bluuebunny/crossref_metadata_2025_split huggingface dataset:
Head-to-head comparison of proprietary PPG and single-lead ECG algorithms for atrial fibrillation detection
Authors: Gruwez H , Evens S , Proesmans T , Smeets C , Haemers P , Pison L , Vandervoort P 
Published: May 2021

Abstract

Funding Acknowledgements
Type of funding sources: None.

Background
Population based screening for atrial fibrillation (AF) has been suggested to reduce stroke. Photoplethysmography (PPG) deriving smartphone apps and single-lead electrocardiography (ECG) tools are attractive devices for screening due to their low cost, convenience, and accessibility. Automated algorithm analysis can serve as pre-screening or remote monitoring for AF, while confirmation on an ECG trace &gt;30s is required to establish the diagnosis. This work directly compares the performance of proprietary algorithms on PPG vs single-lead ECG for the detection of AF.

Purpose
To evaluate and compare the diagnostic performance of a PPG-deriving smartphone app and a single-lead ECG-deriving handheld device for AF detection.

Methods
Patients were recruited from the cardiology ward. After obtaining written informed consent, demographic and medical information were collected. Patients were instructed to perform one measurement using a pulse-deriving smartphone app and one via a single-lead ECG handheld device. A 12-lead electrocardiogram (ECG) was collected and interpreted by a cardiologist as gold standard. Patients with atrial flutter were excluded, with additional exclusions for insufficient quality measurements and unsuccessful measurements resulting due to technical errors. Unclassified single-lead ECG measurements were handled as test-negative. Sensitivity, specificity and accuracy were calculated with respect to the reference diagnosis. McNemar’s analysis was performed to compare the sensitivity and specificity of the proprietary PPG and single-lead ECG AF detection algorithms.

Results
The median age in the study population (n = 300) was 70 years (interquartile range: 51-78), 56.3% were men, and the median CHA2DS2-VASc was 3 (interquartile range: 1-4) with an AF-prevalence of 32.3%. PPG signal and single‑lead ECG quality was sufficient in 272/300 (91.0%) and 278/298 (93.3%) participants, respectively. After excluding atrial flutter patients (n = 25) and insufficient quality measurements, the sensitivity and specificity were 97.6% (95% CI 93.8 to 99.3) and 94.1% (95% CI 86.8 to 98.1) for the PPG signal versus 95.7% (95% CI 91.4 to 98.3) and 91.1% (95% CI 83.2 to 96.1) for the single‑lead ECG signal, respectively. Results demonstrated a 96.4% (95% CI 93.2 to 98.3) accuracy for PPG and 94.1% (95% CI 90.4 to 96.6) for single-lead ECG. No significant differences in sensitivity (P = 0.453) or specificity (P = 0.219) between the proprietary PPG and single-lead ECG algorithms were found.

Conclusion
This study demonstrated equivalent diagnostic performance of PPG and single-lead ECG proprietary AF detection algorithms in smartphone apps.
Does industry funding differ between men and women in electrophysiology and devices research?
Authors: Camm CJF , Crawford W , Olivarius-Mcallister J , Prachee I , Schaefer A , Raouf Z , Bello A , Ginks M , Nicol E 
Published: May 2021

Abstract

Funding Acknowledgements
Type of funding sources: None.

Background
A significant gender bias has been identified in cardiology. Industry funding may be important developing electrophysiology (EP) and devices research. Such funding leads to potential conflicts of interest (COI) which must be disclosed on research presentations. There is limited evidence whether the gender bias in cardiology extends to industry funding of research.
Purpose
To assess whether COI disclosures in EP and devices presentations at the ESC Annual Congress differ between men and women.

Methods
Recorded presentations from the Arrhythmia & Devices section of ESC Annual Congresses 2016-2020 were assessed. Presentations were excluded if the original presentation contained no slides, it was a panel discussion, it was a non-scientific presentation, or part of the presentation was missing. Presentations with multiple speakers were also excluded. Chi-squared and Mann-Whitney U tests were used to assess differences between groups for dichotomous and continuous data respectively.

Results
Of 1,153 presentations assessed, 999 were suitable for inclusion. Women made up 22% (n = 221) of presenters. There was no difference in whether COI declaration slides were missing between women (5.9%, n = 13) and men (7.6%, n = 56), p = 0.38. In those with COI disclosure slides (n = 927), women declared significantly lower median number of COIs (0, IQR 0-3) compared with men (2, IQR 0-8), p &lt; 0.0001. In contrast, women spent a greater time-per-word on their COI disclosure slides (250ms, IQR 125-375ms) compared with men (200ms, IQR 118-333ms), p &lt; 0.0001.

