Retrograde percutaneous coronary intervention of chronic total occlusion via discontinuous septal channels.

OBJECTIVES: The study aims to investigate the safety and feasibility of retrograde CTO intervention via collateral connection grade 0 (CC-0) septal channel and to identify predictors of collateral tracking failure. BACKGROUND: Guidewire crossing a collateral channel is a critical step for successful retrograde percutaneous coronary intervention (PCI) of chronic total occlusion (CTO). METHODS: Retrograde PCI was attempted in 122 cases of CTO with CC-0 septal collaterals from December 2018 to May 2021. A hydrophilic polymer coating guidewire was used for crossing all intended CC-0 collaterals. A multivariable logistic regression analysis was performed to identify the predictors of guidewire tracking failure via the CC-0 collaterals. RESULTS: Successful guidewire tracking via CC-0 septal channel was achieved in 98 (80.3%) of 122 cases. The independent predictors of CC-0 septal channel guidewire tracking failure included well-developed non-septal collateral (OR: 5.297, 95% CI: 1.107-25.353, p = 0.037) and the ratio length of posterior descending artery (PDA) versus the distance of PDA ostium to cardiac apex ≤2/3 (OR: 3.970, 95% CI: 1.454-10.835, p = 0.007). Collateral perforation, target vessel perforation, and cardiac tamponade occurred in 5 (4.1%), 3 (2.5%), and 6 (4.9%) cases, respectively. There were no complications requiring emergency cardiac surgery or revascularization of nontarget vessel. CONCLUSIONS: Retrograde PCI via CC-0 septal channels with a hydrophilic polymer-coated guidewire is feasible and safe in patients with CTO. Well-developed nonseptal collaterals and short PDA length influence the procedure success and the risk of guidewire tracking failure via CC-0 septal channels.

CFTR Suppresses Neointimal Formation Through Attenuating Proliferation and Migration of Aortic Smooth Muscle Cells.

ABSTRACT: Cystic fibrosis transmembrane conductance regulator (CFTR) plays important roles in arterial functions and the fate of cells. To further understand its function in vascular remodeling, we examined whether CFTR directly regulates platelet-derived growth factor-BB (PDGF-BB)-stimulated vascular smooth muscle cells (VSMCs) proliferation and migration, as well as the balloon injury-induced neointimal formation. The CFTR adenoviral gene delivery was used to evaluate the effects of CFTR on neointimal formation in a rat model of carotid artery balloon injury. The roles of CFTR in PDGF-BB-stimulated VSMC proliferation and migration were detected by mitochondrial tetrazolium assay, wound healing assay, transwell chamber method, western blot, and qPCR. We found that CFTR expression was declined in injured rat carotid arteries, while adenoviral overexpression of CFTR in vivo attenuated neointimal formation in carotid arteries. CFTR overexpression inhibited PDGF-BB-induced VSMC proliferation and migration, whereas CFTR silencing caused the opposite results. Mechanistically, CFTR suppressed the phosphorylation of PDGF receptor ß, serum and glucocorticoid-inducible kinase 1, JNK, p38 and ERK induced by PDGF-BB, and the increased mRNA expression of matrix metalloproteinase-9 and MMP2 induced by PDGF-BB. In conclusion, our results indicated that CFTR may attenuate neointimal formation by suppressing PDGF-BB-induced activation of serum and glucocorticoid-inducible kinase 1 and the JNK/p38/ERK signaling pathway.

Successful treatment of complex coronary chronic total occlusions improves midterm outcomes.

BACKGROUND: Data regarding outcomes of percutaneous coronary intervention (PCI) in patients with chronic total occlusion (CTO) is still limited. Our aim was to evaluate clinical outcomes in patients after successful CTO PCI when compared to patients with failed PCI. METHODS: The cohort study enrolled 145 eligible patients with attempted PCI of CTO. Detailed baseline clinical and procedural data, and in-hospital complications were analyzed. The primary end point was occurrence of major adverse cardiac events (MACE). RESULTS: Median follow-up was 11.49±2.01 months. Successful revascularization was associated with a significantly lower 1-year MACE compared to failed revascularization [hazard ratio (HR): 0.026; 95% confidence interval (CI): 0.004-0.176; P=0.0002]. A J-CTO score of ≥3 was associated with a significantly higher 1-year MACE compared with a J-CTO score of <3 in patients undergoing PCI (HR: 4.819; 95% CI: 1.463-15.870; P=0.0097). Moreover, in patients with a J-CTO score ≥3, success of CTO PCI was associated with significantly lower risk of 1-year MACE than failure of CTO revascularization (HR: 0.114; 95% CI: 0.023-0.569; P=0.0081). Multivariate analysis identified the J-CTO score (HR: 2.10; 95% CI: 1.09-4.04; P=0.026) as a positive predictor, and the success of CTO PCI (HR: 0.17; 95% CI: 0.05-0.59; P=0.005) as a negative significant independent predictor of MACEs. CONCLUSIONS: Among patients with CTOs, high J-CTO score was independently associated with worse clinical outcomes. Furthermore, successful PCI was associated with a lower risk of midterm MACE compared with failed revascularization of CTOs.