SIRT3 attenuates coronary atherosclerosis in diabetic patients by regulating endothelial cell function.

BACKGROUND: This study aimed to explore the relationship between the Sirtuin 3 (SIRT3) gene and endothelial cell dysfunction, contributing to the progression of coronary atherosclerosis driven by hyperglycemia. METHODS: We measured serum SIRT3 levels using enzyme-linked immunosorbent assay in 95 patients with type 2 diabetes mellitus (T2DM) who underwent diagnostic coronary angiography. The patients were divided into two groups according to the presence (n = 45) or absence (n = 50) of coronary artery disease (CAD). Human aortic endothelial cells (HAECs) grown in vitro in a medium with various concentrations of glucose (5.5, 11, 16.5, 22, 27.5, 33, and 38.5 mM) for 24 h were assessed for protein expression of SIRT3, peroxisome proliferator-activated receptor alpha (PPAR-α), endothelial nitric oxide (NO) synthase (eNOS), and inducible NO synthase (iNOS) using Western blot analysis. HAECs were subjected to SIRT3 overexpression or inhibition through SIRT3 adenovirus and siRNA transfection. RESULTS: Serum SIRT3 levels were significantly lower in T2DM patients with CAD than in those without CAD (p = 0.048). The in vitro results showed that HG significantly increased SIRT3, PPAR-α, and eNOS protein expression in a concentration-dependent manner. Moreover, iNOS expression was decreased in HAECs in response to HG. Reduced PPAR-α and eNOS levels and increased iNOS levels were observed in SIRT3 silenced HAECs cells. In contrast, SIRT3 overexpression significantly improved PPAR-α and eNOS expression and suppressed iNOS expression. CONCLUSION: SIRT3 was associated with the progression of atherosclerosis in T2DM patients through upregulation of PPAR-α and eNOS and downregulation of iNOS, which are involved in endothelial dysfunction under hyperglycemic conditions.

Astragalus polysaccharide attenuates overexercise-induce myocardial injury via activating AMPK signaling pathway to suppress inflammation and oxidative stress.

Excessive exercise leads to myocardial injury or even sudden exercise death. For the vast sports population, appropriate physiological state is a necessary condition for exercise. The present study aims to investigate the cardioprotective effects and potent mechanism of astragalus polysaccharide (APS) treatment against the exercise-induced myocardial injury via in vitro cell-based assay and in vivo model rat. Efficacies of APS incubation on the inflammatory response and oxidative stress induced by LPS were both explored in H9c2 cells by using CCK-8 and western blotting method, respectively. Normal SD rats were randomly divided into saline-treated overexercise rat group, and APS-treated overexercise rat groups with three doses. Then long-term swimming training load cycle (8 week) were performed on these rats. Finally, the changes on body weight, myocardial morphological and injury indicators, as well as the inflammation-related proteins in overexercise-induced model rats were all assessed. Three concentrations of APS all significantly increased cell viability, and decreased the apoptosis of cardiomyocytes in LPS-treated H9c2 cells. Moreover, chronic treatment of APS at all three doses also could obviously decreased myocardial injury-related indicators. Furthermore, the histopathologic examination exhibited that the APS successfully attenuated the changes of myocardial tissues, reduced the lipid accumulation and the protein levels of IL-1ß, TNF-α and NF-κB. Furthermore, the APS could activate the AMPK signaling pathway, enhance the autophagy and suppress the production of ROS. On conclusions, APS exerted the protective efficacies on overexercise-induced myocardial injury by activating the AMPK signaling pathway to increase autophagy and suppress the inflammation response, oxidative stress, apoptosis of myocardial cells.

The influence of nitroglycerin on the proliferation of endothelial progenitor cells from peripheral blood of patients with coronary artery disease.

