Dawei Wu

Detection of coronary artery anomalies by dual-source CT coronary angiography

AIM To retrospectively evaluate the clinical value of dual-source computed tomography (DSCT) coronary angiography in the diagnosis of coronary artery anomalies. MATERIALS AND METHODS A large cohort of 3625 consecutive patients, who underwent DSCT coronary angiography in our institute, was reviewed for coronary artery anomalies. All images were evaluated by two experienced readers using axial source images, multi-planar reformations (MPR), maximum intensity projections (MIP) and volume rendering (VR). Coronary artery anomalies were found in 36 patients (male 20, female 16, mean age 48 years, range 15-76 years). Of the 36 patients, 19 patients also underwent conventional coronary angiography (CCA). RESULTS The incidence of coronary artery anomalies was 0.99% (36/3625). Six different types of coronary artery anomalies were diagnosed by DSCT coronary angiography: (1) 11 anomalies of the right coronary artery; (2) five anomalies of the left coronary artery; (3) 10 anomalies of the left circumflex artery; (4) two single coronary artery; (5) one anomalous pulmonary origin of the coronary artery; (6) seven coronary artery fistula. Evaluation of the CCA resulted in a precise diagnosis in 53% (10/19) patients. CONCLUSION DSCT coronary angiography is a good diagnostic tool to examine coronary artery anomalies.

Anatomical features of the cisternal segment of the oculomotor nerve: neurovascular relationships and abnormal compression on magnetic resonance imaging

OBJECT The object of this study was to assess the detailed anatomical features and vascular relationships of the cisternal segment of the oculomotor nerve, and to assess the utility of MR imaging in oculomotor nerve palsy caused by abnormal compression related to arteries and tumors. METHODS The anatomy of the oculomotor nerve was depicted using 3D Fourier transformation constructive interference in steady-state (CISS) MR imaging in 196 volunteers (392 total nerves), in 9 patients with paralysis of the oculomotor nerve, and in 1 preoperative patient with cholesteatoma in the pontine cistern. The vessels adjacent to the oculomotor nerve were detected and compared using 3D time-of-flight MR imaging. The 3D CISS multiplanar reconstruction (MPR) images of the oculomotor nerve in cadavers and in specimens from the cadavers were used to verify the oculomotor nerve shown in the 196 patients. The images were assessed with respect to the demonstration of the oculomotor nerve, the optimal display angles on MPR images, the visualized length of the nerve, neurovascular relationships, and abnormal compression caused by arteries and tumors. RESULTS Three-dimensional CISS MR imaging depicted the cisternal segment of the oculomotor nerve with certainty in 100% of the patients in the transverse, sagittal, and coronal planes. Three-dimensional CISS imaging of the oculomotor nerve in 196 volunteers revealed similar results corresponding to 3D CISS MPR images of cadavers and cadaver specimens. The maximum visualized length of the oculomotor nerve was 14.61 +/- 2.33 mm. The angle between the oculomotor nerve and the median sagittal plane was 24.48 +/- 4.57 degrees on the left and 24.48 +/- 5.07 degrees on the right. The posterior cerebral artery was observed to contact the oculomotor nerve in 216 (55.1%) of 392 nerves, and the superior cerebellar artery was observed to contact the oculomotor nerve in 231 (58.9%) of 392 nerves. The abnormal nerve compression in 9 patients with paralysis of the oculomotor nerve was displayed well in all patients. The adjacent relationship of the oculomotor nerve in 1 preoperative patient with cholesteatoma in the pontine cistern was also demonstrated clearly. CONCLUSIONS Use of 3D CISS sequences and 3D time-of-flight sequences enables accurate identification of the cisternal segment of the oculomotor nerve, neurovascular relationships, and abnormal compression caused by arteries and tumors.

Abdominal aortic intimal flap motion characterization in acute aortic dissection: assessed with retrospective ECG-gated thoracoabdominal aorta dual-source CT angiography.

Objectives To evaluate the feasibility of dose-modulated retrospective ECG-gated thoracoabdominal aorta CT angiography (CTA) assessing abdominal aortic intimal flap motion and investigate the motion characteristics of intimal flap in acute aortic dissection (AAD). Materials and Methods 49 patients who had thoracoabdominal aorta retrospective ECG-gated CTA scan were enrolled. 20 datasets were reconstructed in 5% steps between 0 and 95% of the R-R interval in each case. The aortic intimal flap motion was assessed by measuring the short axis diameters of the true lumen and false lumen 2 cm above of celiac trunk ostium in different R-R intervals. Intimal flap motion and configuration was assessed by two independent observers. Results In these 49 patients, 37 had AAD, 7 had intramural hematoma, and 5 had negative result for acute aortic disorder. 620 datasets of 31 patients who showed double lumens in abdominal aorta were enrolled in evaluating intimal flap motion. The maximum and minimum true lumen diameter were 12.2±4.1 mm (range 2.6∼17.4) and 6.7±4.1 mm (range 0∼15.3) respectively. The range of intimal flap motion in all patients was 5.5±2.6 mm (range 1.8∼10.2). The extent of maximum true lumen diameter decreased during a cardiac cycle was 49.5%±23.5% (range 12%∼100%). The maximum motion phase of true lumen diameter was in systolic phase (5%∼40% of R-R interval). Maximum and minimum intimal flap motion was at 15% and 75% of the R-R interval respectively. Intimal flap configuration had correlation with the phase of cardiac cycle. Conclusions Abdominal intimal flap position and configuration varied greatly during a cardiac cycle. Retrospective ECG-gated thoracoabdominal aorta CTA can reflect the actual status of the true lumen and provide more information about true lumen collapse. This information may be helpful to diagnosis and differential diagnosis of dynamic abstraction.

