A Single-Center Study Using IVUS to Guide Rotational Atherectomy for Chronic Renal Disease's Calcified Coronary Artery.

Objective: To assess the effectiveness and safety of an IVUS-guided rotational atherectomy (RA) percutaneous coronary intervention (PCI) in chronic renal patients with complex coronary calcification who are at risk for contrast-related acute kidney injury (AKI). Methods: From October 2018 to October 2021, 48 patients with chronic renal disease who were receiving PCI with RA at the General Hospital of NingXia Medical University were informed for data collection for this research. They were randomly assigned to the IVUS-guided RA group and the Standard RA group, which did not use IVUS. According to a clinical expert consensus document on rotational atherectomy in China, both PCI procedures were performed. The intravascular ultrasound (IVUS) results from the study group were used to describe the morphology of the lesion and to guide the selection of burrs, balloons, and stents. IVUS and angiography were used to evaluate the outcome in the end. IVUS-guided RA PCI and Standard RA PCI groups' effects and results were contrasted. Results: There were no appreciable differences in the clinical baseline characteristics between the IVUS-guided RA PCI group and the Standard RA PCI group. The average estimated glomerular filtration rate (eGFR) of two groups was (81.42 ± 20.22 vs 82.34 ± 22.19) mL/min/1.73 m2. Most of them (45.8% vs 54.2%) was in stage 60-90 mL/min/1.73m2. When compared to the standard RA PCI group, RA in IVUS-Guided group was more performed electively (87.5% vs 58.3%; p = 0.02). The IVUS-guided RA PCI group was associated with shorter fluoroscopy time (20.6 ± 8.4 vs 36 ± 22; p<0.01) and less contrast amount (32 ±16 vs 184 ±116mL; p<0.01) than Standard-RA group. Five patients in the Standard RA PCI group developed contrast-induced nephropathy, which was 5 times than the IVUS-guided RA PCI group (20.8% VS 4.1%; p=0.19). Conclusion: In chronic renal patients with complex coronary calcification, an IVUS-guided RA PCI technique is effective and safe. It can also lower the volume of contrast and perhaps the incidence of contrast-related AKI.

LncRNA BANCR induced vascular smooth muscle cell proliferation by downregulating miR-34c methylation in atherosclerosis.

Aberrant vascular smooth muscle cell (VSMCs) proliferation involves in the development of atherosclerosis. It reported that Long noncoding BRAF-activated noncoding RNA (BANCR) and miR-34c played opposite roles in the regulation of the proliferation of VSMCs, indicating that there might be a potential interaction between them. This study was to investigate the relationship between BANCR and miR-34c in atherosclerosis. Blood (5 ml) was obtained from 56 patients with atherosclerosis and 56 healthy volunteers after they were fasted overnight, and plasma was extracted from the blood. Human Aortic Smooth Muscle Cells (HASMCs) were used to perform in vitro cell experiments. RT-qPCR was performed to measure the expression of BANCR and miR-34c in plasma and HASMCs. Dual luciferase reporter assay detected the interaction between BANCR and miR-34c. CCK-8 assay was used to assess the effects of BANCR and miR-34c overexpression on the proliferation of HASMCs. Western blotting was used to assess the effects of BANCR and miR-34c overexpression on the protein expression of HMGB1, TNF-ɑ and Bcl-2. In this study, we found that BANCR was upregulated, while miR-34c was downregulated in atherosclerosis. Bioinformatics analysis showed that BANCR and miR-34c could directly interact with each other. Moreover, overexpression of BANCR could decrease the expression of miR-34c in HASMCs, but overexpression of miR-34c could not affect the expression of BANCR. Furthermore, overexpression of BACNR increased miR-34c methylation, and knockdown of endogenous BANCR decreased miR-34c methylation. In addition, overexpression of BANCR reduced the effects of miR-34c on HASMCs proliferation and reversed the effects of miR-34c on HMGB1, TNF-ɑ and Bcl-2 expression. BANCR overexpression could induce HASMCs proliferation by downregulating the miR-34c methylation. Therefore given BANCR upregulation in atherosclerosis, its expression may be considered as a novel and useful biomarker for atherosclerosis prevention and prognosis. However considering the possible effects of other underlying diseases on both BANCR expression and miR-34c in atherosclerosis, further investigation is suggested for future research.