Endothelial progenitor cells (EPCs) are associated with vascular repairing and progression of atherosclerotic lesion. It may lead to coronary artery disease (CAD) if circulating EPCs lose their function. Continuous nitroglycerin (NTG) therapy causes increased vascular oxidative stress and endothelial dysfunction. The aim of this study was to investigate the effects of NTG on the proliferation of human peripheral blood-derived EPCs. EPC cultures, collected from 60 CAD patients and cultured for 7-12 days, were treated with different concentrations of NTG (0.0, 0.3, 1.0, 2.0, 7.5, 15.0, and 20.0 mg/l) for 72 h, respectively. The cell counts and proliferative activities of EPC; the levels of vascular endothelial growth factor-A (VEGF-A), nitric oxide (NO) and peroxynitrite (ONOO(-)) in culture medium; and the level of reactive oxygen species (ROS) in adherent cells were measured. Compared with control (0.0 mg/l NTG), the cell number and proliferative activities of EPCs were increased when treated with 1.0 mg/l NTG and reached maximum level when NTG concentration was 7.5 mg/l. However, there was a significant reduction when treated with higher doses of NTG (≥15.0 mg/l). Meanwhile, VEGF-A expression reached its maximal expression with 7.5 mg/l NTG, but gradually declined by incubation with higher doses of NTG. There was a linear relationship between NO level and NTG concentration, but no changes of ONOO(-) and ROS levels were found when EPCs were incubated with 0.3-7.5 mg/l NTG. However, ONOO(-) and ROS levels were significantly increased when incubated with 15 and 20 mg/l NTG. Our data demonstrated that moderate dose of NTG may stimulate the proliferative activities of EPCs isolated from CAD patients.

SIRT3 MEDIATES THE CARDIOPROTECTIVE EFFECT OF THERAPEUTIC HYPOTHERMIA AFTER CARDIAC ARREST AND RESUSCITATION BY RESTORING AUTOPHAGIC FLUX VIA THE PI3K/AKT/MTOR PATHWAY.

ABSTRACT: Background : Postresuscitation cardiac dysfunction is a significant contributor to early death following cardiopulmonary resuscitation (CPR). Therapeutic hypothermia (TH) mitigates myocardial dysfunction due to cardiac arrest (CA); however, the underlying mechanism remains unclear. Sirtuin 3 (Sirt3) was found to affect autophagic activity in recent research, motivating us to investigate its role in the cardioprotective effects of TH in the treatment of CA. Methods : Sprague-Dawley rats were used to establish an in vivo CA/CPR model and treated with a selective Sirt3 inhibitor or vehicle. Survival rate, myocardial function, autophagic flux, and Sirt3 expression and activity were evaluated. H9C2 cells were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) injury in vitro . The cells were transfected with Sirt3-siRNA and treated with the autophagy inhibitor chloroquine or the PI3K inhibitor LY294002, and cell viability and autophagic flux were assessed. Results : Rats exhibited decreased survival and impaired cardiac function after CA/CPR, which were alleviated by TH. Mechanistically, TH restored Sirt3 expression and autophagic flux, which were impaired by CA/CPR. Sirt3 inactivation diminished the capacity of TH to restore autophagic flux and partially abolished the improvements in myocardial function and survival. An in vitro study further showed that TH-induced restoration of disrupted autophagic flux by OGD/R was attenuated by pretreatment with Sirt3-siRNA, and this attenuation was partially rescued by the inhibition of PI3K/Akt/mTOR signaling cascades. Conclusions : Sirt3 mediates the cardioprotective effect of TH by restoring autophagic flux via the PI3K/Akt/mTOR pathway. These findings suggest the potential of Sirt3 as a therapeutic target for CA.

Finite element analysis of a three-dimensional cervical spine model with muscles based on CT scan data.

