef Amirian, MD,
- Choudhury Hasan, MD,
- Usman Baber, MD,
- Jagat Narula, MD, PhD and
- Samin K. Sharma, MD
- ↵∗Division of Cardiology, Mount Sinai Hospital, One Gustave L. Levy Place, Box 1030, New York, New York 10029
Side branch (SB) occlusion remains a major complication of bifurcation lesion treatment. Although plaque and carina shift are suggested as mechanisms of SB occlusion (1), little is known about underlying plaque morphology and composition of the main vessel (MV) and its potential impact on SB occlusion after MV stenting. Optical coherence tomography (OCT) allows precise evaluation of plaque characteristics, and dedicated bifurcation 3-dimensional (3D) quantitative coronary angiography (QCA) software permits highly accurate lesion assessment (2). The primary aim of this study was to identify the predictors of SB occlusion after MV stenting by OCT and dedicated bifurcation 3D-QCA.
Consecutive patients who underwent coronary stent implantation for bifurcation lesions were studied. 134 bifurcation lesions with SB >1.5 mm by 3D-QCA undergoing MV first stenting were analyzed. All lesions showed Thrombolysis in Myocardial Infarction (TIMI) flow grade 3 in MV and SB at the beginning of the procedure and underwent OCT imaging before MV stenting. SB occlusion was defined as TIMI flow grade ≤2 in SB immediately after MV stenting. True bifurcation was defined as Medina classification (1.1.1), (1.0.1), or (0.1.1) (3). Periprocedural myocardial infarction (MI) was defined as troponin I elevation above 5 times the upper limit of normal.
3D-QCA was performed using the QAngio XA 3D, bifurcation edition (Medis, Leiden, the Netherlands). Reference diameters, bifurcation angles, lesion length, minimal lumen diameter (MLD) and area (MLA), and diameter stenosis (DS) were measured. Bifurcation lesions were divided into 3 segments of interest: proximal MV (MVp), distal MV (MVd), and SB ostium. MVp was defined as between the carina tip and 5 mm proximal to SB ostium, MVd between carina tip and 5 mm distal to SB ostium, and SB ostium at just distal site to the carina tip in SB (Figure 1). MLD, MLA, and DS were obtained in each segment.
OCT images of MV pullbacks were analyzed at 1-mm intervals according to previously validated criteria and as we previously described (4). MV in bifurcation area was divided into MVp and MVd (Figure 1). Reference lumen areas were calculated for each lesion, and minimal lumen area and percent lumen area stenosis were calculated for MVp and MVd. A maximal lipid arc, length, volume index, and minimum fibrous cap thickness were assessed for each lipid plaque (4). Distance from the maximal lipid arc site to bifurcation was also measured. A maximal calcium arc, length, and volume index were measured for each calcified plaque in the same way as lipid. OCT thin-cap fibroatheroma as well as spotty calcification were defined as we previously described (4).
Continuous variables were expressed as mean ± SD or median and interquartile range, and compared using Student t or Mann-Whitney U test. Categorical variables were compared by chi-square or Fisher exact test. Multivariate analysis was performed to identify the independent correlates of SB occlusion. DS of the MVp and SB ostium, maximal lipid arc of the MVp, and minimal cap thickness of the MVp were entered into the multivariate model. Results are reported as unit odds ratios (OR) with 95% confidence intervals (CI). Statistical analyses were performed using SPSS 22.0 statistical software (Chicago, Illinois).
SB occlusion occurred in 17 (12.7%) of 134 bifurcation lesions. Periprocedural MI was more frequent in the cases with SB occlusion (17.6% vs. 1.7%; p = 0.015). Baseline clinical, lesion, and procedural characteristics were similar between the 2 groups, including prevalence of true bifurcation. By 3D-QCA, DS of the MVp and SB ostium were significantly greater in the lesions with SB occlusion (47.9% vs. 38.0%; p = 0.018; 41.1% vs. 28.5%; p = 0.002). Bifurcation angles were not significantly different between the 2 groups. By OCT, the lesions with SB occlusion were characterized by higher prevalence of lipid plaque (94.1% vs. 61.5%; p = 0.008). In the MVp, maximal lipid arc was greater (227.2° vs. 129.0°; p < 0.001), and minimal cap thickness was lower (70.0 vs. 110.0 μm; p = 0.009) in the lesions with SB occlusion, whereas there was no difference in each lipid parameter of the MVd. Calcific parameters were similar except for spotty calcification (Table 1). Multivariate analysis identified maximal lipid arc of the MVp (OR: 1.017; 95% CI: 1.004 to 1.030; p = 0.010), and DS of the SB ostium (OR: 1.089; 95% CI: 1.016 to 1.166; p = 0.016) as independent predictors of SB occlusion.
SB ostial disease has been reported as the major cause of SB occlusion (3,5), and we confirmed this finding by 3D-QCA. In the present study, high lipid content of the proximal MV was found to be an independent predictor of SB occlusion. To the best of our knowledge, this is the first report that showed the association between lipid-rich plaque and SB occlusion. Plaque and carina shift are regarded as 2 main mechanisms of SB occlusion, and it appears likely that plaque is shifted mostly from the proximal MV into the SB (1). Lipid-rich plaque in the proximal MV may play an important role in plaque shift. On the other hand, a large calcified plaque was not associated with SB occlusion. A previous study showed that the proportion of calcified plaques in the proximal MV was lower in the lesions with SB occlusion (5). Calcified plaques might be less prone to plaque shift.
In conclusion, high lipid content of the proximal MV and SB ostial stenosis severity are independent predictors of SB occlusion after MV stenting.
Please note: All authors have reported that they have no relationships relevant to the contents of this paper to disclose. Drs. Kini and Yoshimura contributed equally to this work.
- 2016 American College of Cardiology Foundation
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