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Thrombosis following plaque rupture is the main cause of acute coronary syndrome, but not all plaque ruptures lead to thrombosis. There are limited in vivo data on the relationship between the morphology of ruptured plaque and thrombosis.We used optical coherence tomography (OCT) to investigate the morphology of plaque rupture and its relation to coronary artery thrombosis in patients with coronary heart disease. Forty-two patients with coronary artery plaque rupture detected by OCT were divided into two groups (with or without thrombus) and the morphological characteristics of ruptured plaque, including fibrous cap thickness and broken cap site, were recorded.The fibrous cap of ruptured plaque with thrombus was significantly thinner compared to caps without thrombus ((57.00 ± 17.00) µm vs. (96.00 ± 48.00) µm; P = 0.0076).Plaque rupture associated with thrombosis occurs primarily in plaque covered by a thin fibrous cap. Thick fibrous caps are associated with greater stability of ruptured plaque.

Edge dissections after coronary stent implantation are associated with increased short-term risk of major adverse cardiovascular events. The incidence and outcome of edge dissections after coronary stent implantation were reportedly different using different imaging techniques. We used optical coherence tomography (OCT) to assess the incidence, morphological findings and related factors of edge dissections after drug-eluting stent (DES) implantation.Totally 42 patients with 43 de novo lesions in 43 native arteries undergoing DES implantation with OCT imaging were enrolled in this study.Nine edge dissections were detected in 43 arteries after DES implantation. There were four morphological patterns of stent edge dissections indentified in this study: (1) superficial intimal tears (n = 3), (2) subintimal dissections (n = 4), (3) split of media (n = 1), (4) disruption of the fibrotic cap of plaque (n = 1). Stent edge expansion and stent expansion were both higher in the group with dissections than those in the group without dissections (1.682 ± 0.425 vs. 1.229 ± 0.285, P = 0.0290; 1.507 ± 0.445 vs. 1.174 ± 0.265, P = 0.0072).The incidence of stent edge dissections detected by OCT was 21%. Stent edge dissection is related with stent edge expansion and stent expansion.

Glioblastoma multiforme (GBM) is the most malignant kind of astrocytic tumors and is associated with a poor prognosis. In this retrospective study, we assessed the clinical, radiological, genetic molecular and treatment factors that influence clinical outcomes of patients with GBM.A total of 116 patients with GBM who received surgery and radiation between January 2006 and December 2007 were included in this study. Kaplan-Meier survival analysis and Cox regression analysis were used to find the factors independently influencing patients' progression free survival (PFS) time and overall survival (OS) time.Age, preoperative Karnofsky Performance Scale (KPS) score, KPS score change at 2 weeks after operation, neurological deficit symptoms, tumor resection extent, maximal tumor diameter, involvement of eloquent cortex or deep structure, involvement of brain lobe, Ki-67 expression level and adjuvant chemotherapy were statistically significant factors (P0.05) for both PFS and OS in the univariate analysis. Cox proportional hazards modeling revealed that ageor= 50 years, preoperative KPS scoreor= 80, KPS score change after operationor= 0, involvement of single frontal lobe, non-eloquent area or deep structure involvement, low Ki-67 expression and adjuvant chemotherapy were independent favorable factors (P0.05) for patients' clinical outcomes.Age at diagnosis, preoperative KPS score, KPS score change at 2 weeks postoperation, involvement of brain lobe, involvement of eloquent cortex or deep structure, Ki-67 expression level and adjuvant chemotherapy correlate significantly with the prognosis of patients with GBM.

Bevacizumab, a humanized monoclonal antibody against vascular endothelial growth factor, has shown promising activity in recurrent malignant gliomas. We reported the treatment response for the combination of bevacizumab and chemotherapy in a series of six patients with recurrent malignant glioma and investigated the molecular alterations in cancer pathways using the surgical biopsies from these patients.Standard therapy with primary resection followed by adjuvant chemoradiotherapy had failed in all patients. Bevacizumab was administered at a dose of 10 mg/kg every 2 weeks. Concomitantly, four patients received temozolomide (50 mgxm(-2)xd(-1)), one patient irinotecan (125 mg/m(2) every 2 weeks) and one patient topotecan (1.2 mgxm(-2)xd(-1)). Response to therapy was mainly determined by magnetic resonance imaging. The expression of Ras, phosphorylated mitogen activated protein kinase (p-MAPK), phosphorylated AKT (p-AKT), phosphorylated mammalian target of rapamycin (p-mTOR) and phosphorylated signal transducer and activator of transcription 3 (p-STAT3) were semiquantitatively assessed by immunohistochemistry using surgical biopsies before the initial treatment.Five of the six patients had a radiographic response. Three were complete response, and two were partial response. Only one patient had progressive disease. The 6-month progession-free survival (PFS) was 33% and the median PFS was 15 weeks, with a range of 6 to more than 60 weeks. Of the three core pathways analyzed in this study, the Ras/MAPK and phosphatidylinositol-3-kinase (PI3K)/AKT/mTOR pathways were more likely to be associated with the treatment response to bevacizumab. In two younger patients (ages50) with complete response, simultaneous overexpression of p-MAPK, p-AKT and p-mTOR might be the crucial feature.Bevacizumab in combination with chemotherapeutic agents may be an effective strategy for patients with recurrent malignant glioma. Activated MAPK and AKT might be possible biomarkers for selecting suitable patients for this targeted therapy.