bluuebunny/crossref_metadata_2025_split huggingface dataset:
Anatomical predictors of high grade atrioventricular conduction disorders in patients with specific pacemaker implanted after TAVI
Authors: Frey P , Brochier A , Nezzouhairi N , Irles D 
Published: May 2021

Abstract

Funding Acknowledgements
Type of funding sources: None.

OnBehalf
STIM TAVI-MS study

Background
The evolution of atrioventricular conduction disorders after transcatheter aortic valve implantation (TAVI) remains poorly understood. Recent studies have identified short membranous septum (MS) length, deep implantation depth (ID) or their relation as anatomic risk of high-grade AV block and permanent pacemaker implantation.
Purpose : We sought to examine whether the atrioventricular (AV) membranous septum (MS) measured by computed tomography (CT) and the depth of valve implantation measured from the final aortic angiogram could predict high-grade atrioventricular block (HG AVB) after TAVI, based on specific pacemaker memory data.

Methods
STIM-TAVI-MS was a prospective, multicentre observational study that enrolled patients implanted with a specific dual chamber pacemaker after TAVI, with the SafeR algorithm activated, allowing continuous monitoring of atrioventricular conduction. The primary endpoint was the occurrence of late (after Day 7) high-grade atrioventricular block(s) during the year after TAVI. We measured on CT scans the coronal MS lenght, infra-annular MS lenght and the quantification of calcifications, on the final angiogram after TAVI we measured the implant depth (ID) to identifie ΔID-MS corresponding to the difference between implant depth and MS length. The variables were compared with the occurrence of late HG-AVB on PM memory data.
Results : Among 82 patients, (mean age 84,5 years ± 4,8, self-expending valve n = 24, 29,3%), n = 47 (57.3%) had ≥1 late high-grade atrioventricular block. Mean coronal MS length was 8,1 ± 2,5 mm, mean infra annular MS was 3,4 ± 3.1 mm, mean calcification volume was 93.0 ± 88, 85,5± 104 and 141,5 ± 137,5 mm3 for the noncoronary, right coronary and left coronary cusp respectively. Mean implant depth was 7,3 ± 3,3mm, and mean ΔID-MS = -0,7 ± 4,1mm. There were no association between MS length (OR = 1,06; CI 0,91 to 1,24), ID (OR = 1,6; CI 0,85 to 2,9), nor ΔID-MS (OR = 0,67; CI 0,37 to 1,23) and late HG AVB. Calcification volume were not associated with late HG AVB.

Conclusion
In an high risk high grade AV block population after TAVI, anatomical analysis of MS length, degree of calcification, implant depth and ΔID-MS did not predict occurrence of late (&gt; day 7 after TAVI ) high grade AV Blocks. Abstract Figure. CT scan A : aortic plane, B : MS lenght
Assessment of the SyncAV fusion pacing algorithm on exercise capacity in patients with cardiac resynchronisation therapy device
Authors: Green PG , Holdsworth D , Monteiro C , Betts T , Herring N 
Published: May 2021

Abstract

Funding Acknowledgements
Type of funding sources: Foundation. Main funding source(s): British Heart Foundation (BHF) and Local Departmental Research Funding

Background
Fusion pacing as part of cardiac resynchronization therapy (CRT) requires correct timing of left ventricular pacing to right ventricular activation. The SyncAV algorithm, available in Quadra Allure and Assura CRT devices, is designed to allow optimal fusion pacing by dynamic reassessment of intrinsic atrio-ventricular (AV) conduction to adjust the paced/sensed AV delay. However, it is unclear whether AV optimisation continues to maintain resynchronisation during exercise, or whether potential loss of fusion pacing with changes in intrinsic AV conduction could lead to decreased exercise capacity. Cardio-pulmonary exercise testing (CPET) is the gold standard method for assessing exercise performance.

Purpose
To assess exercise capacity using the SyncAV algorithm for fusion pacing, compared with conventional biventricular pacing with fixed AV delays (AVD) for CRT.

Methods
Patients at least 6 months post-CRT implant were recruited in a prospective single-centre randomized single-blind crossover study. Patients performed 2 CPET tests at least 1 week apart, with randomization to either SyncAV with fusion pacing or conventional biventricular pacing with a fixed AVD of 120ms. All other programming was optimised to produce the narrowest QRS duration possible at rest in each case.

