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.

Ulinastatin attenuates diabetes-induced cardiac dysfunction by the inhibition of inflammation and apoptosis.

Ulinastatin exhibits anti-inflammatory activity and protects the heart from ischemia/reperfusion injury. However, whether ulinastatin has a protective effect in diabetic cardiomyopathy is yet to be elucidated. The aim of the present study was to investigate the protective effects of ulinastatin against diabetic cardiomyopathy and its underlying mechanisms.

Strain/strain rate imaging of impaired left atrial function in patients with metabolic syndrome.

Left ventricular (LV) dysfunction has been demonstrated in patients with metabolic syndrome (MetS). However, alterations in left atrial (LA) function in MetS are unknown. We aimed to use strain/strain rate (SR) imaging to investigate the effect of MetS on LA function.

Tribbles homolog 3 is induced by high glucose and associated with apoptosis in human endothelial cells.

Tribbles homolog 3 (TRIB3) is an intracellular kinase-like molecule that modifies cellular survival and metabolism. The present study aimed to investigate the function of TRIB3 regulation in the process of high glucose-induced apoptosis in endothelial cells, with the aim of identifying a novel intervention target for the prevention and treatment of diabetes mellitus. Human umbilical vein endothelial cells (HUVECs) grown in medium with various concentrations of glucose (5.

The application of vWF/ADAMTS13 in essential hypertension.

Background: Plasma von Willebrand factor (vWF), a key player in hemostasis and thrombosis, is released from endothelial cells during inflammation. Hypertension, a progressing in chronic inflammation and cardiovascular syndrome with various causes, results in functional and structural changes of heart and arterial vessels. However little information is available on LA changes during hypertension.

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.

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.

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.

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.

IL-18 overexpression promotes vascular inflammation and remodeling in a rat model of metabolic syndrome.

Although considerable evidence implicates the cytokine interlukin-18 (IL-18) in metabolic syndrome (MetS), the direct effect of IL-18 on vascular changes of MetS remains unknown. We investigated the chronic in vivo effect of IL-18 on development of MetS and vascular inflammation and remodeling by overexpressing IL-18 protein in fructose-fed rats (FFR), a model of MetS using intravenous administration of an adenovirus encoding rat IL-18. Increased serum IL-18 and vascular inflammatory response were found in FFR.

Impaired atrial synchronicity in patients with metabolic syndrome associated with insulin resistance and independent of hypertension.

The risk of developing atrial fibrillation is increased in patients with metabolic syndrome, but atrial conduction properties are uncharacterized in patients who have metabolic syndrome without atrial arrhythmia. We used tissue Doppler imaging to evaluate intra- and interatrial synchronicity in such patients. The imaging was performed in 145 patients with metabolic syndrome and 110 controls.

Impaired left ventricular synchronicity in patients with metabolic syndrome, regardless of hypertension.

Objective: To assess the left ventricular (LV) diastolic and systolic synchronicity in patients with metabolic syndrome.

Methods: Tissue Doppler echocardiography was performed in 235 individuals (135 with metabolic syndrome and 100 controls). Diastolic and systolic synchronicity was determined by measuring the SD of time to peak myocardial early diastolic relaxation and systolic contraction and the maximal difference in time to peak myocardial early diastolic relaxation and systolic contraction with six basal and six middle LV segments.

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.

TRIB3 functional Q84R polymorphism is a risk factor for metabolic syndrome and carotid atherosclerosis.

Objective: To determine the association of TRIB3 Q84R polymorphism with metabolic syndrome (MetS) and carotid atherosclerosis.

Research Design And Methods: A case-control study enrolled 513 Chinese subjects in three groups: control, MetS, and obese. The functional TRIB3 Q84R polymorphism was genotyped among subjects undergoing carotid ultrasonography.

Impaired left ventricular systolic and diastolic function in patients with metabolic syndrome as assessed by strain and strain rate imaging.

The present study aimed to investigate cardiac structural and functional alterations in patients with metabolic syndrome (MS) and to compare those with control subjects. Strain and strain rate (SR) imaging were preformed in 200 patients with MS and 197 normal subjects. The patients were further divided into Group 1 (with three metabolic disorders) and Group 2 (with four metabolic disorders) to elucidate the influence of different metabolic components on left ventricular (LV) functions.

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.

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.

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.

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.

[Mechanism of reversion of myocardial interstitial fibrosis in diabetic cardiomyopathy by valsartan].

Objective: To investigate the mechanism of reversion of myocardial interstitial fibrosis in diabetic cardiomyopathy (DCM) by valsartan.

Methods: Forty male wistar rats were randomly divided into 3 groups: DCM group, n = 16, fed with high-fat diet for 4 weeks and injected intraperitoneally with streptozocin (STZ) once to induce hyperglycemia so as to construct a DCM model, and then perfused into the stomach with normal saline; valsartan group, n = 16, to be constructed into DCM model and then perfused into the stomach with valsartan once daily; and control group (n = 8, fed with normal food and perfused into the stomach with normal saline. Four weeks after feeding (i.

[The role of glucose/TSP-1/TGFbeta1 signal pathways in diabetic cardiomyopathy].

Objective: Hyperglycemia could upregulate transforming growth factor-beta (TGFbeta(1)) via thrombospondin (TSP-1) and induce fibrotic renal disease in the rat in vivo and myocardial fibrosis was related to cardiac dysfunction in diabetic patients. We explored the role of glucose/TSP-1/TGFbeta(1) signal pathways in the development of diabetic cardiomyopathy (DCM).

Methods: Male Wistar rats were fed with high cholesterol diet for 17 weeks, streptozocin (30 mg/kg, i.