Sagittal balance parameters measurement on cervical spine MR images based on superpixel segmentation.

Introduction: Magnetic Resonance Imaging (MRI) is essential in diagnosing cervical spondylosis, providing detailed visualization of osseous and soft tissue structures in the cervical spine. However, manual measurements hinder the assessment of cervical spine sagittal balance, leading to time-consuming and error-prone processes. This study presents the Pyramid DBSCAN Simple Linear Iterative Cluster (PDB-SLIC), an automated segmentation algorithm for vertebral bodies in T2-weighted MR images, aiming to streamline sagittal balance assessment for spinal surgeons. Method: PDB-SLIC combines the SLIC superpixel segmentation algorithm with DBSCAN clustering and underwent rigorous testing using an extensive dataset of T2-weighted mid-sagittal MR images from 4,258 patients across ten hospitals in China. The efficacy of PDB-SLIC was compared against other algorithms and networks in terms of superpixel segmentation quality and vertebral body segmentation accuracy. Validation included a comparative analysis of manual and automated measurements of cervical sagittal parameters and scrutiny of PDB-SLIC's measurement stability across diverse hospital settings and MR scanning machines. Result: PDB-SLIC outperforms other algorithms in vertebral body segmentation quality, with high accuracy, recall, and Jaccard index. Minimal error deviation was observed compared to manual measurements, with correlation coefficients exceeding 95%. PDB-SLIC demonstrated commendable performance in processing cervical spine T2-weighted MR images from various hospital settings, MRI machines, and patient demographics. Discussion: The PDB-SLIC algorithm emerges as an accurate, objective, and efficient tool for evaluating cervical spine sagittal balance, providing valuable assistance to spinal surgeons in preoperative assessment, surgical strategy formulation, and prognostic inference. Additionally, it facilitates comprehensive measurement of sagittal balance parameters across diverse patient cohorts, contributing to the establishment of normative standards for cervical spine MR imaging.

Network pharmacology analysis and animal experiment validation of neuroinflammation inhibition by total ginsenoside in treating CSM.

BACKGROUND: Cervical spondylotic myelopathy (CSM) is a degenerative pathology that affects both upper and lower extremity mobility and sensory function, causing significant pressure on patients and society. Prior research has suggested that ginsenosides may have neuroprotective properties in central nervous system diseases. However, the efficacy and mechanism of ginsenosides for CSM have yet to be investigated. PURPOSE: This study aims to analyze the composition of ginsenosides using UPLC-MS, identify the underlying mechanism of ginsenosides in treating CSM using network pharmacology, and subsequently confirm the efficacy and mechanism of ginsenosides in rats with chronic spinal cord compression. METHODS: UPLC-Q-TOF-MS was utilized to obtain mass spectrum data of ginsenoside samples. The chemical constituents of the samples were analyzed by consulting literature reports and relevant databases. Ginsenoside and CSM targets were obtained from the TCMSP, OMIM, and GeneCards databases. GO and KEGG analyses were conducted, and a visualization network of ginsenosides-compounds-key targets-pathways-CSM was constructed, along with molecular docking of key bioactive compounds and targets, to identify the signaling pathways and proteins associated with the therapeutic effects of ginsenosides on CSM. Chronic spinal cord compression rats were intraperitoneally injected with ginsenosides (50 mg/kg and 150 mg/kg) and methylprednisolone for 28 days, and motor function was assessed to investigate the therapeutic efficacy of ginsenosides for CSM. The expression of proteins associated with TNF, IL-17, TLR4/MyD88/NF-κB, and NLRP3 signaling pathways was assessed by immunofluorescence staining and western blotting. RESULTS: Using UPLC-Q-TOF-MS, 37 compounds were identified from ginsenoside samples. Furthermore, ginsenosides-compounds-key targets-pathways-CSM visualization network indicated that ginsenosides may modulate the PI3K-Akt signaling pathway, TNF signaling pathway, MAPK signaling pathway, IL-17 signaling pathway, Toll-like receptor signaling pathway and Apoptosis by targeting AKT1, TNF, MAPK1, CASP3, IL6, and IL1B, exerting a therapeutic effect on CSM. By attenuating neuroinflammation through the TNF, IL-17, TLR4/MyD88/NF-κB, and MAPK signaling pathways, ginsenosides restored the motor function of rats with CSM, and ginsenosides 150 mg/kg showed better effect. This was achieved by reducing the phosphorylation of NF-κB and the activation of the NLRP3 inflammasome. CONCLUSIONS: The results of network pharmacology indicate that ginsenosides can inhibit neuroinflammation resulting from spinal cord compression through multiple pathways and targets. This finding was validated through in vivo tests, which demonstrated that ginsenosides can reduce neuroinflammation by inhibiting NLRP3 inflammasomes via multiple signaling pathways, additionally, it should be noted that 150 mg/kg was a relatively superior dose. This study is the first to verify the intrinsic molecular mechanism of ginsenosides in treating CSM by combining pharmacokinetics, network pharmacology, and animal experiments. The findings can provide evidence for subsequent clinical research and drug development.

