[Evaluation of very early neointimal coverage post drug-eluting stent implantation using optical coherence tomography].

OBJECTIVE: To investigate the neointimal coverage at the very early phase after drug-eluting stent (DES) implantation using optical coherence tomography (OCT). METHODS: OCT examination was performed immediately after stent deployment and about one week post stenting in 12 patients with coronary artery disease to detect neointimal coverage and stent thrombus. Sirolimus eluting stent implantation was also performed in 5 healthy Chinese minipigs, OCT and histopathology examination were made one week later in these minipigs. RESULTS: (1) Twenty-nine DES were implanted in 12 patients. There was no major cardiovascular event post stenting. The mean time of follow-up was (7.7 ± 2.6) d, the mean percentage of stent coverage was (21.8 ± 17.7)%, and neointimal hyperplasia thickness was (42.9 ± 32.2) µm and the percentage of malapposition struts was (1.5 ± 3.0)%, respectively. Mural stent thrombus was found in 2 of the 12 patients (the percentage is 16.7%). (2) In the minipigs model, OCT evidenced that (43.2 ± 11.5)% struts were covered by neointima with a mean neointimal hyperplasia thickness of (24.0 ± 8.5) µm at one week. Histopathology examination illustrated that the neointima was mainly consisted of proteoglycan, inflammation cells, fibrin and organized thrombus at the very early phase after DES implantation, while endothelial cells were barely found on the neointima. CONCLUSIONS: Neointimal coverage is found as early as one week after DES implantation by OCT. The covered struts rate is very low and the main components of neointima are proteoglycan, inflammation cells, fibrin and organized thrombus. Re-endothelialization is rather poor at the very early phase post DES implantation.

Qingyi decoction protects against myocardial injuries induced by severe acute pancreatitis.

BACKGROUND: We studied the protective effects of Qingyi decoction (QYD) (a Traditional Chinese Medicine) against severe acute pancreatitis (SAP)-induced myocardial infarction (MI). AIM: To study the function and mechanism of QYD in the treatment of myocardial injuries induced by SAP. METHODS: Ultrasonic cardiography, hematoxylin and eosin staining, immunohistochemistry, qRT-PCR, western blot, enzyme-linked immunosorbent assays, and apoptosis staining techniques were used to determine the effects of QYD following SAP-induced MI in Sprague-Dawley rats. RESULTS: Our SAP model showed severe myocardial histological abnormalities and marked differences in the symptoms, mortality rate, and ultrasonic cardiography outputs among the different groups compared to the control. The expression of serum cytokines [interleukin (IL)-1ß, IL-6, IL-8, IL-12, amyloid ß, and tumor necrosis factor-α] were significantly higher in the SAP versus QYD treated group (P < 0.05 for all). STIM1 and Orai1 expression in myocardial tissue extracts were significantly decreased post QYD gavage (P < 0.001). There was no significant histological difference between the 2-aminoethyl diphenylborinate inhibitor and QYD groups. The SAP group had a significantly higher apoptosis index score compared to the QYD group (P < 0.001). CONCLUSION: QYD conferred cardio-protection against SAP-induced MI by regulating myocardial-associated protein expression (STIM1 and Orai1).

Comparison of long-term in-stent vascular response between abluminal groove-filled biodegradable polymer sirolimus-eluting stent and durable polymer everolimus-eluting stent: 3-year OCT follow-up from the TARGET I trial.

The study sought to compare long-term optical coherence tomography (OCT)-based in-stent vascular response between the abluminal groove-filled biodegradable polymer sirolimus-eluting stent (SES) and the durable polymer everolimus-eluting stent (EES) in the TARGET I trial. The TARGET I trial was a prospective, multicenter, randomized clinical trial which enrolled 458 patients with single de novo lesions treated by abluminal groove-filled biodegradable polymer SES and EES. A subset of 43 patients underwent angiography and OCT examinations at 3 years. All OCT images were analyzed at 0.4 mm intervals. A similar increase in angiographic late lumen loss was observed in SES and EES (from 0.05 ± 0.05 vs. 0.05 ± 0.05 mm [p = 0.84] at 9 months to 0.25 ± 0.37 vs. 0.26 ± 0.19 mm [p = 0.99] at 3 years, respectively), without significant differences at 3 years in mean neointimal thickness of stent struts (SES: 0.13 ± 0.02 mm vs. EES: 0.13 ± 0.02 mm, p = 0.80); mean percentage of covered struts (SES: 99.2 % vs. EES: 99.3 %, p = 0.53), or malapposed strut rates (SES: 0.08 % vs. EES: 0.06 %, p = 0.15). The OCT-based in-stent vascular response evaluation found similar vascular healing for the two studied devices, indicating that the luminal loss in EES from 9 months to 3 years cannot be imputed on its coated biocompatible polymer.

