bluuebunny/crossref_metadata_2025_split huggingface dataset:
P6575Evaluation of arrhythmias using an insertable cardiac monitor in patients with hypertrophic cardiomyopathy
Authors: Magnusson P , Morner S 
Published: October 2019

Abstract

Background
Hypertrophic cardiomyopathy (HCM) is a heterogeneous disease associated with arrhythmias. Life-threatening ventricular tachycardia (VT) or fibrillation is the main cause of sudden cardiac death (SCD) in HCM, even though bradycardia does occur. An implantable cardioverter-defibrillator effectively prevents SCD. Non-sustained VT is a risk factor for SCD and part of current risk stratification. Furthermore, atrial fibrillation (AF) is believed to be common in HCM and increases the risk of stroke. Notably, novel oral anticoagulant (NOAC) is recommended in HCM with AF, even in the absence of other risk factors. Routinely, arrhythmias are evaluated by 24–48 hours of ambulatory monitoring occasionally. Thus, the true burden of arrhythmia is unknown but may be elucidated by an insertable cardiac monitor (ICM).

Purpose
The purpose of this study was to ascertain the incidence of NSVT, AF, and significant bradycardia in unselected HCM patients by use of an ICM.

Methods
In total, 30 adults with HCM had an ICM Confirm Rx implanted subcutaneously at the level of the fourth rib on the left side. None had a cardiac device implanted previously since they were considered to be at low risk for SCD according to ESC risk score. The application for monitoring was installed in the patients' phone which also allowed for patient activation in case of symptoms. The ICM was programmed as follows: VT ≥160 beats per minute (bpm) during ≥8 intervals, AF ≥2minute of duration, and bradycardia ≤40 bpm or pause ≥3.0 s. Clin Trial Reg: NCT03259113.

Results
In total, 29 patients, mean age 51.2±12.3 years, 24 (82.8%) males, completed the monitoring and 1 had the phone disconnected the vast majority of time and was excluded for analyses. During a follow-up of 14–18 months, 9 patients (31.0%) had AF and were started on NOAC and potential dose-adjustment of beta-blocker. One of these patients had syncope due to rapidly conducted AF. One of the patients with AF also had episodes of atrial flutter. At least one episode of NSVT was detected in 6 patients (20.7%). In 11 patients (37.9%), sino-atrial block/sinus arrest were seen, typically 30–40 bpm. In 9 patients (31.0%) no significant arrhythmia were detected.

Conclusion
In this first study of ICM in HCM, evaluation of arrhythmia burden in low risk patients with HCM, yielded 31.0% AF, 20.7% NSVT, and 37.9% sino-atrial block/arrest.

Acknowledgement/Funding
Abbott
P6580Prevalence and clinical significance of latent Brugada syndrome in juvenile lone atrial fibrillation
Authors: Fathy E , Gaido L , Quaranta S , Anselmino M , Giustetto C , Kamal Salama M , Ghaleb R , Salh A , Gaita F 
Published: October 2019

Abstract

Introduction
Brugada syndrome (BrS) cause about 20% of sudden cardiac death (SCD) in young healthy adults. Nearly 20% of Brugada patients develop supraventricular arrhythmias, mostly atrial fibrillation (AF). But whether lone AF may be the first clinical manifestation in young patients with latent BrS remains unclear.

Purpose
To estimate the prevalence and clinical significance of latent Brugada ECG pattern in young population (age ≤45 years) with lone AF.

Methods
A total of 78 patients with lone atrial fibrillation (mean age 35±7) were selected from 111 young patients with juvenile atrial fibrillation (age ≤45 years) between January 2015 and November 2017. All patients were clinically evaluated. Moreover 12 lead-24H Holter ECG and pharmacological class 1C antiarrhythmic drug (AAD) test were done for high suspicious cases of Brugada ECG. The diagnosis of Brugada ECG pattern was established according to the second consensus report criteria 2005 and since 2013, according to HRS/EHRA/APHRS expert consensus statement.