BACKGROUND: The incidence of cervical spondylosis is increasing, gradually affecting people's normal lives. Establishing a finite element model of the cervical spine is one of the methods for studying cervical spondylosis. MRI (Magnetic Resonance Imaging) still has certain difficulties in transitioning from human imaging to establishing muscle models suitable for finite element analysis. Medical software provides specific morphologies and can generate muscle finite element models. Additionally, there is little research on the static analysis of cervical spine finite element models with solid muscle. PURPOSE: A new method is proposed for establishing a finite element model of the cervical spine based on CT (Computed Tomography) data and medical software, and the model's effectiveness is validated. Human movement characteristics based on the force distribution in various parts are analyzed and predicted. METHODS: The muscle model is reconstructed in medical software and a three-dimensional finite element model of the entire cervical spine (C0-C7) is established by combining muscle models with CT vertebral data models. 1.5 Nm of load is applied to the finite element model to simulate the cervical spine movement. RESULTS: The finite element model was successfully established, and effectiveness was verified. Stress variations in various parts under six movements were obtained. The effectiveness of the model was basically verified. CONCLUSION: The finite element model of the cervical spine for mechanical analysis can be successfully established by using medical software and CT data. In daily life, the C2-3, C3-4, C4-C5 intervertebral discs, rectus capitis posterior major, longus colli, and obliquus capitis inferior are more prone to injury.

Elevated lipoprotein-associated phospholipase A2 is associated with progression of nonculprit lesions after percutaneous coronary intervention.

Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an enzyme that hydrolyzes oxidized phospholipids to generate bioactive proatherogenic products. Nonculprit lesions have been assumed to contribute to the pathogenesis of recurrent acute coronary syndrome (ACS). The role of LP-PLA2 in the progression of nonculprit coronary lesions after successful percutaneous coronary intervention (PCI) remains unclear. Our study included 123 patients with ACS who underwent initial PCI and a long-term follow-up (mean interval, one year) with coronary angiography. Among them, 19 patients were diagnosed as the progression of nonculprit lesions, based on the presence of at least one of the following factors: (1) ≥ 10% reduction in the diameter of a preexisting ≥ 50% stenosis; (2) ≥ 30% reduction in the diameter of a < 50% stenosis; and (3) early-onset stenosis with ≥ 30% reduction in the diameter of a segment that was normal on the primary angiogram. Blood sampling was drawn from all patients at 12-14 hours after PCI. The ACS patients with progression had higher total cholesterol (4.47 ± 1.02 mmol/L vs. 3.59 ± 0.57 mmol/L, P < 0.05), higher levels of Lp-PLA2 activity (14.39 ± 6.13 nmol/min/ml vs. 8.86 ± 3.14 nmol/min/ml, P < 0.001) and a higher proportion of multi-vessel disease than those without progression. Multivariate logistic regression analysis showed that Lp-PLA2 activity (ß = 0.024, P = 0.005) was an independent predictor for rapid progression of nonculprit coronary lesions. In conclusion, elevated Lp-PLA2 activity is associated with rapid progression of nonculprit coronary lesions in ACS patients who underwent PCI.

[Application of noninvasive brain-edema dynamic monitoring in critically ill patients with traumatic brain injury].

Brain edema could be secondary to cerebral lesion caused by a variety of reasons, severe cases may result in brain herniation or even death. Accurate real-time monitoring of cerebral edema, rational application of dehydrating drugs, and timely treatment of cerebral edema were very important for patients. However, there were defects in the monitoring methods commonly used in clinical practice. Noninvasive brain-edema monitoring was a new method, which can quantify the degree of brain edema by electromagnetic disturbance and directly reflect the state of brain edema. This article reviews the application of noninvasive brain-edema monitoring in the treatment of in critically ill patients with traumatic brain injury.

An integrative view on the carotid artery alterations in metabolic syndrome.

