38 research outputs found

    Additional file 1 of The optimal antithrombotic strategy for post-stroke patients with atrial fibrillation and extracranial artery stenosis—a nationwide cohort study

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    Additional file 1: Fig. S1. Risks of clinical events of patients receiving different stroke prevention strategies compared to “AP” only excluding patients experiencing mortality within 1 year and adjusting “mortality” as the competing risk

    ROC curve for the ADMA levels in predicting adverse events.

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    <p>The area under the curve for ADMA levels in predicting adverse events was 0.767 (95% confidence interval  =  0.654–0.879). ADMA  =  asymmetric dimethylarginine; ROC curve  =  receiver-operator characteristics curve.</p

    ADMA levels in AF and non-AF patients.

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    <p>The ADMA levels were higher in AF patients compared to non-AF patients. In addition, non-PAF patients had higher levels of ADMA than PAF patients. ADMA  =  asymmetric dimethylarginine; AF  =  atrial fibrillation; PAF  =  paroxysmal atrial fibrillation. *P value <0.05, PAF or non-PAF versus no AF. <sup>+</sup>P value <0.05, Non-PAF versus PAF.</p

    Event-free survival curve for patients with different ADMA levels.

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    <p>Kaplan-Meier survival analysis showed that the patients with an ADMA level ≥ 0.55 µmol/L were associated with a higher event rate compared to patients with an ADMA level <0.55 µmol/L (33.3% versus 9.3%, p = 0.001). ADMA  =  asymmetric dimethylarginine.</p

    A novel noninvasive surface ECG analysis using interlead QRS dispersion in arrhythmogenic right ventricular cardiomyopathy

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    <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

    (A) Scatter plot and (B) ROC curves of the IQRSD between V4-V5 and between V6-I.

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    <p>The IQRSD between V4-V5 separated definite ARVC from RVOT VT (borderline cases), while the IQRSD between V6-1 differentiated Group 1 Group 2. Right panel: ROC curves of IQRSD between V4-V5 and between V6-I. The area under the curve further improved after a combination of the IQRSD between V4-V5 and V6-I. (IQRSD: interlead QRS dispersion; ROC: receiver-operator characteristic).</p

    Linear regression models on the relationship between PA-PDI interval and pericardial fat.

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    <p>hs-CRP = high sensitivity C-reactive protein; LV = left ventricle; LVEF = left ventricular ejection fraction; LVIDD = left ventricular internal dimension at end-diastole; SE = standard error; WBCs = white blood cells.</p
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