Results
According to the study protocol, we considered two groups of patients, group 1: 13 patients (16.7%; mean age 37±8) were diagnosed with type 1 Brugada ECG pattern (3 during class 1C AADs therapy and 10 induced by class 1C AAD test), group 2: 65 patients (83%; mean age 35±7) diagnosed as lone AF without type 1 Brugada ECG. The clinical characteristics of the two groups are described in table 1. Regarding to group 1, two patients had positive electrophysiological study with subsequent ICD implantation and genetic test for SCN5A mutation was positive in 3 patients.
Table 1. G1, G2 clinical characteristics Patients characteristics Group 1 (n=13) Group 2 (n=65) P value Mean age (years) 37±8 35±7 0.42 Gender (Male %) 7 (54%) 54 (83%) 0.02 Family history of BrS 2 (15%) 0 (0%) 0.03 Family history of SCD 1 (8%) 1 (1.5%) 0.20 Syncope 4 (31%) 5 (8%) 0.02 Sick Sinus Syndrome 1 (8%) 7 (11%) 0.70 Paroxysmal AF 12 (92%) 54 (83%) 0.40 Suspected basal ECG for BrS 13 (100%) 28 (43%) <0.01 Statistical test is considered significant when p value <0.05.

Conclusions
Up to our knowledge this study is the first one that estimate the prevalence of latent BrS in juvenile lone AF patients. Young patients with lone AF had a high prevalence of latent BrS. Syncope, family history of SCD and family history of BrS are significant indicators of the presence of latent BrS in young patients with lone atrial fibrillation.
P6591Arrhythmogenic effects of non-steroidal anti-inflammatory drugs (NSAID)
Authors: Frommeyer G , Baeumer S , Ellermann C , Eckardt L 
Published: October 2019

Abstract

Background
Clinical and experimental data suggest potential deleterious effects of non-steroidal anti-inflammatory drugs (NSAID) in cardiac disease. The aim of the present study was to characterize potential direct arrhythmogenic effects of ibuprofen or indometacin on cardiac electrophysiology.

Methods and results
In 13 isolated rabbit hearts, indometacin was administered in increasing concentrations (10, 30 and 50μM) after obtaining baseline data. In further 13 hearts, ibuprofen was infused (10, 30 and 50μM). Eight endo- and epicardial monophasic action potentials and a simultaneously recorded 12-lead ECG showed a significant decrease of QT-interval in indometacin- (50μM: −60ms, p<0.05) and ibuprofen-treated hearts (50μM: −81ms, p<0.01). This was accompanied by a similar decrease of action potential duration (APD). Effective refractory period (ERP) was also reduced by indometacin (−24ms, p<0.05) and ibuprofen (−22ms, p<0.05) while spatial dispersion of repolarisation remained stable with both drugs.
Programmed ventricular stimulation and burst stimulation were employed for provocation of ventricular arrhythmias. In the indomethacin group 7 episodes of ventricular arrhythmias were inducible at baseline. The incidence was increased to 22 (10μM), 37 (30μM) and 51 (50μM) with higher concentrations of indometacin. In the ibuprofen group 15 episodes were inducible at baseline. After infusion of 10μM ibuprofen, also 15 episodes of ventricular arrhythmias occurred while 34 episodes were inducible with 30μM ibuprofen.

Conclusion
Infusion of the NSAID ibuprofen and indometacin resulted in a significant abbreviation of myocardial repolarization and a shortening of ventricular refractory periods. This resulted in an enhanced inducibility of ventricular arrhythmias and may contribute to the proposed deleterious effects of NSAID in the presence of cardiac disease.
P6594Granger Causality-based analysis to accurately identify specific electrophenotypes of myocardial fibrillation
Authors: Handa B S , Li X , Qureshi N , Mann I , Kanagaratnam P , Peters N S , Ng F S 
Published: October 2019

Abstract

Background
Clinical identification of fibrillation drivers remains challenging in both atrial and ventricular fibrillation (VF). In this study, we developed novel tools using granger causality (GC) analysis for quantifying the causal relationship between neighbouring fibrillatory signals. We tested whether it was adaptable to low resolution, limited coverage and sequentially acquired data for quantifying global organisation of VF and mapping regions with stable rotational drivers (RDs).