Aspercitrininone A, novel antibacterial polyketide featuring unusual spiral skeleton from Aspergillus cristatus.

Aspercitrininone A (1), a novel polyketide featuring an unprecedented tetracyclic 6/6/6/5 spiral skeleton, was obtained from the rice fermentation cultures of the fungus Aspergillus cristatus together with five known compounds (2-6). Their structures were determined by HRESIMS data, 1D and 2D NMR spectroscopic analysis, and electronic circular dichroism (ECD) calculations. Aspercitrininone A was revealed as a new type of C/D cycle spiral structure and an unusual addition product of o-quinoid form citrinin with 2-methylterrefuranone. Compounds 1, 4, and 5 exhibited potent antibacterial activities with minimal inhibitory concentration (MIC) values from 13.2 to 67.3 µg/mL against four strains of human pathogenic bacteria in vitro.

A systematic review and meta-analysis of chondroitinase ABC promotes functional recovery in rat models of spinal cord injury.

BACKGROUND: To comprehensively assess the neurologic recovery potential of chondroitinase ABC (ChABC) in rats after spinal cord injury (SCI). METHODS: The PubMed, Embase, ScienceDirect, Web of Science, and China National Knowledge Infrastructure databases were searched for animal experiments that evaluated the use of ChABC in the treatment of SCI up to November 2022. Studies reporting neurological function using the Basso, Beattie, and Bresnahan (BBB) scale, as well as assessments of cavity area, lesion area, and glial fibrillary acidic protein (GFAP) levels, were included in the analysis. RESULTS: A total of 46 studies were ultimately selected for inclusion. The results of the study showed that rats with SCI that received ChABC therapy exhibited a significant improvement in locomotor function after 7 days compared with controls (32 studies, weighted mean difference (WMD) = 0.58, [0.33, 0.83], p < 0.00001). Furthermore, the benefits of ChABC therapy were maintained for up to 28 days according to BBB scale. The lesion area was reduced by ChABC (5 studies, WMD = -20.94, [-28.42, -13.46], p < 0.00001). Meanwhile, GFAP levels were reduced in the ChABC treatment group (8 studies, WMD = -29.15, [-41.57, -16.72], p < 0.00001). Cavity area is not statistically significant. The subgroup analysis recommended that a single injection of 10 µL (8 studies, WMD = 2.82, [1.99, 3.65], p < 0.00001) or 20 U/mL (4 studies, WMD = 2.21, [0.73, 3.70], p = 0.003) had a better effect on improving the function. The funnel plot of the BBB scale was found to be essentially symmetrical, indicating a low risk of publication bias. CONCLUSIONS: This systematic review and meta-analysis has indicated that ChABC could improve functional recovery in rats after SCI.

Analysis of gene expression profiles and experimental validations of a rat chronic cervical cord compression model.

