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Background Acquired long QT syndrome (aLQTS) is often associated with poor clinical outcomes. Objective The purpose of this study was to examine the important predictors of all-cause mortality of aLQTS patients by applying both random survival forest (RSF) and non-negative matrix factorization (NMF) analyses. Methods Clinical characteristics and manually measured electrocardiographic (ECG) parameters were initially entered into the RSF model. Subsequently, latent variables identified using NMF were entered into the RSF as additional variables. The primary outcome was all-cause mortality. Results A total of 327 aLQTS patients were included. The RSF model identified 16 predictive factors with positive variable importance values: cancer, potassium, RR interval, calcium, age, JT interval, diabetes mellitus, QRS duration, QTp interval, chronic kidney disease, QTc interval, hypertension, QT interval, female, JTc interval, and cerebral hemorrhage. Increasing the number of latent features between ECG indices, which incorporated from n = 0 to n = 4 by NMF, maximally improved the prediction ability of the RSF-NMF model (C-statistic 0.77 vs 0.89). Conclusion Cancer and serum potassium and calcium levels can predict all-cause mortality of aLQTS patients, as can ECG indicators including JTc and QRS. The present RSF-NMF model significantly improved mortality prediction.

Acquired long QT syndrome (ALQTS) has long been overlooked in clinical practice. Recent studies reported that severe ALQTS (QTc ≥500 ms) in hospitalized patients is associated with increased all-cause mortality.The purpose of this study was to determine the role of ALQTS in the clinical outcomes of hospitalized patients.Electronic medical records were reviewed to identify severe ALQTS in hospitalized patients in a single study center from September 1, 2013, to February 28, 2014. Up to 1-year follow-up was conducted in the ALQTS subjects and compared with age-, gender-, and admitting diagnosis-matched hospitalized patients with a normal QT interval.Severe ALQTS (QTc 529 ± 38 ms) was seen in 0.7% (293/41,649) of hospitalized patients, of whom 86% were treated in noncardiology departments. All-cause mortality was 32% in the ALQTS group vs 14% in the control group (P.001) during follow-up of 255 ± 63 days. Syncope and life-threatening ventricular arrhythmia were more frequent in patients with severe ALQTS (6% vs 0.6%, P .0001). Cerebral hemorrhage (odds ratio [OR] 6.405, 95% confidence interval [CI] 2.341-17.525), cancer (OR 5.937, 95% CI 2.658-13.260), infection (OR 2.207, 95% CI 1.124-4.333), and end-stage disease (OR 2.092, 95% CI 1.045-4.191) are the major contributors to all-cause mortality in ALQTS.Severe ALQTS is not uncommon in hospitalized patients. It can be easily overlooked because the majority of patients with severe ALQTS are treated in noncardiology departments. The clinical outcome of severe ALQTS is poor. Removing QT-prolonging factors may reduce the risks of fatal arrhythmia and sudden death in patients with ALQTS.

The TThis systematic review and meta-analysis evaluated the significance of the TPubMed, Embase, Cochrane Library, and CINAHL Plus databases were searched through November 30, 2016.Of the 854 studies identified initially, 33 observational studies involving 155,856 patients were included in our meta-analysis. TThe T

Background Different P-wave morphologies during sinus rhythm as displayed on standard ECGs have been postulated to correspond to differences in interatrial conduction. Objective The purpose of this study was to evaluate the hypothesis by comparing P-wave morphologies using left atrial activation maps. Methods Twenty-eight patients (mean age 49 ± 9 years) admitted for ablation of paroxysmal atrial fibrillation were studied. Electroanatomic mapping of left atrial activation was performed at baseline during sinus rhythm with simultaneous recording of standard 12-lead ECG. Unfiltered signal-averaged P waves were analyzed to determine orthogonal P-wave morphology. The morphology was subsequently classified into one of three predefined types. All analyses were blinded. Results The primary left atrial breakthrough site was the fossa ovalis in 8 patients, Bachmann bundle in 18, and coronary sinus in 2. Type 1 P-wave morphology was observed in 9 patients, type 2 in 17, and type 3 in 2. Seven of eight patients with fossa ovalis breakthrough had type 1 P-wave morphology, 16 of 18 patients with Bachmann bundle breakthrough had type 2 morphology, and both patients with coronary sinus breakthrough had type 3 P-wave morphology. Overall, P-wave morphology criteria correctly identified the site of left atrial breakthrough in 25 (89%) of 28 patients. Conclusion In the vast majority of patients, P-wave morphology derived from standard 12-lead ECG can be used to correctly identify the left atrial breakthrough site and the corresponding route of interatrial conduction.