Optical coherence tomography assessment of a PLGA-polymer with electro-grafting base layer versus a PLA-polymer sirolimus-eluting stent at three-month follow-up: the BuMA-OCT randomised trial.

AIMS: To compare stent strut coverage using optical coherence tomography (OCT) at three-month follow-up between a PLGA-polymer with electro-grafting base layer sirolimus-eluting stent (SES) (BuMA) and a PLA-polymer SES (EXCEL). METHODS AND RESULTS: This prospective, single-centre, non-inferiority randomised BuMA-OCT trial enrolled patients with de novo coronary artery lesions, treated with either the BuMA or the EXCEL stent. The study primary endpoint was OCT-evaluated stent strut coverage at three months. Secondary endpoints were neointimal thickness of stent struts, and incomplete stent apposition evaluated with OCT. A total of 80 patients were randomly assigned to receive the BuMA (n=40) or the EXCEL (n=40) stent. In OCT follow-up (achieved in 86.3% of cases: BuMA, n=33; EXCEL, n=36), the percentage of stent strut coverage was significantly higher in the BuMA vs. the EXCEL group (strut level: 94.2% vs. 90.0%, p<0.01; p(non-inferiority)<0.0001; p(superiority) <0.0001), while the proportion of malapposed struts (strut level: 1.28% vs. 1.80%, p=0.51) and the mean neointimal thickness (strut level: 0.07±0.03 mm vs. 0.06±0.02 mm, p=0.31) were similar. Rates of myocardial infarction (periprocedural non-Q-wave, 7.5% vs. 7.5%, p=1.00) and target lesion failure (7.5% vs. 7.5%, p=1.00) were similar between groups, with no cardiac death or stent thrombosis. CONCLUSIONS: In the BuMA-OCT randomised trial, the novel BuMA PLGA-polymer with electro-grafting base layer SES was superior to the EXCEL PLA-polymer SES in the primary endpoint of stent strut coverage at three-month follow-up.

Excitotoxicity effects of glutamate on human neuroblastoma SH-SY5Y cells via oxidative damage.

OBJECTIVE: To investigate the mechanisms of excitotoxic effects of glutamate on human neuroblastoma SH-SY5Y cells. METHODS: SH-SY5Y cell viability was measured by MTT assay. Other damaged profile was detected by lactate dehydrogenase (LDH) release and by 4', 6-diamidino-2-phenylindole (DAPI) staining. The cytosolic calcium concentration was tested by calcium influx assay. The glutamate-induced oxidative stress was analyzed by cytosolic glutathione assay, superoxide dismutase (SOD) assay and extracellular malondialdehyde (MDA) assay. RESULTS: Glutamate treatment caused damage in SH-SY5Y cells, including the decrease of cell viability, the increase of LDH release and the alterations of morphological structures. Furthermore, the concentration of cytoplasmic calcium in SH-SY5Y cells was not changed within 20 min following glutamate treatment, while cytosolic calcium concentration significantly increased within 24 h after glutamate treatment, which could not be inhibited by MK801, an antagonist of NMDA receptors, or by LY341495, an antagonist of metabotropic glutamate receptors. On the other hand, oxidative damage was observed in SH-SY5Y cells treated with glutamate, including decreases in glutathione content and SOD activity, and elevation of MDA level, all of which could be alleviated by an antioxidant Tanshinone IIA (Tan IIA, a major active ingredient from a Chinese plant Salvia Miltiorrhiza Bge). CONCLUSION: Glutamate exerts toxicity in human neuroblastoma SH-SY5Y cells possibly through oxidative damage, not through calcium homeostasis destruction mediated by NMDA receptors.