Cervical spondylotic myelopathy (CSM) is a severe non-traumatic spinal cord injury (SCI) wherein the spinal canal and cervical cord are compressed due to the degeneration of cervical tissues. To explore the mechanism of CSM, the ideal model of chronic cervical cord compression in rats was constructed by embedding a polyvinyl alcohol-polyacrylamide hydrogel in lamina space. Then, the RNA sequencing technology was used to screen the differentially expressed genes (DEGs) and enriched pathways among intact and compressed spinal cords. A total of 444 DEGs were filtered out based on the value of log2(Compression/Sham); these were associated with IL-17, PI3K-AKT, TGF-ß, and Hippo signaling pathways according to the GSEA, KEGG, and GO analyses. Transmission electron microscopy indicated the changes in mitochondrial morphology. Western blot and immunofluorescence staining revealed neuronal apoptosis, astrogliosis and microglial neuroinflammation in the lesion area. Specifically, the expression of apoptotic indicators, such as Bax and cleaved caspase-3, and inflammatory cytokines, such as IL-1ß, IL-6, and TNF-α, were upregulated. The activation of IL-17 signaling pathway was observed in microglia instead of neurons or astrocytes, the activation of TGF-ß and inhibition of Hippo signaling pathways were detected in astrocytes instead of neurons or microglia, and the inhibition of PI3K-AKT signaling pathway was discovered in neurons rather than microglia of astrocytes in the lesion area. In conclusion, this study indicated that neuronal apoptosis was accompanied by inhibiting of the PI3K-AKT pathway. Then, the activation of microglia IL-17 pathway and NLRP3 inflammasome effectuated the neuroinflammation, and astrogliosis was ascribed to the activation of TGF-ß and the inhibition of the Hippo pathway in the chronic cervical cord of compression. Therefore, therapeutic methods targeting these pathways in nerve cells could be promising CSM treatments.

Establishment and Comparison of Two Different Animal Models of Graves' Orbitopathy.

Purpose: The purpose of this study was to construct an animal model of Graves' ophthalmopathy (GO) by comparing recombinant adenovirus expressing human thyrotropin receptor A subunit (Ad-TSHR A) gene immunization and dendritic cell (DC) immunization. We evaluated the animal models that are closer to the pathology of human GO, and laid the foundation for the study of GO. Materials and Methods: Ad-TSHR A was injected intramuscularly into female BALB/c mice to induce the GO animal model. A GO animal model was constructed using TSHR combined with IFN-γ-modified primary DC immunized female BALB/c. The animal models constructed by the above two methods were evaluated in terms of ocular appearance, serology, pathology, and imaging to assess the modeling rate of the animal models, respectively. Results: Both modeled mice exhibited increased serological indexes of free thyroxine (FT4) and TSH receptor antibodies (TRAbs) levels and decreased TSH (P < 0.01). Thyroid pathology analysis revealed the number of thyroid follicles increases, the size varies, and the follicular epithelial cells proliferate to varying degrees in a cuboidal or tall columnar pattern, with a small amount of lymphocytic infiltration visible. Adipose tissue behind the eyeball was accumulated, the muscle outside the eyeball was broken and fibrotic, and hyaluronic acid (HA) behind the eyeball was increased. The animal model of GO constructed by immunization of TSHR with IFN-γ-modified DC had a modeling rate of 60%, whereas that of Ad-TSHR A gene immunization was 72%. Conclusions: Both gene immunization and cellular immunization can be used to construct GO models, and the modeling rate of gene immunization is higher than that of cellular immunization. Translational Relevance: In this study, two innovative methods, cellular immunity and gene immunity, were used to establish GO animal models, which improved the success rate to a certain extent. To our knowledge, this study presents the first cellular immunity modeling idea of TSHR combined with IFN-γ for the GO animal model, which provides an animal model basis for understanding the pathogenesis of GO and developing new treatment methods.

Melatonin restores endoplasmic reticulum homeostasis to protect injured neurons in a rat model of chronic cervical cord compression.