Methods
Eighteen Sprague-Dawley rat hearts were perfused ex vivo for optical mapping studies. VF with differing degrees of organisation was induced with carbenoxolone (10–50μM, n=8), or prior maturation of patchy ventricular fibrosis (n=10) generated by ischaemia-reperfusion. After phase mapping, the data was downsampled to 25% of full resolution to develop validated GC-based tools. The causality pairing index (CPI), a global measure of organisation, quantified propagational effects between all neighboring signals. Low-resolution GC-vector maps localized areas harboring RDs and quantified the prevalence of RDs over time using a novel index called circular interdependence value (CIV). These GC-based tools were then adapted to analyze low-resolution multi-electrode electrograms of sixteen persistent-AF (psAF) patients presenting for a first ablation procedure.

Results
A spectrum of fibrillatory organisation and mechanisms in VF was observed. In rat VF there was a positive correlation between CPI and the number of stable RDs (R2=0.41, p=0.004), and CIV showed a significant difference in driver vs non-driver regions (0.91±0.05 vs 0.35±0.06, p=0.0002). Similarly, in psAF patients, there was a positive correlation between CPI and the number of stable RDs (R2=0.56, p≤0.001). GC vector mapping showed that 8/16 of patients had at least one RD area, and 8/16 had chaotic activity with no RDs.

Conclusion
Mechanisms of myocardial fibrillation occurs along a spectrum between organized activity with discrete areas harboring RDs and disorganised myocardial activation with no RDs. GC maps can be utilised for identifying regions localising RDs with sequential mapping in limited spatial resolution and coverage. In psAF GC-based analysis accurately identified specific fibrillatory mechanisms from low-resolution mapping. GC vector mapping holds potential for development with human fibrillation data as a mapping tool for driver guided ablation.

Acknowledgement/Funding
BHF Programme Grant PG/16/17/32069
P6595The optogenetic defibrillation of ventricular arrhythmia in myocardial infarction rats in vivo
Authors: Wang X I , Cheng Y , Rao P , Wang L 
Published: October 2019

Abstract

Introduction
Optogenetics is a low-invasive, flexible and highly selective intervention that enables electrical excitation with light on myocardium overexpressing light-sensitive proteins. Optical illumination can control the simultaneous exciting of the whole myocardium under the spot, which is more conducive to recovery from electrical disturbance to sinus rhythm.

Purpose
We explored optogenetic defibrillation for different illumination parameters how to affect defibrillation rates and the possible mechanism of continuous illumination defibrillation.

Methods
Systemic delivery via right jugular vein injection of (AAV9-CAG-hChR2(H134R)-mCherry) were performed in juvenile SD rats to achieve the light sensitive protein Channelrhodopsin-2 (ChR2) transfer throughout the whole heart. We intubated and ventilated rats, opened chest and recorded the ECG. After ligation of the left anterior descending coronary artery, ventricular arrhythmia was induced by electrical burst stimulation (10v, 50Hz, 2s). Cardiac epicardium illumination with 470nm blue laser was performed to investigate the effects of optogenetic defibrillation and its underlying mechanism. Every heart accepted 30 pulses of 20ms duration on 8Hz to test the light intensity threshold for 1:1 capture. Different illumination modes of multiple light intensity (2,4,8,10,20 times threshold intensity), pulse duration (20, 50, 200, 500 and 1000ms) and illumination position (RV apex, RV, RVOT, septum, LV) were applied in each attempt for 4 repetitions with 1 s interval.