Results
Nine patients (5 male, age 70 ± 10 years, mean ± standard deviation) were recruited, with both ischaemic and non-ischaemic aetiology of heart failure. All had clinical or echocardiographic response to CRT. There was no difference in peak oxygen consumption (V̇O2max) between programming (1.47 ± 0.57 vs 1.50 ± 0.65 l/min for fixed AVD and SyncAV groups respectively, p = 0.59), or oxygen consumption at anaerobic threshold (VT1) (0.72 ± 0.20 vs 0.74 ± 0.25 l/min, p = 0.57). There was no difference in oxygen pulse (V̇O2/heart rate - a surrogate of stroke volume) at peak (12.3 ± 3.8 vs 13 ± 5.0 ml/beat , p = 0.28) or VT1 (8.4 ± 2.2 vs 8.7 ± 2.1 ml/beat, p = 0.67) and also no change in time to V̇O2max (1400 ± 491 vs 1367 ± 543 seconds, p = 0.38) or VT1 (518 ± 211 vs 534 ± 200 seconds, p = 0.75). Average heart rate at the median stage of exercise showed no difference between programming (96 ± 18 vs 93 ± 15 bpm respectively, p = 0.32). There was no difference in BORG Rating of Perceived Exertion (BORG-RPE) score at either peak exercise (median 19 [interquartile range (IQR) 2] vs 17 [IQR 2], p = 0.23) or at the median stage of exercise (median 13 [IQR 1] vs 13 [IQR 2], p = 0.30).

Conclusion
Fusion pacing using the SyncAV algorithm does not appear to improve exercise capacity compared to optimised conventional biventricular pacing with fixed AVD.
Outcome of catheter ablation of arrhythmias in adult congenital heart disease with high density multi-electrode mapping with automatic annotation algorithm
Authors: Gomes J , Saeed Y , Kawada S , Benson L , Downar E , Nair K 
Published: May 2021

Abstract

Funding Acknowledgements
Type of funding sources: None.

Introduction
Arrhythmias are frequently encountered in adult congenital heart disease (ACHD) and respond poorly to pharmacological therapies. Catheter ablation is challenging due to anatomical variation and complexity of the arrhythmia substrate. High density multi electrode mapping (MEM) with automatic annotation of activation time may aid mapping of arrhythmia, decrease procedure time and improve the accuracy of targeting of ablation therapy.

Purpose
To compare the acute and long term outcomes and procedural characteristics of catheter ablation in ACHD patients with and without automatic annotation of activation with MEM.

Methods
Retrospective analysis of the acute and long term outcomes of ACHD patients in a single centre undergoing ablation procedures from 1 Jan 2014 to 18 August 2017 was undertaken. 2 groups were identified.
Group 1 included patients who had arrhythmia mapping performed with the CARTO 3D electroanatomic mapping system without the use of automatic signal annotation. Most patients in this group had sequential mapping performed with the ablation catheter (78%), the rest had multi-electrode mapping with the PentaRay 20 pole catheter.
Group 2 included patients who had arrhythmia mapping performed with the CARTO 3D electroanatomic mapping system using the automated CONFIDENSE mapping algorithm.

Results
Group 1: n = 27, mean age 44.6 +/-3 years. Male 46.6%. Group 2: n = 38, mean age 44.0 +/- 1.9 years. Male 56.7%. All patients had CHD of at least moderate complexity. 25% of patients in group 1 and 45% in group 2 were repeat ablations. 45 arrhythmias were induced in group 1 of which 29 were targeted and 74 arrhythmias were induced in group 2 of which 46 were targeted. Acute success rates (after attempts at reinduction) were 96.3% in group 1 and 94.7% in group 2. Recurrences of arrhythmia occurred significantly less in patients in group 2 compared to group 1 (44.7% and 70.4% respectively, p &lt; 0.05) after a follow up duration of 17.3+/-0.43 months in group 2 and 45.3 +/-1.19 months in group 1. Fluoroscopy time, procedure time and ablation time were not significantly different between groups.

Conclusions
The use of multi-electrode mapping with an automatic annotation algorithm was associated with a significantly lower risk of recurrence during the follow up period of this study.
Hypertension burden and the risk of new-onset atrial fibrillation: a nationwide population-based study
Authors: Lee SR , Park CS , Choi EK , Ahn HJ , Han KD , Oh S , Lip GYH 
Published: May 2021

Abstract

Funding Acknowledgements
Type of funding sources: None.