Cervical spondylotic myelopathy (CSM) refers to a chronic injury of the cervical cord caused by cervical intervertebral disc degeneration. Endoplasmic reticulum (ER) homeostasis is essential to counteract neuronal apoptosis. ER stress, an integral part of ER homeostasis, was observed in a rat model of chronic cervical cord compression in our previous study. However, the correlation between ER homeostasis and CSM remains unknown. The antioxidant melatonin is known to exert therapeutic effects in acute spinal cord injury, but the specific effects and their potential mechanisms in the pathological processes of CSM require further exploration. The present study hypothesized that ER homeostasis is essential for neuronal apoptosis in the CSM and that melatonin maintains this homeostasis. The results showed that ER stress led to neuronal apoptosis in rats with chronic cervical cord compression. Conversely, melatonin attenuates protein kinase R-like ER kinase-eukaryotic initiation factor 2α-C/EBP-homologous protein, inositol-requiring enzyme 1, and transcription factor 6 signaling pathways to release ER stress and prevents Bax translocation to the mitochondrion, thereby promoting motor recovery and protecting neurons in vivo. It also rescued primary rat cortical neurons from ER stress-induced glutamate toxicity in vitro. Moreover, melatonin remodels the ER morphology and restores homeostasis via ER-phagy in injured neurons. FAM134B, CCPG1, RTN3, and Sec. 62 are four known ER-phagy receptors. In this study, Sec. 62 was identified as a key melatonin factor in promoting ER-phagy and restoring ER homeostasis in damaged neurons in vivo and in vitro. In conclusion, melatonin suppresses neuronal apoptosis by reducing ER stress and promoting ER-phagy to restore ER morphology and homeostasis. The current results suggested that melatonin is a promising treatment for CSM owing to its restorative effect on ER homeostasis; however, well-designed randomized controlled trials must be carried out to further investigate its clinical effects.

Consideration in Randomized Placebo-Controlled Trial on Neck Pain to Avoid the Placebo Effect in Analgesic Action.

Background: In neck pain treatment, many therapies are focused on etiology, while it is well-known that placebo analgesia is also present in these therapies. The specific efficacy for etiology may be underestimated by ignoring their actual placebo effect. In this study, a logistic regression analysis is used to explore the risk factors causing different placebo responses in patients with neck pain among two RCTs. The probability of the placebo effect is predicted based on these risk factors. Methods: Trial A and Trial B were similarly designed, randomized, double-/single-blind, placebo-controlled trials in patients treating neck pain with Qishe pill or Shi-style manipulation. Both studies set a placebo pill twice a day or traction for every other day as control. For further analyses on the placebo effect in neck pain management, logistic regression was used to assess subgroup-placebo interactions. The odds ratio assessed a significant influence on the placebo effect. Results: In this pooled analysis, the total number of patients recruited for these two studies was 284, of which 162 patients received placebo treatment (placebo drug or traction for every other day). No statistically significant differences are found at baseline between the participants with placebo effect and non-placebo effect in the gender, age, and disease duration except in VAS and NDI at the initial time. There are numerically more patients with placebo effect in the shorter disease duration subgroup (< 4 months [76%]), higher initial VAS subgroup (>60 mm [90%]), and worse initial NDI subgroup (>24 [72%]) compared with the gender and age subgroup. An ROC curve is established to assess the model-data fit, which shows an area under the curve of 0.755 and a 95% confidence interval of 0.677-0.830. Participants who show placebo effect after 2 weeks have significantly lower VAS scores after 4 weeks, while there is no significant difference in NDI improvement between the two groups after 4 weeks. Conclusion: Neck pain patients with shorter disease duration are more likely to overscore their pain severity, because of their less experience in pain perception, tolerance, and analgesia expectation.

Non-surgical treatment with XSHHD for ruptured lumbar disc herniation: a 3-year prospective observational study.