BACKGROUNDS: Metabolic syndrome (MetS) is a multiple risk factor paradigm widely considered in risk management. We aimed to investigate carotid artery alterations in MetS and the underlying risk factors. MATERIALS AND METHODS: A total of 400 Chinese subjects were recruited, divided into control (n = 200) and MetS (n = 200) groups. Clinical and laboratory characteristics were collected. All subjects underwent carotid ultrasonography. RESULTS: Cardiovascular risk profiles were worse in the MetS than control group (all P < 0.05). After adjusting for MetS and age, the MetS group showed significantly increased mean intima-media thickness (IMT(mean)) and significantly impaired carotid elastic properties (all P < 0.05), as compared to control group. Waist circumference (WC) was positively correlated with IMT(mean) (r = 0.130, P = 0.038), systolic carotid diameter (r = 0.139, P = 0.026) and diastolic carotid diameter (r = 0.168, P = 0.007). systolic blood pressure (SBP) and diastolic blood pressure were positively correlated with IMT(mean) (r = 0.201, P = 0.004; r = 0.168, P = 0.008, respectively), but negatively with arterial compliance coefficient (r = -0.421, P < 0.001; r = -0.230, P < 0.001, respectively). Serum level of high-density lipoprotein (HDL) negatively correlated with IMT(mean) (r = -0.195, P = 0.002). Plaque index was positively correlated with fasting blood glucose (r = 0.205, P = 0.001) after adjusting for the other risk factors. Significantly impaired carotid elastic properties (all P < 0.05) independently correlated with IMT(mean) . Furthermore, age (ß = 0.255, P < 0.001), SBP (ß = 0.224, P < 0.001), WC (ß = 0.202, P < 0.001) and high-density lipoprotein cholesterol (HDL-C) (ß = -0.163, P = 0.001) were independently associated with IMT(mean). CONCLUSION: Carotid alterations consequent upon MetS ultimately developed subclinical and clinical atherosclerosis, the underlying risk factors for which were abdominal obesity, hypertension, ageing and low level of HDL-C.

Plasma lipoprotein-associated phospholipase A2 in patients with metabolic syndrome and carotid atherosclerosis.

BACKGROUND: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a recently identified and potentially useful plasma biomarker for cardiovascular and atherosclerotic diseases. However, the correlation between the Lp-PLA2 activity and carotid atherosclerosis remains poorly investigated in patients with metabolic syndrome (MetS). The present study aimed to evaluate the potential role of Lp-PLA2 as a comprehensive marker of metabolic syndrome in individuals with and without carotid atherosclerosis. METHODS: We documented 118 consecutive patients with MetS and 70 age- and sex-matched healthy subjects served as controls. The patients were further divided into two groups: 39 with carotid plaques and 79 without carotid plaques to elucidate the influence of Lp-PLA2 on carotid atherosclerosis. The plasma Lp-PLA2 activity was measured by using ELISA method and carotid intimal-media thickness (IMT) was performed by ultrasound in all participants. RESULTS: Lp-PLA2 activity was significantly increased in MetS subgroups when compared with controls, and was higher in patients with carotid plaques than those without plaques (P < 0.05). Furthermore, we found that significant difference in Lp-PLA2 was obtained between patients with three and four disorders of metabolic syndrome (P < 0.01). Age (ß = 0.183, P = 0.029), LDL-cholesterol (ß = 0.401, P = 0.000) and waist-hip ratio (ß = 0.410, P = 0.000) emerged as significant and independent determinants of Lp-PLA2 activity. Multiple stepwise regression analysis revealed that LDL-cholesterol (ß = 0.309, P = 0.000), systolic blood pressure (ß = 0.322, P = 0.002) and age (ß = 0.235, P = 0.007) significantly correlated with max IMT, and Lp-PLA2 was not an independent predictor for carotid IMT. CONCLUSIONS: Lp-PLA2 may be a modulating factor for carotid IMT via age and LDL-cholesterol, not independent predictor in the pathophysiological process of carotid atherosclerosis in patients with MetS.

Expression of STAMP2 in monocytes associates with cardiovascular alterations.