Background
The association between the cumulative hypertension burden and the development of atrial fibrillation (AF) is unclear.

Purpose
We aimed to investigate the relationship between hypertension burden and the development of incident AF.
Methods and Results: Using the Korean National Health Insurance Service database, we identified 3,726,172 subjects who underwent four consecutive annual health checkups between 2009 and 2013, with no history of AF. During the median follow-up of 5.2 years, AF was newly diagnosed in 22,012 patients (0.59% of the total study population, 1.168 per 1,000 person-years). Using the BP values at each health checkup, we determined the burden of hypertension (systolic blood pressure [SBP] ≥130 mmHg or diastolic blood pressure [DBP] ≥80 mmHg), stratified as 0 to 4 per the hypertension criteria. The subjects were grouped according to hypertension burden scale 1 to 4: 20% (n = 742,806), 19% (n = 704,623), 19% (n = 713,258), 21% (n = 766,204), and 21% (n = 799,281). Compared to normal people, subjects with hypertension burdens of 1, 2, 3, and 4 were associated with an 8%, 18%, 26%, and 27% increased risk of incident AF, respectively. On semi-quantitative analyses with further stratification of stage 1 (SBP 130-139 mmHg or DBP 80-89 mmHg) and stage 2 (SBP ≥140 mmHg or DBP ≥90 mmHg) hypertension, the risk of AF increased with the hypertension burden by up to 71%.

Conclusions
Both a sustained exposure and the degree of increased blood pressure were associated with an increased risk of incident AF. Tailored blood pressure management should be emphasized to reduce the risk of AF. Abstract Figure.
Evaluation of the device independent nature of a photoplethysmography-deriving smartphone app
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
Smartphone apps using photoplethysmography (PPG) technology enable digital heart rhythm monitoring through their built-in camera, without the need for additional, specific, or costly hardware. This may positively impact the availability and scalability of remote monitoring. However, the diversity of smartphone specifications on the consumer market may raise concerns regarding the robustness of AF detection algorithms between various devices.
Purpose
To study the device independency of AF detection performance by a PPG-based smartphone application.
Methods
Patients from the cardiology department were consecutively enrolled. Patients were handed 7 iOS models and 1 Android model and were asked to consecutively perform one PPG measurement per device. A 12-lead electrocardiogram (ECG) was collected during the same consultation and interpreted by a cardiologist as reference diagnosis. To allow an objective comparison across the devices, patients who failed to perform one successful measurement on each device were excluded. Additional exclusions were atrial flutter rhythms and insufficient quality results. Sensitivity, specificity and accuracy were calculated with respect to the reference diagnosis. McNemar’s analysis was used for the head-to-head comparison of the sensitivity and specificity of the proprietary algorithm on the different smartphone devices.
Results
A total of 150 patients participated in the study with a median CHA2DS2-VASc score of 3 (interquartile range: 1-5). The median age of the study population was 70 (interquartile range: 56-79) years. In total, 54.7% of the population was male and the AF-prevalence was 35.3%. After the exclusion of patients with atrial flutter (n = 14) and patients who did not successfully perform a PPG measurement on each device (n = 5), diagnostic-grade results of 131 patients were used to calculate the performance of the proprietary algorithm. The sensitivity and specificity of the AF detection algorithm ranged from 90.9% (95% CI 75.7-98.1) to 100.0% (95% CI 91.0-100) and 94.5% (95% CI 86.6-98.5) to 100.0% (95% CI 94.6-100), respectively. The overall accuracy across the devices ranged from 94.4% (95% CI 88.3-97.9) to 99.0% (95% CI 94.6-100). Head-to-head comparisons of the results did not reveal significant differences in sensitivity (P = 0.125-1.000) or specificity (P = 0.375-1.000) of the proprietary AF detection algorithm among the different devices.