BACKGROUND: Lumbar disc herniation (LDH) is mainly caused by annular fiber disruption with a discrete leakage of nucleus pulposus pressing on a nerve, resulting in back pain and radiating pain. Most patients with LDH can be treated conservatively, but there are many different conservative treatments. Furthermore, most previous studies did not evaluate the long-term efficacy of these treatments and the prognosis. Therefore, an effective and safe therapeutic strategy is lacking for patients with LDH. In this study, we evaluated Xiao Sui Hua He decoction (XSHHD) in the treatment of LDH. METHODS: This was a rigorous prospective observational 3-year follow-up study. We recruited 69 participants with ruptured lumbar disc herniation (RLDH) between February 2014 and February 2016. Patients took XSHHD orally twice a day for 6 months. The primary outcome measurements were visual analogue scale (VAS) pain score, Oswestry disability index (ODI) and straight leg raising test (SLRT). The secondary outcome measurements was nucleus pulposus protrusion volume on magnetic resonance imaging (MRI). Clinical outcomes were measured at baseline (Visit 1), and at 3, 6, 12, and 36 months (Visit 2, 3, 4, and 5, respectively).. RESULTS: Sixty-three patients were followed-up for 3 years after treatment. SLRT and ODI after non-surgical treatment improved significantly compared with baseline (P < .001). There were no statistically significant differences at 6 months vs 36 months for SLRT and ODI. VAS scores (leg, back) after 3 years of treatment were statistically significantly different compared with baseline (P < .001; Z = - 6.93, - 6.637). The baseline protrusion volume was 2018.61 ± 601.16 mm3, and the volume decreased significantly to 996.51 ± 387.42 mm3 at 36 months (t = 12.863; P < .001). The volume of protrusion resorption rate (VPRR) at 36 months was 47.24 ± 23.99%, with significant resorption in 23 cases, partial resorption in 23 cases, no resorption in 15 cases, and increased volume in 2 cases. CONCLUSIONS: This study showed that non-surgical treatment with XSHHD was effective, and the study clarified the natural outcomes in LDH.

Investigation of growth characteristics and semimetal-semiconductor transition of polycrystalline bis-muth thin films.

The preferred orientation growth characteristics and surface roughness of polycrystalline bis-muth (Bi) thin films fabricated on glass substrates using the molecular beam epitaxy method were investigated at temperatures ranging from 18 to 150°C. The crystallization and morphology were analyzed in detail and the polycrystalline metal film structure-zone model (SZM) was modified to fit the polycrystalline Bi thin film. The boundary temperature between Zone T and Zone II in the SZM shifted to higher temperatures with the increase in film thickness or the decrease of growth rate. Furthermore, the effect of the thickness and surface roughness on the transport properties was investigated, especially for Bi thin films in Zone II. A two-transport channels model was adopted to reveal the influence of the film thickness on the competition between the metallic surface states and the semiconducting bulk states, which is consistent with the results of Bi single-crystal films. Therefore, the polycrystalline Bi thin films are expected to replace the single-crystal films in the application of spintronic devices.

Piezochromism and hydrochromism through electron transfer: new stories for viologen materials.

While viologen derivatives have long been known for electrochromism and photochromism, here we demonstrated that a viologen-carboxylate zwitterionic molecule in the crystalline state exhibits piezochromic and hydrochromic behaviors. The yellow crystal undergoes a reversible color change to red under high pressure, to green after decompression, and finally back to yellow upon standing at ambient pressure. Ultraviolet-visible spectroscopy, X-ray photoelectron spectroscopy, electron paramagnetic resonance X-ray diffraction and DFT calculations suggested that the piezochromism is due to the formation of radicals via pressure-induced electron transfer from carboxylate to pyridinium, without a crystallographic phase transition. It was proposed that electron transfer is induced by pressure-forced reduction of intermolecular donor-acceptor contacts. The electron transfer can also be induced by dehydration, which gives a stable green anhydrous radical phase. The color change is reversible upon reabsorption of water, which triggers reverse electron transfer. The compound not only demonstrates new chromic phenomena for viologen compounds, but also represents the first example of organic mechanochromism and hydrochromism associated with radical formation via electron transfer.

Expression of intestinal CD40 after experimental traumatic brain injury in rats.