BACKGROUND: Metabolic and inflammatory pathways crosstalk at many levels. In this study, we aimed to investigate the expression of six-transmembrane protein of prostate 2 (STAMP2) in macrophages and tried to search for the association between the decreased STAMP2 expression, if any, and carotid atherosclerosis as well as cardiac adaptations. MATERIALS AND METHODS: A total of 97 unrelated Chinese subjects were recruited including 48 subjects with metabolic syndrome (MetS) and 49 controls. Clinical and biochemical characteristics were collected from subjects, with quantification of STAMP2 in monocyte/macrophages. All subjects underwent ultrasonography. RESULTS: STAMP2 expression in macrophages was significantly decreased in MetS as compared with the control group (10.25 +/- 9.20 vs. 15.20 +/- 9.18, P = 0.009), especially in women patients. Partial correlation analysis showed that STAMP2 expression in macrophages correlated with BMI (r = -0.375, P = 0.045), age (r = 0.414, P = 0.026) and HDL (r = 0.377, P = 0.044) after controlling for systolic blood pressure (SBP). Furthermore, STAMP2 expression was correlated with PI (r = -0.454, P = 0.013), LVEF (r = -0.503, P = 0.005), LA-ESR (r = -0.424, P = 0.022), LA-S (r = 0.469, P = 0.010) and mitral E/A ratio (r = 0.492, P = 0.005) after controlling for SBP. Still, in multivariable analysis, STAMP2 expression was independently associated with IMT(mean), PI and mitral E/A ratio. CONCLUSIONS: In MetS patients, especially women patients, STAMP2 expression was down-regulated in peripheral blood mononuclear cell, which was correlated with carotid atherosclerosis and cardiac adaptation.

Continuous "Snowing" Thermotherapeutic Graphene.

Finding the best applications of graphene, and the continuous and scalable preparation of graphene with high quality and high purity, are still two major challenges. Herein, a "pulse-etched" microwave-induced "snowing" (PEMIS) process is developed for continuous and scalable preparation of high-quality and high-purity graphene directly in the gas phase, which is found to have excellent thermotherapeutic effects. The obtained graphene exhibits small size (≈180 nm), high quality, low oxygen content, and high purity, together with a high gas-solid conversion efficiency of ≈10.46%. Considering the intrinsic characteristics of this high-purity and small-sized biocompatible graphene, in particular the low-frequency microwave absorption property as well as the good thermal transformation ability, a graphene-based combination therapeutic system is demonstrated for microwave thermal therapy (MTT) for the first time, exhibiting a high tumor ablation rate of ≈86.7%. This is different from the principle of ions vibrating in a confined space used by current MTT sensitization materials. Not limited to this application, it is foreseen that this PEMIS-based high-quality graphene will allow the search for further suitable applications of graphene.

[Prevention strategies for traumatic cardiac arrest].

The fatality rate of traumatic cardiac arrest (TCA) is extremely high, and it is very different from that of non-traumatic cardiac arrest (NTCA) in resuscitation strategy. Only when the standard resuscitation process is combined with rapid treatment of various reversible causes can the mortality rate of patients be decreased. In this paper, the key factors leading to TCA are reviewed, such as hypovolemic shock, asphyxia, tension pneumothorax, pericardial tamponade, crush syndrome, craniocerebral injury, cerebral hernia, and the control measures are elaborated respectively, so as to provide references for clinical treatment of patients with severe trauma, and reduce TCA incidence and mortality.

Impaired elastic properties of the aorta in fat-fed, streptozotocin-treated rats. Vascular remodeling in diabetic arteries.

BACKGROUND: Vascular complications associated with diabetes are the major cause for the increased morbidity and mortality in diabetic patients. However, the progression of vascular complications in diabetes is not well understood. We aimed to investigate the biomechanical and biochemical changes associated with vascular dysfunction in diabetic rats. METHODS: Male Wistar rats were randomly divided into two groups: normal control (n = 8) and fat-fed, streptozotocin-treated diabetic rats (n = 11). After 16 weeks, Peterson's modulus of elasticity (Ep) and cross-sectional distensibility (CD) were calculated and compared between the two groups. Aortas were harvested from rats for histopathological and electron-microscopic analysis. RESULTS: Collagenous fibers were scattered in the extracellular matrix and invaded the elastic lamina in the aortas of diabetic rats, suggesting a significant accumulation of collagen in diabetic vessels. Compared with normal rats, diabetic rats showed significantly reduced aortic distensibility (CD: 0.10 +/- 0.04 vs. 0.17 +/- 0.08 kPa(-1), p = 0.033) and an increased aortic stiffness index (Ep: 0.25 +/- 0.13 vs. 0.15 +/- 0.05 x 10(6) dyn/cm(2), p = 0.045). Ep was positively and CD negatively correlated with glucose and collagen in diabetic rats. CONCLUSIONS: In diabetic rats, elastic properties of the aorta are impaired, being closely related to hyperglycemia-induced vascular wall remodeling.