Results
We demonstrated that ventricular arrhythmias could be terminated by illumination of the right ventricle at 20 times threshold intensity in 1s (figure A) with the successful defibrillation rate of 95±2.673% (mean ±SEM; N=7). Herein, the successful optogenetic defibrillation rate was strongly depending on light intensity (N=5, n=50 episodes, p=0.0118) and duration of illumination (N=5, n=50 episodes, p<0.0001) (figure B.C). Notably when there were higher intensity and longer pulse duration, the higher defibrillation rate appeared. There was no significant difference in the defibrillation rate among different illumination positions (N=5, n=25episodes per position, p=0.1177) (figure D). To explore the underlying mechanism of optogenetic defibrillation, we performed the same illumination mode during sinus rhythm in 2 rats (figure E. F. G). We observed that higher light intensity and longer pulse duration were more conducive to induce an episode of higher frequency focal excitement.
Views of optogenetic defibrillation

Conclusions
We demonstrated that optogenetic defibrillation is a highly effective intervention and the possible mechanism is partly attributed to overdrive suppression. We believe that optogenetic approach is potentially to be translated into more efficient and pain-free clinical termination of ventricular arrhythmia.

Acknowledgement/Funding
The national natural science foundation of China (81772044)
P6600Cardiac electrical biomarker retains memory of myocardial ischaemia not severe enough to cause myonecrosis
Authors: Chattopadhyay S , Adjei F , Kardos A 
Published: October 2019

Abstract

Background
“Cardiac electrical biomarker” (CEB) is a numerical index measured by the Vectraplex ECG (vECG) System with Vectraplex AMI software that detects changes in the cardiac electrical fields from dipolar to multipolar vectors during myocardial ischemia. CEB has been validated with ECG traces derived from patients with acute myocardial infarction. However the threshold of CEB for diagnosis of NSTEMI is varied between studies.

Purpose
To examine the effect of myocardial ischemia during transient coronary occlusion on CEB and the time-course of its recovery.

Method
Seventy-five consecutive patients with normal (without Q waves, ST-T changes, arrhythmias, bundle branch blocks, left ventricular hypertrophy etc) surface ECG (sECG) had CEBs measured from vECGs recorded before, during and 1, 2 and 3 hours after balloon occlusion during elective percutaneous coronary intervention (PCI). HsTnI was measured before and 1, 2 and 3 after the procedure. The balloon was inflated to the clinically indicated pressures till the appearance of symptoms and/or ST changes or to a maximum of 90 seconds. Ischemia induction during balloon occlusion was confirmed by the presence of ST-T changes on sECG and/or TIMI-0 flow on angiogram. Multiple vECGs were recorded at each balloon occlusion. Every vECG used to derive CEBs was adjudicated for quality by 2 observers blinded to the results. vECGs with wandering baseline, transient arrhythmias, bundle branch blocks etc. were discarded. The highest CEBs derived from best traces were analysed. The pre- and post-PCI CEBs, were compared with the maximum CEB during balloon occlusion using Wilcoxon rank and Friedman test.

Results
Fifteen subjects with negative FFR and 2 subjects with totally occluded arteries that could not be revascularised were excluded. Mean duration of balloon occlusion resulting in the highest CEB was 54.1 secs. The maximum CEB was reached in 20, 27 and 11 patients during pre-dilatation, stent deployment and post-dilatation respectively. The CEB increased with balloon inflation (pre-PCI median (interquartile range, IQR) 53.5 (31–105) vs balloon occlusion 202 (108–332), p<0.0001). The CEB during balloon occlusion gradually recovered over 1, 2 and 3 hrs post-PCI (vs 74.5 (35–135), p<0.0001; vs 66 (37–118), p<0.0001; vs 58.5 (29–97), p<0.0001 respectively). The 1hr (p=0.0011) and 2hr (p=0.0352) post-PCI CEB remained higher than pre-PCI CEB and returned to the pre-PCI level at 3h post-PCI (p=0.4433). All except 2 patients had normal 3hr TnI; both being below the threshold for diagnosis of peri-procedural MI.
Figure 1

Conclusion
CEB increases with short transient coronary artery occlusion not severe enough to cause myocardial necrosis and took 3 hours to return to the pre-procedural level suggesting its feature of “ischemic memory”. Thus CEB may have a value in detecting an ischemic episode in patients with chest pain but without a raised hs-Tn.