BACKGROUND: Nuclear factor kappa B (NF-κB) has been shown to be activated in the intestine after traumatic brain injury (TBI), and results in gastrointestinal mucosal injury. In addition, CD40 has a major role in the activation of NF-κB and is up-regulated in inflammatory bowel disease. However, we found no study in the literature investigating the intestinal expression of CD40 after TBI. Hence, we designed the current study to explore the intestinal expression pattern of CD40 after TBI in rats. We hypothesized that CD40 could mediate inflammation and ultimately contribute to acute intestinal mucosal injury after TBI. METHODS: We randomly divided rats into control and TBI groups at 3, 6, 12, 24, and 72 h, respectively. We assessed the expression of CD40 by quantitative real-time polymerase chain reaction, Western blotting, and immunohistochemical study, and detected the levels of tumor necrosis factor-α (TNF-α), intracellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) by enzyme-linked immunosorbent assay. RESULTS: The mRNA and protein levels of -CD40 increased by 3 and 6 h, peaked at 6 and 12 h, and remained elevated until 24 and 72 h post-injury, respectively. Levels of TNF-α, VCAM-1, and ICAM-1 also markedly increased in jejunum tissue after TBI. Interestingly, there was a positive relationship between the expression of CD40 and that of TNF-α, VCAM-1, and ICAM-1. CONCLUSIONS: CD40 could be markedly elevated in intestine after TBI in rats, and it might have an important role in the pathogenesis of acute intestinal mucosal injury mediated by inflammatory response.

[Clinical and angiographic outcomes of coronary drug-eluting stenting in treating vasospastic angina patients with severe organic stenosis].

OBJECTIVE: To evaluate the clinical and angiographic outcomes of vasospastic angina patients with severe organic stenosis treated by drug-eluting stents. METHODS: Between January 2006 and December 2010, severe organic stenosis (diameter stenosis more than 70%) was evidenced in 7 out of 46 vasospastic angina patients and treated with drug-eluting stents. Coronary angiography was repeated at 6 - 18 months after percutaneous coronary intervention and the patients were clinically followed up. The clinical and angiographic outcomes were observed. RESULTS: Nine drug-eluting stents [mean diameter 2.75 - 3.50 (3.08 ± 0.24) mm, length 24 - 33 (27.3 ± 3.6) mm] were successfully implanted in these 7 patients. Stents were implanted into left anterior descending artery (LAD) in 5 patients (71.4%), right coronary artery (RCA) in 1 patient (14.3%), both LAD and RCA in 1 patient (14.3%). Transient RCA spasm and distal LAD spasm were observed during percutaneous coronary intervention of LAD in 2 patients. Anginal attack at rest with transient ST segment elevation at V(1)-V(3) leads occurred 24 hours after LAD stenting in 1 patient. Follow-up coronary angiography showed significant in-stent restenosis or focal edge restenosis (diameter stenosis more than 50%) in 3 patients (42.9%), mild neointimal proliferation but without significant restenosis in 2 patients (28.6%), and no neointimal proliferation in 2 patients (28.6%). During clinical follow-up of 17 to 50 months after percutaneous coronary intervention, 2 patients (28.6%) remained asymptomatic, while effort angina and/or rest angina was documented in the remaining 5 patients (71.4%). CONCLUSIONS: Our results from this small patient cohort suggest that drug eluting stent implantation for severe organic stenosis in patients with vasospastic angina is linked with high incidence of restenosis and recurrent chest pain. Further observation in larger patient cohort is warranted to clarify the efficacy of this strategy for treating vasospastic angina patients with severe organic stenosis.

[Clinical and angiographic characteristics of patients with slow coronary flow].