Therapy for myocardial infarction: In vitro and in vivo evaluation of puerarin-prodrug and tanshinone co-loaded lipid nanoparticulate system.

Myocardial infarction (MI) is the leading cause of morbidity and mortality worldwide. Nanoparticle systems carrying drugs have already been developed to treat MI. To improve the efficiency of tanshinone (TAN), and to achieve the synergistic effect of TAN and puerarin (PUE), PUE-prodrug and TAN co-loaded solid lipid nanoparticles (SLN) was structured and utilized for MI treatment in the present research. PUE-prodrug was synthesized by an esterification reaction. PUE-prodrug and TAN co-loaded SLN (PUEp/TAN-SLN) were prepared by a single emulsification followed by a solvent evaporation method. The physicochemical properties of SLN were characterized and the in vivo infarct therapy effects were evaluated in MI rats. PUE-prodrug and TAN contained SLN showed a size of 112.6 ± 3.1 nm. The SLN encapsulation reduced the cytotoxicity of drugs and was a safer system. PUEp-SLN exhibited a 1.7-fold increase in comparison to PUE-SLN (21.2 ± 2.1 versus 12.5 ± 1.5 mg/L), in the mean time a 3.4-fold increase compared with free PUE in heart drug concentration (21.2 ± 2.1 versus 6.3 ± 0.9 mg/L). In vivo infarct therapy efficiency of double drugs loaded PUEp/TAN-SLN (17 ± 1.9%) was significantly better than the single drug loaded PUEp-SLN (31 ± 1.6%) and TAN-SLN (40 ± 2.2%). PUE-prodrug contained, double drugs co-loaded SLN can be utilized as promising candidate delivery system for cardioprotective drugs in treatment of myocardial infarction.

Predictive value of fasting blood glucose for serious coronary atherosclerosis in non-diabetic patients.

OBJECTIVE: To determine if high fasting blood glucose (FBG) level is an independent predictor of serious coronary lesions in patients with coronary artery disease (CAD). METHODS: We enrolled 64 patients who had symptoms of chest discomfort and who underwent coronary angiography. FBG was determined from blood samples and the extent of coronary artery lesions was analyzed according to Gensini score. We examined the relationships among diabetes, FBG, and coronary artery severity. RESULTS: Diabetes and FBG were significantly and positively related to Gensini score. Diabetes, but not FBG, was independently correlated with the occurrence of a Gensini score >41. However, FBG was significantly associated with Gensini score >41 in non-diabetic patients. CONCLUSION: Hyperglycemia is an independent predictor of severe CAD in non-diabetic patients. Clinicians should be aware of this and should carry out appropriate early interventions.

Fetal Dermal Mesenchymal Stem Cell-Derived Exosomes Accelerate Cutaneous Wound Healing by Activating Notch Signaling.

Fetal dermal mesenchymal stem cells (FDMSCs), isolated from fetal skin, are serving as a novel MSC candidate with great potential in regenerative medicine. More recently, the paracrine actions, especially MSC-derived exosomes, are being focused on the vital role in MSC-based cellular therapy. This study was to evaluate the therapeutic potential of exosomes secreted by FDMSCs in normal wound healing. First, the in vivo study indicated that FDMSC exosomes could accelerate wound closure in a mouse full-thickness skin wound model. Then, we investigated the role of FDMSC-derived exosomes on adult dermal fibroblast (ADFs). The results demonstrated that FDMSC exosomes could induce the proliferation, migration, and secretion of ADFs. We discovered that after treatment of exosomes, the Notch signaling pathway was activated. Then, we found that in FDMSC exosomes, the ligands of the Notch pathway were undetectable expect for Jagged 1, and the results of Jagged 1 mimic by peptide and knockdown by siRNA suggested that Jagged 1 may lead the activation of the Notch signal in ADFs. Collectively, our findings indicated that the FDMSC exosomes may promote wound healing by activating the ADF cell motility and secretion ability via the Notch signaling pathway, providing new aspects for the therapeutic strategy of FDMSC-derived exosomes for the treatment of skin wounds.