Conclusions
Women made up a minority of presenters in EP/devices talks at the ESC annual congress. Women were less likely to have COIs which may suggest that they are less likely to receive industry funding. Despite this, women spent a greater amount of time-per-word on their COI slides. The lower number of declared COIs in women highlights another potential area of gender bias in cardiology that needs further investigation so that it can be addressed.
Taurine blunts doxorubicin cardiotoxicity: chronic and acute effects
Authors: Cobet V , Tacu L , Hajawi O , Rotaru V , Frasineac V , Braniste A 
Published: May 2021

Abstract

Funding Acknowledgements
Type of funding sources: None.
Aim. To study the functional statement of the isolated heart inherent to doxorubicin cardiotoxicity under the chronic and acute action of taurine.
Material and methods. Doxorubicin (Dx) cardiotoxicity manifested by heart failure development was reproduced classically by anthracycline i/p administration in rats in cumulative dose of 16 mg/kg (4 mg/kg four times during 2 weeks) – Dx series. Series with chronic action of taurine (Tr) included rats receiving this aminoacid daily per os during Dx administration (100 mg/kg) – Dx + Tr series. Rats of both series were sacrificed by euthanasia and the isolated heart was perfused by Krebs solution according to Langendorff (isovolumic heart) and Neely-Rovetto (working heart) methods in conditions of diverse hemodynamic and neuroendocrine efforts applying. Acute action of taurine was studied during its infusion in the perfusate of isolated hearts in final concentration of 40 µM. The hearts of intact rats constituted the control series.
Results. Chronic action of taurine has identified certain important functional benefits, the most important being underlined beneath. The first, taurine reversed the negative inotropic effect of isolated heart on endothelin-1 (ET-1) action (10-7 M), detected in Dx series and manifested by both systolic pressure of left ventricle (LV) and cardiac output fall by about 9,1%. Taurine assured increase of these indices during ET-1 stimulation. The second, Tr notably improved both isovolumic relaxation and contraction of myocardium exhibited by significant enhancement of Veragut index (118,6 ± 9,6 vs 94,8 ± 6,5 1/sec), +dP/dPmax (8389 ± 445 vs 7216 ± 363 mm Hg/sec) and -dP/dTmax (7526 ± 378 vs 5684 ± 322 mm Hg/sec) during efforts with volume and resistance. The third, Tr significantly decreased LV end diastolic pressure (LVSDP) when coronary pressure of isovolumic heart elevated by 50% (from 80 up to 120 cm H20 column): 16,2 ± 1,2 vs 18,8 ± 1,4 mm Hg. Acute Tr action manifested by: (i) significant LVSDP diminution during 30 min of ischemia (52,4 ± 3,1 vs 63,7 ± 4,4 mm Hg) and on 45th min of reperfusion (18,3 ± 1,3 vs 22,8 ± 1,4 mm Hg), (ii) increased time of LV extrasystole appearance when the glucose content of Krebs solution was reduced by 50% (28,6 ± 2,8 vs 22,5 ± 2,4 min), and (iii) increased time of LV tachyarrhythmia appearance when the potassium content of Krebs solution raised up to 6,5 meq/L (9,2 ± 0,5 vs 6,9 ± 0,3 min).
Conclusion. Taurine, a natural calcium modulator of the heart, notably improves functional reserves of the myocardium exposed to cardiotoxic action of Dx, and could be seen as a relevant remedy of primary and secondary prophylaxis of Dx induced heart failure in oncologic patients.
Directed graph mapping is able to distinguish between the true and false rotors in a complex in-silico excitation pattern
Authors: Van Nieuwenhuyse E , Martinez-Mateu L , Saiz J , Panfilov A V , Vandersickel N 
Published: May 2021

Abstract

Funding Acknowledgements
Type of funding sources: Public grant(s) – EU funding. Main funding source(s): Supported in part by Dirección General de Polı́tica Cientı́fica de la Generalitat Valenciana PROMETEU 2020/043
Background
In realistic in-silico studies (Figure1, top row) it was shown that phase mapping PM (Figure 1, A) can detect the correct rotor as well as phantom rotors as an artefact of interpolation or due to the far field (Figure 1, B). After interpretation of the LAT, the far field detections could not be distinguished from the true rotor driving the excitation pattern. This can contribute to failure in Atrial Fibrillation (AF) ablation procedures.

