Abstract
Aims
This study aimed to use intravascular ultrasound (IVUS) data to reveal the mechanism of lesion progression in the native coronary circulation proximal to bypass grafts after coronary artery bypass grafting (CABG).
Methods and results
We reviewed IVUS images in 86 patients with an angiographically significant left main coronary artery (LMCA) stenosis. Overall, 41 patients underwent CABG more than 6 months (mean 8.2 ± 6.1 years) previously and had at least one patent graft to the left coronary artery system. The number of patent grafts to the left coronary artery was 1.4 ± 0.7. Comparing patent graft vs. non-CABG groups, external elastic membrane and lumen areas and remodeling index at the minimum lumen area (MLA) site trended smaller with no difference in the plaque & media area. In addition, patients in the patent graft group had more LMCA calcium whether defined by cross-sectional (arc at the MLA site of 141 ± 109° vs. 88 ± 108°, P = 0.025) or longitudinal measurements (calcium length index, calculated as LMCA calcium length divided by total LMCA length, 0.69 ± 0.38 vs. 0.50 ± 0.42, P = 0.035).
Conclusions
Negative remodeling may be the main mechanism of lesion progression proximal to a patent bypass graft, and more calcium was found in LMCA after CABG compared with non-CABG patients.
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Conflict of interest
Dr. Shang receives fund from Zhejiang Provincial Nature Science Foundation (Y2090393) and grant from Boston Scientific Corporation, China. Drs. Pu and Guo receive grants from Boston Scientific Corporation, China. Drs. Mintz and Maehara receive grants/research support from Boston Scientific Corporation and Volcano Corporation. Drs. Leon and Stone are the members of the advisory boards for Boston Scientific Corporation. Dr. Moses is a consultant for Boston Scientific Corporation.
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Shang, Y., Mintz, G.S., Pu, J. et al. Bypass to the left coronary artery system may accelerate left main coronary artery negative remodeling and calcification. Clin Res Cardiol 102, 831–835 (2013). https://doi.org/10.1007/s00392-013-0598-6
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DOI: https://doi.org/10.1007/s00392-013-0598-6