Impaired left ventricular synchronicity in hypertensive patients with ventricular hypertrophy.

OBJECTIVES: The influence of left ventricular hypertrophy (LVH) on left ventricular synchronicity, and the prevalence of left ventricular dyssynchrony in hypertensive patients with LVH are unknown. The purpose of this study was to determine the influence of LVH on left ventricular synchronicity in hypertensive subjects. METHOD: Tissue Doppler imaging (TDI) was performed in 115 hypertensive and 30 control individuals. Hypertensive patients were divided into a LVH group and a non-LVH group according to the left ventricular mass index (LVMI). Diastolic and systolic asynchrony was determined by measuring the maximal differences in time to peak myocardial systolic contraction (Ts-max) and early diastolic relaxation (Te-max) between any two of the left ventricular segments and the standard deviation of time to peak myocardial systolic contraction and early diastolic relaxation of all 12 segments. RESULTS: Ts-max was greater in both the non-LVH and LVH groups than in controls, (96.68 +/- 26.21 versus 79.30 +/- 25.19 versus 53.20 +/- 15.24 ms, both P < 0.001) and in the LVH group than in the non-LVH group (96.68 +/- 26.21 versus 79.30 +/- 25.19 ms, P < 0.01). Te-max was prolonged in both patient groups, being most advance in the LVH group (67.39 +/- 11.01 versus 57.18 +/- 11.42 versus 46.72 +/- 13.24 ms, both P < 0.001 versus control group and P < 0.001 versus non-LVH group). LVH patients had shown a greater prevalence of both systolic and diastolic asynchrony than non-LVH patients. A Ts-max value greater than 88 ms had 68% sensitivity and 71% specificity for detecting hypertensive patients with LVH. CONCLUSION: Left ventricular systolic synchronicity was impaired in hypertensive patients with LVH. TDI was shown to be useful for the detection of myocardial abnormalities in such patients.

Increased serum visfatin in patients with metabolic syndrome and carotid atherosclerosis.

OBJECTIVE: Visfatin is a newly identified adipocytokine and recent studies indicated that visfatin may have potential proinflammatory effect. However, its pathophysiological role in the metabolic syndrome (MetS) is not fully understood. In this study we investigated whether serum visfatin levels is altered in patients with the MetS, and compared the levels of visfatin between patients with and without carotid plaques. DESIGN AND METHOD: A total of 139 patients with MetS and 105 controls were included. The patients were further divided into two groups: 40 with carotid plaques and 99 without carotid plaques. Serum visfatin was measured by using enzyme immunoassay method and carotid intimal-media thickness (IMT) was measured by ultrasound in all subjects. RESULTS: Serum visfatin was elevated in both MetS patients with and without carotid plaques compared to controls (log visfatin: 1.14 +/- 0.14 vs. 0.99 +/- 0.17 ng/ml vs. 0.93 +/- 0.23 ng/ml, P < 0.001 and P < 0.05 vs. control group, respectively), and in patients with carotid plaques more than in patients without carotid plaques (P < 0.001). Multiple stepwise regression analysis revealed that only LDL-cholesterol correlated with visfatin, and visfatin independently correlated with max IMT in the patients with MetS. A log visfatin > 1.08 ng/ml had 70% sensitivity and 67% specificity for detecting patients with carotid plaques. CONCLUSIONS/INTERPRETATION: Our results showed that serum visfatin was increased in patients with MetS, especially in those with carotid plaques. Visfatin may be an inflammatory marker of MetS.