Objective
We tested if the recently developed tool Directed Graph mapping (DGM) is less prone to far-field effects and interpolation artefacts than PM on the same in-silico data. DGM represents the excitation pattern as a directed network, from which the rotational activity is detected as cycles in that network.

Methods
Starting from the electrograms (EGMs) of the 64 electrode basket catheter, we interpolated to 957 equidistant electrodes and calculated local activation times (LATs) of the interpolated EGMs (Figure 1, C). We varied the minimal allowed conduction velocity and calculated the corresponding networks for the complete simulation time. Detections were considered as correct if they were located in the same region of the true core of the phasemaps. The false detections were classified in multiple different regions (Figure 1, D).

Results
We find that by proper choice of CVs in the graphs it is possible to achieve a 80% detection of true rotors with 26% detection of false rotors. Reducing restrictions on the CVs increased the detection rate of the false rotors. False rotors due to artifacts were not detected by DGM (Figure 1, last row).

Conclusion
DGM is able to distinguish between true and far field rotors. False detections due to interpolation artifacts as seen in the PM protocol were not observed. The velocity limits in the graph construction play a keyrole in eliminating the far field effects. Abstract Figure 1
Genotype-phenotype association in patients with arrhythmic variant of non-compaction cardiomyopathy
Authors: Rineiska N , Komissarova S , Chakova N , Dolmatovich T , Niyazova S 
Published: May 2021

Abstract

Funding Acknowledgements
Type of funding sources: None.
Purpose. To evaluate the genotype-phenotype association in Belarusian patients with non-compaction cardiomyopathy (NCCM) and clinically significant ventricular arrhythmias.
Methods. The study included 170 unrelated pts with NCCM prospectively observed in the RSPC "Cardiology", who underwent 24-hour Holter ECG monitoring for 12 months after entering the study. The median follow-up was 36 months [6; 152,0]. The median age of pts was 42 [18; 69] years, men – 63,2%. The arrhythmic phenotype of NCСM was diagnosed by the presence of unexplained syncope; nonsustained ventricular tachycardia, defined as ≥3 consecutive ventricular contractions lasting &lt;30 seconds with a frequency of ≥120 bpm; the presence of ≥ 500 ventricular premature beats (VPB) per day. The diagnosis of NCCM was established on the basis of the following criteria: 1) Echocardiography of the R. Jenni criteria; 2) CMR of the S. Petersen and A. Jaquier criteria. The mutations search in the coding sequences of 174 genes was performed in 30 unrelated pts with NCCM using next generation sequencing (NGS).
Results. In 76 out of 170 (44,7%) pts, clinically significant arrhythmias were the leading manifestation of the disease. Nonsustained VT was recorded in 54 (71,1%) pts, sustained VT – in 15 (19,7%) pts, VPB more than 500 per day – in 50 (65,8%), chronic AF with episodes of nonsustained VT was noted in 34 (44,7%) pts. During the follow-up period (median follow-up of 36 months), devices (ICD/CRT-D) were implanted in 15 (19,7%) pts, appropriate shocks were observed in two of them; three pts died, among which SCD occurred in one patient with CRT-D therapy, which was ineffective in stopping sustained VT. NGS sequencing revealed 40 changes in the nucleotide sequence (5 pathogenic mutations, 30 variants with uncertain significance (VUS), 5 new substitutions) in 27 genes in 26 (86,7%) probands. The proportion of mutations in sarcomeric proteins genes was 26,9%, and in ion channel proteins genes was 23,1%. Nucleotide changes in genes encoding structural proteins accounted for 11,5%. In 38,5% of cases, not one, but two or more rare mutations were detected, and in 30,8% – amino acid replacements were found in proteins of different functional classes.
Conclusions. The frequency of multiple mutations was higher (38,5%) in the group of pts with the arrhythmic NCCM phenotype. In the group of pts with implantable devices (ICD/CRT-D), mutations in the genes of sarcomeric proteins were observed more often. The genetic characteristics of pts, along with their clinical characteristics, are markers of a high risk of developing life-threatening arrhythmias and can be additionally used for predicting adverse events in pts with NCCM, as well as for early diagnosis of the disease in their relatives.
UBLED AF study for safety and efficacy between uninterrupted edoxaban, warfarin and rivaroxaban for AF/Fl ablation patients
Authors: Kumar N , Elbanhawy N , Chalil S , Abozguia K 
Published: May 2021

Abstract

Funding Acknowledgements
Type of funding sources: None.

