25 research outputs found
Representative flow cytometry analysis for quantifying the number of circulating endothelial progenitor cells (EPCs).
<p>Upper left shows mononuclear cells (MNCs) were gated by forward/sideward scatter (FSC/SSC) in patients with nonalcoholic fatty liver disease (NAFLD) (A) and without NAFLD (B). The numbers of circulating EPCs were defined as CD34<sup>+</sup>, CD34<sup>+</sup>KDR<sup>+</sup>, and CD34<sup>+</sup>KDR<sup>+</sup>CD133<sup>+</sup>, respectively.</p
The association between EPC levels (% and cells/10<sup>5</sup> events) and the severity of non-alcoholic fatty liver disease (values presented as means ± standard error; FL, fatty liver; Mild, mild fatty liver; Moderate, moderate fatty liver; Severe, severe fatty liver).
<p>The association between EPC levels (% and cells/10<sup>5</sup> events) and the severity of non-alcoholic fatty liver disease (values presented as means ± standard error; FL, fatty liver; Mild, mild fatty liver; Moderate, moderate fatty liver; Severe, severe fatty liver).</p
Comparison of the EPC adhesive function (A), migration (B), and tube formation capacities (C) in subjects with or without fatty liver (values presented as means ± SD; HPF: high-power field; *P<0.05).
<p>Comparison of the EPC adhesive function (A), migration (B), and tube formation capacities (C) in subjects with or without fatty liver (values presented as means ± SD; HPF: high-power field; *P<0.05).</p
Simple correlation and multivariate analysis of factors associated with nonalcoholic fatty liver disease.
<p>OR: odds ratio; CI: confidence interval; EPC: endothelial progenitor cell; hsCRP: high sensitivity C-reactive protein; ADMA: asymmetric dimethylarginine.</p>*<p>Multivariate analysis: adjusted for metabolic syndrome and uric acid levels.</p
The Association between Heme Oxygenase-1 Gene Promoter Polymorphism and the Outcomes of Catheter Ablation of Atrial Fibrillation
<div><p>A length polymorphism of GT repeats in the promoter region of the human heme oxygenase-1 (HO-1) gene modulates its gene transcription to protect against myocardial injury. The present study investigated the association between HO-1 promoter polymorphisms and the outcomes of catheter ablation of atrial fibrillation (AF). The allelic frequencies of GT repeats in the HO-1 gene promoter were screened in 205 random individuals who underwent catheter ablation for drug refractory AF.In the patients who received catheter ablation, those with AF recurrence had fewer GT repeats (53.4±7.1 vs. 56.1±6.5, p = 0.004), a lower incidence of hyperlipidemia, more non-paroxysmal AF, and a larger left atrial diameter. After conducting a multivariate logistic analysis, the number of GT repeats (Odds ratio: 0.94, 95% CI 0.90–0.99, p = 0.01) and the diameter of the left atrium (Odds ratio: 1.08, 95% CI 1.02–1.15, p = 0.01) remained independent predictors. The carriers of GT repeats, which were <29 in both alleles, were associated with a lower sinus maintenance rate after catheter ablation (38.5% vs. 60.1%, p = 0.003). The patients were divided into paroxysmal and non-paroxysmal AF groups; the number of GT repeats was associated with AF recurrence only in the patients with paroxysmal AF. The number of GT repeats, combined with LAD, was significant for predicting AF recurrence after catheter ablation (p = 0.01). The number of GT repeats was not found to be associated with differences in the left atrial diameter, the biatrial voltage, or the levels of bilirubin, ferritin, iron, C-reactive protein, or von-Willibrand factor. In conclusions, HO-1 gene promoter polymorphisms were associated with AF recurrence after catheter ablation.</p> </div
A novel noninvasive surface ECG analysis using interlead QRS dispersion in arrhythmogenic right ventricular cardiomyopathy
<div><p>Background</p><p>This study investigated the feasibility of using the precordial surface ECG lead interlead QRS dispersion (IQRSD) in the identification of abnormal ventricular substrate in arrhythmogenic right ventricular cardiomyopathy (ARVC).</p><p>Methods</p><p>Seventy-one consecutive patients were enrolled and reclassified into 4 groups: definite ARVC with epicardial ablation (Group 1), ARVC with ventricular tachycardia (VT, Group 2), idiopathic right ventricular outflow tract VT without ARVC (Group 3), and controls without VT (Group 4). IQRSD was quantified by the angular difference between the reconstruction vectors obtained from the QRS-loop decomposition, based on a principal component analysis (PCA). Electroanatomic mapping and simulated ECGs were used to investigate the relationship between QRS dispersion and abnormal substrate.</p><p>Results</p><p>The percentage of the QRS loop area in the Group 1–2 was smaller than the controls (P = 0.01). The IQRSD between V1-V2 could differentiate all VTs from control (P<0.01). Group 1–2 had a greater IQRSD than the Group 3–4 (V4-V5,P = 0.001), and Group 1 had a greater IQRSD than Group 3–4 (V6-Lead I, P<0.001). Both real and simulated data had a positive correlation between the maximal IQRSD (γ = 0.62) and the extent of corresponding abnormal substrate (γ = 0.71, both P<0.001).</p><p>Conclusions</p><p>The IQRSD of the surface ECG precordial leads successfully differentiated ARVC from controls, and could be used as a noninvasive marker to identify the abnormal substrate and the status of ARVC patients who can benefit from epicardial ablation.</p></div
Noncontact mapping findings of triggers.
<p>BO = breakout; EA = earliest activation; Eg = electrogram; PNV = peak negative value; Other abbreviations are the same as <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0140167#pone.0140167.t001" target="_blank">Table 1</a>.</p><p>Noncontact mapping findings of triggers.</p
Radiofrequency ablation and follow-up.
<p>RF = radiofrequency; Other abbreviations are the same as <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0140167#pone.0140167.t001" target="_blank">Table 1</a>.</p><p>Radiofrequency ablation and follow-up.</p
Baseline Clinical Characteristics of 35 Patients.
<p>* Measured by ventriculogram</p><p><sup>†</sup> Data are presented as median (range).</p><p>ARVC = arrhythmogenic right ventricular cardiomyopathy; ICD = implantable cardioverter-defibrillator; LVEF = left ventricular ejection fraction; NS = nonsignificant; PVC = premature ventricular contraction; RVEF = right ventricular ejection fraction; RVOT = right ventricular outflow tract; VT = ventricular tachycardia.</p><p>Baseline Clinical Characteristics of 35 Patients.</p
Dynamic substrate map and isopotential maps of noncontact mapping.
<p>(A) Normalized peak negative voltage (PNV) distribution of the RV in a posterior caudal view. The orange border zone rerepresents areas with voltages around 30% of the peak negative potential. (B) Isopotential map shows the activation sequence (frames 1–4). Color scale has been set so that white indicates the most negative potential and purple indicates the least negative potential. Virtual electrodes (V1-1 to V1-4) are placed along the propagation of activation wavefront from EA site (Frame 1) to BO site (Frame 4). The green arrows indicate the activation wavefron propagating from EA to BO site, then spreading out at BO site. The virtual unipolar electrograms reveal a QS pattern at the origin.</p