Felodipine attenuates vascular inflammation in a fructose-induced rat model of metabolic syndrome via the inhibition of NF-kappaB activation.

AIM: Metabolic syndrome is associated with an increased incidence of atherosclerosis. Clinical studies have shown that calcium channel blockers (CCB) inhibit the progression of atherosclerosis. However, the underlying mechanism is unclear. We investigated the inhibitory effect of felodipine on adhesion molecular expression and macrophage infiltration in the aorta of high fructose-fed rats (FFR). METHODS: Male Wistar rats were given 10% fructose in drinking water. After 32 weeks of high fructose feeding, they were treated with felodipine (5 mg x kg(-1) x d(-1)) for 6 weeks. The control rats were given a normal diet and water. The aortic expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) and the infiltration of macrophages were measured by real-time RT-PCR and/or immunohistochemistry. NF-kappaB activity was measured by electrophoretic mobility shift assay (EMSA). RESULTS: After 32 weeks of high fructose feeding, FFR displayed increased body weight, systolic blood pressure (SBP), serum insulin, and triglycerides when compared with the control rats. The aortic expressions of ICAM-1 and VCAM-1 were significantly increased in FFR than in the control rats and accompanied by the increased activity of NF-kappaB. FFR also showed significantly increased CD68- positive macrophages in the aortic wall. After treatment with felodipine, SBP, serum insulin, and the homeostasis model assessment decreased significantly. In addition to reducing ICAM-1 and VCAM-1, felodipine decreased macrophages in the aortic wall. EMSA revealed that felodipine inhibited NF-kappaB activation in FFR. CONCLUSION: Felodipine inhibited vessel wall inflammation. The inhibition of NF-kappaB may be involved in the modulation of vascular inflammatory response by CCB in metabolic syndrome.

Possible beneficial effect of olmesartan medoxomil on left atrial function in patients with hypertension : noninvasive assessment by acoustic quantification.

BACKGROUND AND OBJECTIVE: Hypertension alters the diastolic properties of the left ventricle and results in deterioration in the structure and function of the left atrium. We aimed to evaluate whether olmesartan medoxomil has an effect on left atrial function in hypertensive patients. METHODS: Fifty hypertensive patients and 20 controls were included in the study. Hypertensive patients were treated with olmesartan medoxomil for 8 weeks. Before and after treatment, study participants were examined by acoustic quantification and tissue Doppler imaging. Left atrial reservoir function was assessed by end-diastolic volume (EDV), end-systolic volume (ESV), reservoir volume (RV) and peak filling rate (PFR). Left atrial booster pump function was assessed by atrial emptying volume (AEV), atrial emptying fraction (AEF) and peak atrial emptying rate (PAER). Left atrial conduit function was assessed by rapid emptying volume (REV), rapid emptying fraction (REF), REV/AEV ratio, and the ratio of peak rapid emptying rate and PAER (PRER/PAER). RESULTS: Atrial RV and PFR were significantly increased in hypertensive subjects (48.30 +/- 19.28 mL vs 34.35 +/- 14.26 mL, p < 0.001; 267.26 +/- 126.52 mL/s vs 206.81 +/- 107.17 mL/s, p < 0.05) compared with controls, while the REV/AEV ratio was decreased in hypertensive patients compared with controls (2.86 +/- 0.85 vs 3.69 +/- 2.13, p < 0.001). After therapy with olmesartan medoxomil, atrial RV (48.30 +/- 19.28 mL vs 40.50 +/- 17.59 mL) and PFR decreased (267.26 +/- 126.52 mL/s vs 220.40 +/- 108.56 mL/s, p < 0.05) and the REV/AEV ratio increased (2.86 +/- 0.85 vs 3.14 +/- 0.43, p < 0.05) in hypertensive patients. CONCLUSION: Our novel findings indicate that left atrial function is impaired in hypertensive patients, and that olmesartan medoxomil can improve left atrial function in this context. Our study also showed that acoustic quantification is useful for non-invasive evaluation of the benefits of treatment on left atrial function.