Acknowledgement/Funding
None
33Can anti-hypertensive thiazide diuretics also reduce fragility fracture risk?
Authors: Sousa J P , Ribeiro J , Puga L , Lourenco C , Goncalves L 
Published: October 2019

Abstract

Introduction
A great deal of fractures are related to osteoporosis. Thiazide diuretics have been associated with reduced age-related bone loss, by decreasing urinary calcium excretion. On the other hand, they can also induce hyponatremia, which is a risk factor for fracture occurrence, potentially jeopardizing hypocalciuric protective effects. Recently, a secondary analysis of the ALLHAT trial found that chlorthalidone may reduce hip and pelvic fractures, when compared to lisinopril.

Purpose
To compare fracture outcomes of hypertensive thiazide users with those of hypertensive patients not treated with thiazides.

Methods
MEDLINE, EMBASE, Cochrane and SCOPUS databases were comprehensively searched, from inception to the first of February of 2019, for cohort studies mentioning thiazide diuretic usage and fracture rates. Literature search, study eligibility, including methodological quality assessment, and data extraction were independently conducted by two investigators. Meta-analysis was performed using generic inverse variance outcome and, due to heterogeneity of the original studies, a random effects model. Confounder-adjusted relative risk (RR) was pooled. Primary outcome was total fracture rate, whereas hip and women-specific fracture risk were regarded as secondary endpoints.

Results
Fourteen eligible studies were identified. Overall, 3,601,779 patients were included and 290,885 incidental fractures were recorded. Prototype patient was middle-aged to old and three studies only enrolled females. Clinical follow-up was documented at a median of five years. Thiazide diuretic users, as compared with non-users, had a significant 11% reduction in total fractures (RR=0.86, 95% confidence interval [CI]=0.82–0.97, p=0.008, i2=77%). Seven studies, encompassing 553,614 patients and 5,005 cases, allowed for estimation of hip fracture risk, with thiazides demonstrating an even larger effect (RR=0.78, 95% CI=0.68–0.89, p=0.0004, i2=45%). Likewise, four studies, incorporating 149,024 patients and 150.998 cases, were able to provide insight into women fracture risk, in whom thiazides seem to exert no significant protective effect (RR=1.00, 95% CI=0.78–1.27, p=0.98, i2=77%).

Conclusion
Thiazide diuretics may convey a decreased risk of fracture, particularly in the potentially lethal hip location. This protective secondary effect of thiazides should be considered in hypertension clinic, with osteoporotic men seeming the best candidates for this therapy.
45Association of types of dietary fats and all-cause and cause-specific mortality: a prospective cohort study and meta-analysis of prospective studies with 1,148,117 participants
Authors: Mazidi M , Mikhailidis D P , Sattar N , Toth P P , Judd S , Blaha M J , Hernandez A V , Banach M 
Published: October 2019

Abstract

Background
The associations between dietary fats with mortality are poorly delineated.

Purpose
Using a large prospective cohort we evaluated the link between total fat, mono-unsaturated (MUFA), polyunsaturated (PUFA) and saturated fatty acid (SFA) consumption and all-cause, coronary heart disease (CHD), stroke, and diabetes (T2D)-associated mortality in a representative sample of US adults. We then added our results to a systematic review and meta-analysis.

Methods
We evaluated 35,080 participants from the National Health and Nutrition Examination Surveys (NHANES) 1988–1999 (19.2 years follow-up) and 1999–2010 (12 years follow-up), with vital status available through December 31, 2011. Cox proportional hazard regression models were used to evaluate the association between baseline quartiles of fat consumption (g/day, 24h recall) and all-cause or cause-specific mortality. For the systematic review, selected databases were searched up to November 2018 and 29 prospective cohorts (n=1,148,117) met inclusion criteria. The DerSimonian-Laird method and generic inverse variance methods were used for random effects meta-analyses.