OBJECTIVE: To analyze the clinical and angiographic characteristics of patients with slow coronary flow (SCF). METHODS: In this retrospective study, 140 patients with SCF and 140 control subjects without SCF were included. SCF were diagnosed by the combination of TIMI flow grade method and TIMI frame count method. All subjects had angiographically normal coronary arteries. The clinical and laboratory data were obtained from medical records at admission. RESULTS: Compared to control group, patients with SCF were younger [(57.8 +/- 10.7) years vs. (59.8 +/- 8.2) years], rate of smokers (59.3% vs. 46.4%) and diabetes mellitus (49.3% vs. 30.7%), fasting blood glucose (FBG) level [(7.8 +/- 2.8) mmol/L vs. (6.2 +/- 2.0) mmol/L, P < 0.05] and triglyceride (TG) level [(2.11 +/- 1.93) mmol/L vs. (1.67 +/- 1.01) mmol/L, P < 0.05] were higher, while high density lipoprotein cholesterol (HDL-C) level [(1.05 +/- 0.35) mmol/L vs. (1.42 +/- 0.74) mmol/L, P < 0.01] and apolipoprotein A1 (apoA1) level [(1.10 +/- 0.19) mmol/L vs. (1.31 +/- 0.31) mmol/L, P < 0.01] were lower. Among the 140 SCF patients, left anterior descending artery (LAD), left circumflex artery (LCX) and right coronary artery (RCA) were involved at the same time in 92 patients. Among the three vessels, RCA is the most frequent involved vessel (n = 119). After adjusting for other risk factors, current smoking (OR = 1.92, 95% CI: 1.04 - 3.57, P < 0.05), DM history (OR = 2.44, 95% CI:1.32-4.76, P < 0.01), FBG (OR = 2.13, 95% CI:1.16-3.98, P < 0.05), TG (OR = 1.47, 95% CI:1.03-2.13, P < 0.05), HDL-C (OR = 0.47, 95% CI:0.24-0.85, P < 0.05) and apoA1 (OR = 0.55, 95% CI:0.40 - 0.75, P < 0.01) were independent factors for SCF (all P < 0.05). CONCLUSIONS: Our results demonstrated that patients with SCF were prone to have a significant metabolic disorder compared to the control group. Patients with high levels of FBG, TG and low levels of HDL-C were more likely to suffer from SCF, which maybe explained by the development of coronary endothelium and microvascular dysfunction.

[Determinants of success percutaneous coronary intervention in patients with chronic total coronary artery occlusion].

OBJECTIVE: To evaluate the in-hospital outcome and determinants relating to success rate of percutaneous coronary intervention (PCI) for patients with chronic total occlusion (CTO) using contemporary techniques. METHODS: A total of 1485 patients with total occluded coronary artery were identified from January 2004 to December 2008 in Zhongshan hospital. Of them, 638 patients were affirmed as CTO and 447 patients underwent PCI. The clinical data and the in-hospital outcome of patients underwent PCI were retrospectively analyzed. RESULTS: Procedure success was achieved in 382 patients (85.5%). Coronary perforation (C-F type dissection or coronary perforation) occurred in 27 patients (6.0%), cardiac tamponade developed in 6 out of the 27 patients, 2 patients (0.4%) received in-hospital repeat revascularization. Two patients (0.4%) died post PCI: one died of acute stent thrombosis and the other one died of refractory heart and respiratory failure.Compared with patients of successful recanalization, patients failure to recanalization were more aged [(62.9 ± 10.4)years vs. (65.9 ± 9.9) years, P < 0.05] and excessive tortuosity (16.2% vs. 38.5%, P < 0.01), absence stump (47.1% vs. 80.0%, P < 0.01) and excessive calcification (36.9% vs. 72.3%, P < 0.01) were more common. Multiple logistic regression analysis revealed that excessive calcification (OR: 3.866, P < 0.01), absence stump (OR: 3.346, P < 0.05) and excessive tortuosity (OR: 3.055, P < 0.01) were independent predictors for the procedural failure. CONCLUSIONS: PCI for patients with CTO is safe and effective. Apart from progress on the equipment development, procedural success rates are closely related with the clinical and angiographic features of CTO.

[Virtual histology intravascular ultrasound assessment of coronary atherosclerotic plaques in diabetic patients].

OBJECTIVE: To evaluate the components and characteristics of coronary atherosclerotic plaques in type 2 diabetic patients using virtual histology intravascular ultrasound (VH-IVUS). METHODS: In vivo atherosclerotic plaques (over 50% angiographic diameter stenosis) of the three main coronary arteries were analyzed by gray-scaled IVUS with planar and volumetric VH-IVUS in consecutive patients examined between September 2008 and March 2009. Patients were divided into two groups: diabetic mellitus (DM) group with 22 patients (39 lesions) and non-DM group with 46 patients (69 lesions). RESULTS: At the minimal lumen area (MLA) site, the percentage of NC (necrotic core) area (19.4% +/- 1.2% vs. 15.1% +/- 1.1%, P = 0.015) and dense calcium (DC) area (15.2% +/- 1.6% vs. 10.7% +/- 1.1%, P = 0.016) were significantly larger while fibrotic tissue (FT) area (56.7% +/- 2.3% vs. 64.8% +/- 1.8%, P = 0.007) was smaller in DM group than in non-DM group. Likewise, volumetric VH-IVUS analysis showed that the percentage of NC volume (21.3% +/- 1.3% vs. 16.5% +/- 1.1%, P = 0.008) and DC volume (16.6% +/- 1.4% vs. 11.3% +/- 1.1%, P = 0.003) were significantly larger while FT volume (55.1% +/- 2.1% vs. 63.9% +/- 1.8%, P = 0.003) was significantly smaller in DM group than in non-DM group. Moreover, significantly higher incidence of VH-TCFA (thin-cap fibro atheromas) was evidenced in the DM group than in the non-DM group (69.2% vs. 42.0%, P = 0.009). However, the remodeling index and the positive remodeling frequency were similar between the 2 groups. CONCLUSION: Incidence of necrotic core, dense calcium plaque and vulnerable plaques in stenotic lesions was higher in DM patients than in non-DM patients.