Introduction
Catheter ablation in patients with atrial fibrillation (AF)/atrial flutter carries a risk of thromboembolism and major bleeding. Oral anticoagulation is advised for prevention of thromboembolic complications.
Purpose
In light of recent prospective trial data on the safety and efficacy of uninterrupted edoxaban in patients undergoing AF/flutter ablation, real-world data was aimed to compared.

Methods
A total of 228 patients who underwent AF/atrial flutter ablation over 14 months at our centre were retrospectively analyzed. All patients received uninterrupted oral anticoagulation for at least 4 weeks prior to ablation and 3 months post-ablation. Both bleeding and thromboembolic events were assessed at 24 hours comparing patients on warfarin, rivaroxaban and edoxaban.

Results
Mean age of patients were 68.5 +/- 8 years in the warfarin group (N = 86), 63.4 +/- 10.6 years; in the edoxaban group (N = 63) and 62.3 +/- 11.6 years in the rivaroxaban group (N = 79). CHADSVASc scores were 2.43 +/- 1.34, 1.68 +/- 1.34 and 1.64 +/- 1.38 respectively. The mean left atrial sizes were 42.7 +/- 6.8 mm, 42.0 +/- 6 mm and 41.1 +/- 6.5 mm respectively. The study endpoint was death, acute thromboembolism or major bleeding. There was 1 pericardial effusion (1.2%) in the warfarin group, 1 pericardial effusion and 1 transient ischaemic attack (2.5%) in the rivaroxaban group and 1 pericardial effusion needing drainage (1.6%) in the edoxaban group. There were no significant differences in the study endpoints between groups.

Conclusion
This real-world study demonstrated no significant difference in safety and efficacy between uninterrupted edoxaban, warfarin and rivaroxaban in patients undergoing AF/flutter ablation.
Aminophylline affects the cardiac rat inward rectifier potassium current in a dual way
Authors: Ramalho NJD , Svecova O , Kula R , Simurdova M , Simurda J , Bebarova M 
Published: May 2021

Abstract

Funding Acknowledgements
Type of funding sources: Public Institution(s). Main funding source(s): Ministry of Education, Youth and Sports of the Czech Republic

Introduction
Aminophylline, a bronchodilator used in clinical practice to treat namely severe astma attacks, often induces atrial fibrillation in patients. Modifications of the inward rectifier potassium current IK1 are known to play a role in the genesis of fibrillation.

Purpose
We aimed to investigate the effect of aminophylline at clinically-relevant concentrations between 3 and 100 µM on IK1 in isolated rat ventricular myocytes.

Methods
Experiments were performed by the whole cell patch clamp technique on enzymatically isolated rat right ventricular myocytes at room temperature. IK1 was measured as the current sensitive to 100 µM Ba2+.

Results
We observed a dual steady-state effect of aminophylline at most of the applied concentrations. Either inhibition or activation was apparent in individual cells during application of aminophylline at a given concentration. The smaller was magnitude of the control IK1, the more likely was activation of the current in the presence of aminophylline and vice versa (tested at 10 and 30 µM). The effect was voltage-independent and fully reversible during the subsequent wash-out. The mean aminophylline effect was inhibitory at all concentrations (10, 15, 4, and 23%-inhibition at -50 mV at 3, 10, 30, and 100 µM, respectively). Using a modified version of the population model of IK1 channels that we published before, the dual effect can be explained by interaction of aminophylline with two channel populations in a different way, the first one being inhibited and the second one being activated by the drug. Considering various fractions of these two channel populations in individual cells, varying effects observed in the measured cells can be simulated.