Low Shear Stress Induced HMGB1 Translocation and Release via PECAM-1/PARP-1 Pathway to Induce Inflammation Response

Low shear stress (LSS) plays a critical role in the site predilection of atherosclerosis through activation of cellular mechanosensors, such as platelet endothelial cell adhesion molecule 1 (PECAM-1). Poly(ADP-ribose) polymerase 1 (PARP-1) is a nuclear enzyme that regulates the expression of various inflammatory cytokines. The nuclear enzyme high mobility group box 1 (HMGB1) can induce inflammation response by binding to toll-like receptor 4 (TLR4). In the present study, we aimed to investigate the role and mechanism of HMGB1 in LSS induced inflammation in human umbilical vein endothelial cells (HUVECs). HUVECs were stimulated by undisturbed shear stress (USS, 1 Pa) and LSS (0.4 Pa) in our experiments. Gene expression was inhibited by small interfering RNA (siRNA). ICAM-1 expression was regulated by LSS in a time dependent manner. LSS can induce HMGB1 translocation from nucleus to cytoplasm and release. Compared with the USS, LSS could increase the protein expression of PECAM-1 and PARP-1 as well as the secretion of TNF-α and IL-1β. LSS induced the translocation of HMGB1 from nucleus to cytoplasm. Inhibition of HGMB1 reduced LSS-induced inflammatory response. Inhibition of PARP-1 suppressed inflammatory response through inhibiting TLR4 expression and HMGB1 translocation. PECAM-1 inhibition reduced LSS-induced ICAM-1 expression, TNF-α and IL-1β secretion, and monocytes adhesion. LSS can induce inflammatory response via PECAM-1/PARP-1/HMGB1 pathway. PARP-1 plays a fundamental role in HMGB1 translocation and TLR4 expression. Inhibition of PARP-1 may shed light on the treatment of HMGB1 involved inflammation during atherosclerosis.

Notch1 inhibition reduces low shear stress-induced plaque formation

Low shear stress (LSS) contributes to the pathogenesis of inflammatory diseases, such as atherosclerosis. Notch1 is a type I transmembrane receptor that critically determines the growth, differentiation, and survival of various cell types, but its role and mechanism in LSS-induced inflammatory response remains undetermined. Apolipoprotein E-deficient (ApoE(-/-)) mice were fed with high fat diet and administered intraperitoneally with DAPT (a γ-secretase inhibitor). Perivascular shear stress modifiers were placed around the right carotid arteries to induce LSS. The left carotid arteries with undisturbed shear stress (USS) were used as the control. LSS increased Delta-like 1 (DLL-1) protein expression and the expression of Notch1 and NICD, while DAPT administration reduced NICD expression. Compared with the LSS group, DAPT reduced LSS-induced plaque formation and intercellular adhesion molecule 1 (ICAM-1) expression. Human umbilical vein endothelial cells (HUVECs) were exposure to undisturbed shear stress (USS, 1Pa) or LSS (0.4Pa). Notch1 was inhibited by siRNA or DAPT. RT-PCR and western blotting analysis showed that LSS upregulated the expression of Notch1 in a time-dependent manner. Caveolin-1 (CAV1) inhibition by siRNA could reduce Notch1 and NICD expression. Compared with USS, LSS increased inflammatory response, including IL-1β and IL-6 secretion, ICAM-1 and inducible nitric oxide synthase (iNOS) expression, and THP-1 cells adhesion. Notch1 inhibition by siRNA or DAPT could reduce these inflammatory responses by reduction of NF-κB phosphorylation, upregulation of IkBα expression, and inhibition of nuclear translocation of NF-κB, while Notch1 activation by DLL-4 had an adverse effect. The Notch signaling system is therefore a potential target for modulating LSS-induced inflammation response during atherosclerosis.