Results
In fully adjusted models from our prospective study, there was a negative association between total fat (hazard ratio [HR]:0.90, 95% confidence interval [CI]: 0.82, 0.99, Q4 vs. Q1) and PUFA (0.81,95% CI: 0.78–0.84) consumption and all-cause mortality (Figure), whereas SFA were positively associated with mortality (1.08, 95% CI: 1.04–1.11). In the meta-analysis we found a significant negative association between total fat (HR: 0.89, 95% CI: 0.82–0.97, I2:27%), MUFA (0.93, 95% CI: 0.87–0.99, I2:56%) and PUFA (0.86, 95% CI: 0.80–0.93, I2:63%) consumption and all-cause mortality. No significant association was observed between total fat and both CVD and CHD mortality (0.92, 95% CI: 0.79–1.08, I2:46%, and 1.03, 95% CI: 0.99–1.09, I2:42%, respectively), while a positive association between SFA intake and CHD mortality (1.10, 95% CI: 1.01–1.20, I2:52.6%) was observed. Neither MUFA nor PUFA were associated with CVD and CHD mortality. Inverse associations were observed between MUFA (0.80, 95% CI: 0.67–0.96, I2:0%) and PUFA (0.84, 95% CI: 0.80–0.90, I2:0%) intakes and stroke mortality.
All-cause death and total fat intake.

Conclusions
Our results highlight differential associations of total fat, MUFA and PUFA intake with all-cause mortality, but no association of them with CVD and CHD mortalities. SFA intake was significantly associated with higher all-cause mortality inNHANES and with CHD mortality in our meta-analysis. The type of fat intake appears to be associated with important health outcomes.

Acknowledgement/Funding
None
65Utilization of percutaneous left atrial appendage closure in patients with atrial fibrillation in the United States: analysis from national inpatient sample 2016
Authors: Wu L , Ho K 
Published: October 2019

Abstract

Introduction/Background
In recent years, the percutaneous left atrial appendage closure (LAAC) has been gaining its popularity in the US. However its use in the US in recent years has not been well described.

Purpose
To provide an updated cross-sectional survey of performance of percutaneous LAAC in the US at national database level.

Methods
We use ICD-10 disease and procedure code to identify all the percutaneous LAAC performed in 2016 in US from national inpatient sample database. The demographic feature, comorbidity, mean time to procedure, mortality, complication rate, length of stay, total cost were described. Procedure related complication Including any vascular, cardiac, respiratory, neurologic and renal complications defined by AHRQ as patient safety indicators.

Results
There is approximately a total of 7550 percutaneous LAAC performed in the US in 2016. The majority of the patients were elderly (mean age 66.83±0.34), white (80.41%) male (59.04%). The mean Charlson Comorbidity Index score is 1.74, with hypertension (76.75%), diabetes (29.23%) being the most common comorbidity. The mean time to procedure is 1.98±0.11 days. The procedure related mortality is 2.06%, whereas the complication rate is 19.6%. The average length of stay is 10.77 day, with an average total cost of 239.67 thousand dollars.
Baseline characterlistisc and outcomes Total percutaneous LAAC (estimated from sample) 7550 Age, years 66.83±0.34 Male, % 59.04 White, % 80.41 Mean Charlson Comorbidity Index 1.74±0.31 Hypertension, % 76.75 Diabetes, % 29.23 CKD, % 21.42 Mean Time to procedure, days 1.98±0.11 Mortality, % 2.06 Length of Stay, days 10.77±0.25 Any Complication, % 19.6 Total Cost, thousand dollars 239.67±10.01 Values are reported as mean ± SD. Categorical variables are represented as frequency.

Conclusion
A total of 7550 percutaneous LAAC was performed in US in 2016. The procedure related mortality is 2.06%, with an average time to procedure of 1.98 days and a length of stay of 10.77 days.