Conclusions
Aminophylline at clinically-relevant concentrations affects IK1 in rat ventricular myocytes in a dual way, showing both the steady-state activation and inhibition in various cells, even at the same concentration. It may be related to a different effect of the drug on various Kir2.x subunits forming the heterotetrameric IK1 channels present at the cell membrane of a single cell.
IP3R1/GRP75/VDAC1 complex mediated endoplasmic reticulum stress-mitochondrial oxidative stress in diabetic atrial remodeling
Authors: Liu T , Yuan M , Gong M , He J , Zhang Z , Meng L , Tse G , Zhao Y , Bao Q , Zhang Y , Yuan M , Liu X , Wang F , Li G 
Published: May 2021

Abstract

Funding Acknowledgements
Type of funding sources: Foundation. Main funding source(s): National Natural Science Foundation of China

Background
Mitochondrial oxidative stress is an important mechanism of atrial remodeling and atrial fibrillation (AF) in the setting of diabetes. Currently, endoplasmic reticulum (ER) stress is regarded as the key link from homeostasis to dysfunction, and is a central feature of metabolic diseases such as type 2 diabetes. However, the molecular mechanisms underlying these processes have not been fully elucidated.

Objective
To explore the potential role of ER stress-mitochondrial oxidative stress in atrial remodeling and AF induction in diabetes.

Methods
Mouse atrial cardiomyocytes (HL-1 cells) , type 2 diabetic rats and GRP75 conditional knockout mice were used as models systems. These findings were correlated with biomarker findings in human diabetic patients with confirmed atrial fibrillation.

Results
In the diabetic rat atria, significant ER stress was observed. Treatment with tunicamycin (TM), an ER stress agonist, mass spectrometry (MS) demonstrated many known ER stress and calmodulin proteins, including Heat shock protein family A (Hsp70) member (Hspa) 5 (GRP78) and Hspa9 (GRP75) and in situ proximity ligation assay (PLA) indicated that TM led to increased protein expression of the IP3R1 (inositol 1,4,5-trisphosphate receptors 1)/GRP75 (glucose-regulated protein 75)/VDAC1 (voltage-dependent anion channel 1) complex in HL-1 cells. Silencing of GRP75 using siRNA in HL-1 cells and GRP75 conditional knockout in our mouse model led to impaired calcium transport from the ER to mitochondria, and alleviated mitochondrial oxidative stress and calcium overload. Moreover, GRP75 deficiency attenuates atrial remodeling and AF progression in Myh6-Cre+/Hspa9flox/flox + TM mice.

Conclusions
The IP3R1/GRP75/VDAC1 complex mediates endoplasmic reticulum stress-mitochondrial oxidative stress plays an important role in diabetic atrial remodeling. Abstract Figure
The increase of extracellular Ca2+ from physiological concentrations to hypercalcemia impairs sino-atrial automaticity
Authors: Torrente AG , Fossier L , Baudot M , Torre E , Bidaud I , Mesirca P , Mangoni ME 
Published: May 2021

Abstract

Funding Acknowledgements
Type of funding sources: Foundation. Main funding source(s): ESC FRM Lefoulon Delalande

Aims
To investigate whether extracellular hypercalcemia alters the conduction through L-type Ca2+ channels (LTCCs), impairing the pacemaker activity of the heart.

Introduction
In the sino-atrial node (SAN), membrane currents and the dynamics of intracellular Ca2+ ([Ca2+]i) generate the pacemaker activity of the heart. SAN dysfunctions (SNDs) harm heart automaticity and have been associated with abnormal dynamics of [Ca2+]i. The LTCCs, Cav1.2 and Cav1.3 carry the main Ca2+ influx of SAN cells, which is necessary to sustain [Ca2+]i dynamics. Modified extracellular Ca2+ ([Ca2+]o) could alter Ca2+ influx through these channels. For example, cancer and hyperparathyroidism can raise [Ca2+]o, causing an extracellular hypercalcemia that could alter [Ca2+]i dynamics and impair SAN activity and heart automaticity.

Methods and results
To test this hypothesis, we measured contractions, [Ca2+]i release and L-type Ca2+ current (ICa,L) in spontaneous cells of the murine SAN. Then, we recorded rate and propagation of the spontaneous action potentials (APs) generated by the SAN tissue ex-vivo.
In spontaneously beating SAN cells, we observed that the modification of [Ca2+]o affected [Ca2+]i and cell contractility through changes of ICa,L. In particular, the increase of [Ca2+]o dysregulated pacemaker activity, likely through excessive Ca2+ influx mediated by Cav1.2.
[Ca2+]o increase to hypercalcemia induced arrhythmia also in the intact SAN tissues, activating ectopic leading regions of pacemaking and impairing conduction towards the atria.

Conclusions
Hypercalcemia causes excessive Cav1.2-mediated Ca2+ influx, which alters [Ca2+]I leading to pacemaker impairment. Modulation of LTCC may reduce pacemaker dysfunctions, preventing SND progression.