Conclusion
This study demonstrated the device-independent nature of the PPG-deriving smartphone application with respect to 12-lead ECG diagnosis.
PDE4B and PDE4D differentially regulate cardiac pacemaker activity
Authors: Pereira De Vasconcelos WPV , Gomez AMG , Fischmeister RF , Vandecasteele GV , Mika DM 
Published: May 2021

Abstract

Funding Acknowledgements
Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Agence Nationale de la Recherche (ANR)
Background Heart rate (HR) is generated by spontaneous electrical activity in the sinoatrial node (SAN) and is modulated by the autonomic nervous system. During sympathetic stimulation, the activation of β-adrenergic receptors (βAR) increases cAMP levels, leading to positive chronotropic effect. Among the 6 cardiac cAMP-PDE families, PDE4 is critical for controlling excitation-contraction coupling (ECC) during β-stimulation in atrial and ventricular myocytes. PDE4 may also be important for automaticity. 3 genes encode for PDE4 in the heart (pde4a, 4b, 4d). We propose to investigate their respective contribution to the regulation of pacemaker activity.
Methods Total PDE activity in mouse SAN was determined as the cAMP-hydrolytic activity measured in the absence of PDE inhibitor and the fraction corresponding to PDE4 activity was assessed by including the PDE4 inhibitor Ro-20-1724. The in vitro pacemaker activity was assessed by measuring spontaneous Ca2+ transients in Fluo4-loaded-SAN tissue from wild-type (WT) and PDE4KO mice. Images were obtained using confocal microscopy. Telemetry EKG was recorded in conscious mice in control (CTRL) conditions, after pharmacological denervation with atropine (1 mg/kg) and propranolol (2 mg/kg) and after β-stimulation with isoproterenol (ISO, 1.5 mg/kg). HR variability was evaluated by calculating the SDNN (standard deviation of RR intervals) parameter.
Results Ro-20-1724 (10 µM) increased beating rate of intact SAN and increased PKA-phosphorylation of key ECC actors (ryanodine receptor, phospholamban and contractile proteins). PDE4 activity was found to account for 60% of total cAMP-PDE activity in SAN. PDE4A, 4B and 4D isoforms were found to be expressed in mouse SAN. In PDE4BKO SAN, the effect of ISO on SAN beating rate was higher than in WT. Ablation of PDE4D induced decreased beating rate in CTRL and ISO conditions and increased Ca2+ spark frequency compared to WT SAN. In vivo, PDE4BKO and PDE4DKO mice displayed increased resting HR during day and night. HR variability was decreased in PDE4BKO, but not in PDE4DKO mice during the day, and decreased in both genotypes at night compared to WT mice. After atropine + propranolol denervation, the rhythmic phenotype was only maintained in PDE4BKO but not in PDE4DKO mice. The response to β-AR stimulation with ISO was higher in PDE4BKO than in PDE4DKO. In addition, under ISO we observed an increased number of premature beats and atrioventricular blocks in PDE4DKO, but not in PDE4BKO mice.
Conclusion PDE4B and PDE4D differentially regulate cardiac pacemaker activity. While PDE4B clearly controls intrinsic SAN automaticity, PDE4D might be important for ANS-mediated regulation of HR and conduction.
Post myocardial infarction ionic remodelling promotes repolarisation dispersions and abnormalities in acute and chronic stages
Authors: Zhou X , Wang Z , Tomek J , Wang L , Rodriguez B 
Published: May 2021

Abstract

Funding Acknowledgements
Type of funding sources: Foundation. Main funding source(s): Wellcome Trust

Background
Sudden cardiac death after a myocardial infarction (MI) was reported in both the acute stage and the chronic stage with the development of heart failure (HF). Around 50% of these deaths were due to ventricular tachyarrhythmia which is related to the temporal dispersion of repolarisation caused by the post-MI remodelling of ionic currents. While variable extent of ionic current changes was observed in multiple animal species in different post-MI phases, the proarrhythmic effects of such remodelling in post infarction human hearts is not fully explored.

Purpose
The goal of this study is to explore the proarrhythmic effects of post-MI ionic remodelling in human ventricular myocyte models of electrophysiology for both the acute and the chronic stages.

Methods
The ToR-ORd human ventricular cellular model was used as the baseline model, and a new formulation of the calcium activated potassium current was implemented. We constructed and calibrated a population of 253 human ventricular cell models (POM) to represent electrophysiological variability of normal zone (NZ) myocytes. For the acute phase, three types of border zone (BZ) remodelling (Acute BZ1-3) were introduced based on dog experimental data collected within one week after infarction. For the chronic phase with the development of HF, BZ (Chronic BZ) and one type of remote zone (RZ) remodelling (Chronic RZ1) were introduced based on minipig data collected 5 months post-MI. Another type of RZ remodelling (Chronic RZ2) was introduced based on experimental data from failing human hearts. The cellular models were paced at cycle lengths of 1000ms, 500ms, 400ms and 300ms for 500 beats before the analysis of repolarization abnormalities.