Previous in vitro studies have suggested full repolarization of the epicardium coincides with the peak of the T wave (T(peak)) and that of the M cells coincides with the end of the T wave (T(end)). However, in vivo validation of the theory is lacking.Monophasic action potentials (MAPs) were recorded using the CARTO mapping system from 51 +/- 10 epicardial sites and 64 +/- 9 endocardial sites of the left ventricle in 10 pigs and from 41 +/- 4 epicardial sites and 53 +/- 2 endocardial sites of the right ventricle in two of the 10 pigs. End of repolarization (EOR) times over the epicardium (EOR(epi)), endocardium (EOR(endo)), and over both (EOR(total)) were obtained. QT(peak) and QT(end) intervals were measured from simultaneously recorded 12-lead ECG.Minimal and maximal EOR(total) were observed in the left ventricle in all pigs. Minimal EOR(total) was on the epicardium in five pigs, and maximal EOR(total) was on the endocardium in nine pigs. Minimal, mean, and maximal QT(peak) intervals all were significantly smaller than maximal EOR(epi) (322 +/- 23 ms, P.01). No significant difference was found between maximal QT(end) interval (338 +/- 30 ms) and maximal EOR(endo) (339 +/- 24 ms, difference = 1 +/- 19 ms, P =.92), between maximal QT(end) interval and maximal EOR(total) (341 +/- 24 ms, difference = 2 +/- 18 ms, P =.69), or between minimal QT(peak) interval (283 +/- 28 ms) and minimal EOR(total) (282 +/- 20 ms, difference = 0 +/- 15 ms, P =.95).In in vivo pig models, T(peak) does not coincide with full repolarization of the epicardium but coincides well with the earliest EOR, whereas the T(end) corresponds with the latest EOR. These findings suggest that not only the transmural gradients but also the apicobasal repolarization gradients contribute to genesis of the T wave.

The purpose of this study was to analyze the velocities across the coronary sinus ostium (cross-CSo) and within the coronary sinus (intra-CS) in patients with and without paroxysmal atrial (AF) fibrillation and to estimate the interatrial conduction deterioration area in AF patients.Interatrial conduction delay in AF patients has been reported. However, localization of the interatrial conduction delay still is not clear.Thirteen patients with paroxysmal AF and 10 control patients with AV nodal reentrant tachycardia or ectopic atrial tachycardia were enrolled in the study. Right atrial and CS mapping were performed using the CARTO electroanatomic mapping system during sinus rhythm and during distal CS pacing. The activation times and spatial distances of cross-CSo and intra-CS were measured between paired sites, from which the activation velocities of cross-CSo and intra-CS were obtained.During sinus rhythm, the activation velocities of cross-CSo in the AF group (1.2 +/- 0.2 m/s) were significantly slower than those in the control group (2.9 +/- 1.6 m/s, P.05). During distal CS pacing, the cross-CSo velocities of the AF group (1.0 +/- 0.5 m/s) also appeared slower than those in the control group (1.4 +/- 0.2 m/s, P = .07). However, no difference was found in intra-CS activation velocities between the two groups (2.8 +/- 1.9 vs 3.2 +/- 2.2 m/s and 1.5 +/- 0.3 vs 1.4 +/- 0.3 m/s, P.05 during sinus rhythm and distal CS pacing, respectively).Interatrial conduction at the posteroparaseptal region across the CS ostium was significantly slower in patients with paroxysmal AF than in control patients, further supporting the link between interatrial conduction deterioration and paroxysmal AF.