Isoquercitrin protects against pulmonary hypertension via inhibiting PASMCs proliferation

Pulmonary vascular remodelling is a common feature among the heterogeneous disorders that cause pulmonary arterial hypertension (PAH), and pulmonary arterial smooth muscle cells (PASMCs) proliferation impact the long‐term prognosis of the patient. Isoquercitrin (IQC) is a flavonoid with anti‐oxidative, anti‐inflammatory and anti‐proliferative activations. This study aimed to investigate whether IQC could prevent PASMCs proliferation and vascular remodelling in monocrotaline (MCT) induced PAH. Male Wistar rats were administered with Vehicle or 0.1% IQC maintain feed after MCT (40 mg/kg) injection. Haemodynamic changes, right ventricular hypertrophy and lung morphological features were assessed 3 weeks later. MCT‐induced PAH, pulmonary vascular remodelling and PASMCs proliferation in Vehicle‐treated rats. IQC reduced the right ventricle systolic pressure (RVSP), the ratio of RV/LV+S and the RV hypertrophy. IQC significantly alleviated the expression of proliferating cell nuclear antigen (PCNA), smooth muscle α‐actin (α‐SMA), and the percentage of fully muscularized small arterioles. In vitro studies, PASMCs were pretreated with IQC and stimulated with platelet‐derived growth factor (PDGF)‐BB (20 ng/mL). IQC suppressed PDGF‐BB‐induced PASMCs proliferation and caused G0/G1 phase cell cycle arrest. IQC downregulated the expression of Cyclin D1 and CDK4 as well as inhibited p27Kip1 degradation. Meanwhile, IQC negatively modulated PDGF‐BB‐induced phosphorylation of PDGF‐Rβ, Akt/GSK3β and ERK1/2. IQC ameliorated MCT‐induced pulmonary vascular remodelling via suppressing PASMCs proliferation and blocking PDGF‐Rβ signalling pathway.

Ischemia-modified albumin is a predictor of short-term mortality in patients with severe sepsis

Purpose: One of the most important events leading to morbidity and mortality in patients with severe sepsis is the development of global tissue hypoperfusion and oxidative damage. Ischemia‐modified albumin (IMA), an albumin generated under ischemic and oxidative conditions, is a marker of oxidative stress and hypoperfusion. Here, we investigated whether IMA level could predict short‐term mortality with severe sepsis. Methods: A prospective cohort study was conducted from April 2014 to October 2014 in intensive care units in a tertiary hospital. At the onset of severe sepsis, serum IMA level was measured, and baseline and laboratory data, infection sources, and underlying diseases were recorded; Sequential Organ Failure Assessment and Acute Physiology and Chronic Health Evaluation II scores were calculated. Multivariate logistic regression and receiver operating characteristic curve analyses were used to evaluate predictors of mortality. Kaplan‐Meier analysis was used to compare survival at day 28. Results: A total of 117 patients with severe sepsis were included (overall 28‐day mortality, 24.8%). The IMA level was higher in nonsurvivors than in survivors (P < .05). It was a strong predictor of 28‐day mortality (area under the receiver operating characteristic curve, 0.742; P < .001), and the optimal cutoff for IMA level maximizing sensitivity and specificity was 110 U/mL. On multivariate logistic regression, Acute Physiology and Chronic Health Evaluation II score and IMA level were independent risk factors for death. Survival rate was reduced with very high IMA level (≥110 U/mL; P < .05). Conclusions: The IMA level, especially at least 110 U/mL, may be a useful predictor of death for patients with severe sepsis.

Predictive Value of Serum Albumin Level for the Prognosis of Severe Sepsis Without Exogenous Human Albumin Administration.

Background: The prognostic significance of serum albumin levels in patients with sepsis has previously been reported; however, these studies have not excluded the potential confounding effect of exogenous albumin administration. In this study, we investigate the predictive value of serum albumin for the prognosis of severe sepsis without the interference of exogenous albumin administration. Methods: A prospective cohort study was conducted from April to November 2014 in the internal and surgical intensive care units of a tertiary care hospital. During the study period, due to a supply shortage, patients were not treated with human albumin. Serum albumin levels were measured, and laboratory and clinical data were collected at the onset of severe sepsis. Prognostic factors were analyzed using receiver operating characteristic curve and multivariate Cox proportional hazard regression analysis. Survival was assessed by Kaplan-Meier method. Results: One hundred sixteen patients were included in the study. The overall 28-day mortality was 26.7%. The most common infection sources were lower respiratory tract, abdomen/pelvis, and bloodstream. Compared to patients who survived, those who died had lower serum albumin levels and higher Acute Physiology and Chronic Health Evaluation II (APACHE II) and Sequential Organ Failure Assessment (SOFA) scores. Receiver operating characteristic curves demonstrate that albumin level is a strong predictor of 28-day mortality, and the optimal cutoff value maximizing sensitivity and specificity is 29.2 g/L. Through multivariate Cox regression analysis, low serum albumin levels (<29.2 g/L) and APACHE II scores are identified as independent risk factors for mortality. Patients with lower serum albumin levels more often had abdominal/pelvic sources of infection, acute kidney or liver injury, septic shock, and higher APACHE II and SOFA scores. The 28-day survival rate was lower for patients with serum albumin below 29.2 g/L than for patients with serum albumin at or above this level. Conclusion: Having excluded potential confounding effect of exogenous albumin administration, low serum albumin levels are associated with an increased risk of death in patients with severe sepsis.