[Clinical manifestations of young and aged patients with coronary artery disease].

OBJECTIVE: To analyze clinical characteristics in young and aged patients with coronary artery disease (CAD). METHODS: The clinical and coronary angiographic data were compared between young (PCAD, male < 55 years old, n = 74, female < 65 years old, n = 71) and aged (CAD, male > 55 years old, n = 106, female > 65 years old, n = 111) patients. Seventy-one patients excluded with CAD by angiography served as controls (non-CAD). The traditional risk factors (including age, smoking, blood pressure, lipid profile, blood glucose, BMI, family history), coronary angiographic changes were analyzed and compared among various groups. RESULTS: (1) Compared with CAD group, PCAD patients had significantly higher rate of smoking (50.3% vs. 38.0%, P < 0.05), significantly higher positive CAD family history rate (29.7% vs. 19.9%, P < 0.05) and significantly higher TG level [(2.13 +/- 1.89) mmol/L vs. (1.78 +/- 1.14) mmol/L, P < 0.05], while had significantly fewer traditional risk factors (2.50 +/- 1.28 vs. 2.76 +/- 1.43, P < 0.05) and lower hypertension rate (59.3% vs. 73.3%, P < 0.05). There were significantly more PCAD patients with acute coronary syndrome (66.2% vs. 42.6%, P < 0.05), more PCAD patients had single vessel lesion (51.0% vs. 30.4%, P < 0.05), lower average lesion score (4.86 +/- 2.30 vs. 5.92 +/- 2.66, P < 0.05). (2) The logistic regression results showed that positive CAD family history (P = 0.029, OR = 1.766, 95% CI 1.060 - 2.940) and smoking (P = 0.066, OR = 1.561, 95% CI 0.971 - 2.510) are important independent risk factors for the development of PCAD. CONCLUSIONS: Smoking, positive family history and the increased TG might contribute to the pathogenesis of PCAD.

[The clinical characteristics of systemic lupus erythematosus associated with coronary artery disease].

OBJECTIVE: To summarize the clinical characteristics of systemic lupus erythematosus (SLE) associated with coronary artery disease (CHD). METHODS: This is a retrospective analysis. We studied the traditional cardiovascular risk factors, first onset of cardiac events, diagnosis, treatment and activity of the disease in 11 SLE patients with CHD. The results were statistically analyzed using independent-samples test and Fisher's exact test. RESULTS: (1) SLE patients with CHD had an average age of (53.9 +/- 8.1) years old. (2) The mean number of CHD risk factors per patient was 1.3 +/- 0.8. (3) The level of lipids was significantly elevated after therapy with corticosteroids (The P values for TC, LDL-C, HDL-C and TG were 0.013, 0.003, 0.016 and 0.006, respectively). (4) The SLEDAI was 12.0 +/- 10.3 when the first cardiac event happened. (5) SLE patients with CHD often had severe lesions of the coronary artery, manifested as diffuse stenosis and severe calcification. CONCLUSIONS: Conventional CHD risk factors cannot fully account for premature CHD in SLE patients. SLE patients with CHD often had severe lesions of the coronary artery and poor prognosis, so we should treat it as early as possible to delay the progress of CHD and use non-invasive examinations for early diagnosis in order to improve the prognosis.