Results
For both the acute and the chronic stages post-MI, the extent of repolarisation dispersion between BZ and the corresponding NZ and RZ varied from 2ms up to 120ms, and largely depended on the level of potassium current remodelling. A weaker calcium transient was always observed in the BZ. Early after depolarisations (EADs) and repolarisation failure (RF) were observed in the chronic stages, caused by the reactivation of L-type calcium current due to the augmentation of late sodium current and the inhibition of hERG current. Beat-to-beat repolarization alternans was observed in both the acute and the chronic stages, with the key ionic mechanisms being the inhibition of SERCA activity and the slower calcium release due to enhanced CaMKII.

Conclusions
Post-MI ionic remodelling of the acute and chronic stages can cause a substantial dispersion of repolarisation in human hearts by inducing the prolongation of action potential durations, EADs, RFs, and alternans, providing substrates for the generation and maintenance of lethal reentrant waves. Abstract Figure. BZ and RZ ionic current remodelling
Glucagon-like peptide-1 directly increases heart rate and shortens atrial refractoriness: an in vivo and ex vivo study in pigs
Authors: Lubberding AF , Veedfald S , Sattler SM , Linz BM , Eggertsen CHE , Lilleoer TMB , Qazi S , Moeller C , Tfelt-Hansen J , Holst JJ , Jespersen T 
Published: May 2021

Abstract

Funding Acknowledgements
Type of funding sources: Foundation. Main funding source(s): Novo Nordisk Foundation Synergy program Novo Nordisk Foundation Center for Basic Metabolic Research

Background
Treatment with glucagon-like peptide-1 receptor agonists (GLP-1 RAs) in patients with type 2 diabetes not only reduces hyperglycaemia, but also improves cardiovascular outcomes. However, GLP-1 RA treatment also increases heart rate: an apparent paradox.

Purpose
Whether the heart rate increase is a direct effect, and whether GLP-1 affects other aspects of cardiac electrophysiology, remain unclear. To answer these questions we investigated the effect of GLP-1 infusion on cardiac electrophysiology in vivo and ex vivo in pigs and pig hearts, respectively, during sinus rhythm and pacing.

Methods
Anaesthetised pigs (n = 8) received infusions of GLP-1 (10 pmol/kg/min). Electrocardiogram, atrial monophasic action potentials and atrial conduction velocity data were collected and atrial and ventricular effective refractory periods (ERP) were measured. For the ex vivo studies, pig hearts (n = 7) were excised, retrogradely perfused and exposed to consecutive bolus perfusions of 2 and 4 nmol GLP-1, 100 nmol of the GLP-1 receptor antagonist exendin-9-39 and a final 4 nmol bolus of GLP-1. The same electrophysiological parameters were measured.

Results
In anaesthetised pigs, GLP-1 increased heart rate, cardiac output and diastolic pressure, while systemic vascular resistance was decreased. Infusion of GLP-1 decreased PQ interval in sinus rhythm (P = 0.019, n = 8) and during atrial pacing (P = 0.027, n = 6) with 8 ± 3 % and 12 ± 3 %, respectively. Additionally, GLP-1 decreased atrial ERP at all pacing cycle lengths (P = 0.04, n = 7), while ventricular ERP was unaffected (P = 0.29, n = 7). In the isolated perfused heart, GLP-1 increased heart rate with 13 ± 2 bpm (P = 0.001, n = 7). This increase in heart rate was completely abolished by pre-administration of exendin-9-39. Atrial ERP shortened after GLP-1 perfusion (P = 0.01, n = 7) comparable to the in vivo studies, with an average decrease of 11 ± 2 %. This effect was also abolished by exendin-9-39.

Conclusion
GLP-1 increases heart rate through activation of the GLP-1 receptor in the isolated perfused heart, suggesting a direct effect of GLP-1 rather than activation through the central nervous system. Additionally, GLP-1 affects atrial electrophysiology, but not ventricular electrophysiology, in vivo and ex vivo independent of the increase in heart rate.