17 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
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
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
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
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
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
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
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) Scatter plot and (B) ROC curves of the IQRSD between V4-V5 and between V6-I.
<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
(A, B) 3D electroanatomic map and (C, D) corresponding reconstruction vectors of precordial ECG (lower panel) in two ARVC patients.
<p>The spatial inhomogeneity between leads V1 and V2 (C) and between leads V6 and I (D) indicate corresponding epicardial unipolar scar (green area, less than 5.5 mV) at the right ventricle site and left lateral left ventricle, respectively.</p
Long-Term Outcome of Non-Sustained Ventricular Tachycardia in Structurally Normal Hearts
<div><p>Background</p><p>The impact of non-sustained ventricular tachycardia (NSVT) on the risk of thromboembolic event and clinical outcomes in patients without structural heart disease remains undetermined. This study aimed to evaluate the association between NSVT and clinical outcomes.</p><p>Methods</p><p>The study population of 5903 patients was culled from the “<b>R</b>egistry of 24-hour <b>E</b>CG <b>m</b>onitoring at <b>T</b>aip<b>e</b>i Veterans General Hospital” (REMOTE database) between January 1, 2002 and December 31, 2004. Of that total, we enrolled 3767 patients without sustained ventricular tachycardia, structural heart disease, and permanent pacemaker. For purposes of this study, NSVT was defined as 3 or more consecutive beats arising below the atrioventricular node with an RR interval of <600 ms (>100 beats/min) and lasting < 30 seconds.</p><p>Result</p><p>There were 776 deaths, 2042 hospitalizations for any reason, 638 cardiovascular (CV)-related hospitalizations, 350 ischemic strokes, 409 transient ischemic accident (TIA), 368 new-onset heart failure (HF), and 260 new-onset atrial fibrillation (AF) with a mean follow-up duration of 10 ± 1 years. In multivariate analysis, the presence of NSVT was independently associated with death (hazard ratio [HR]: 1.362, 95% confidence interval [CI]: 1.071–1.731), CV hospitalization (HR: 1.527, 95% CI: 1.171–1.992), ischemic stroke (HR: 1.436, 95% CI: 1.014–2.032), TIA (HR 1.483, 95% CI: 1.069–2.057), and new-onset HF (HR: 1.716, 95% CI: 1.243–2.368). There was no significant association between the presence of NSVT and all-cause hospitalization or new-onset AF.</p><p>Conclusion</p><p>In patients without structural heart disease, presence of NSVT on 24-hour monitoring was independently associated with death, CV hospitalization, ischemic stroke, TIA, and new onset heart failure.</p></div