bluuebunny/crossref_metadata_2025_split huggingface dataset:
3035Synergy of artificial intelligence and single lead EKG to detect and localize STEMI
Authors: Vieira D , Mehta S , Fernandez F , Villagran C , Frauenfelder A , Ceschim M , Matheus C , Torres M A , Mazzini J , Quintero S , Pisana L , Safie R , Nola F , Krisciunas S , Cecilio S 
Published: October 2019

Abstract

Background
The cumbersome, standard 12-lead electrocardiogram (EKG) challenges an efficient detection of ST-Elevation Myocardial Infarction (STEMI) in pre-hospital (ambulances) and hospital (portable devices) settings. We believe that our machine-learning algorithm embedded into a single lead EKG will be successful in acute care settings.

Purpose
To incorporate Artificial Intelligence-guided, single lead EKG interpretation, to facilitate easy and accurate STEMI detection in urgent situations.

Methods
This is an observational, retrospective, case-control study. A subset sample was generated from the International Telemedical Systems (ITMS) database that contains cardiologist annotated EKG records. Subset: A total of 2,542 exclusively confirmed STEMI diagnosis EKG records from enrolled healthcare centers in Mexico, Colombia, and Brazil; including specific ischemic heart wall (anterior, inferior, and lateral). Following discharge of treated patients, confirmation of STEMI diagnosis was obtained as feedback from healthcare centers. Records were anonymized EKG that excluded all medical information. Sample: A Standard 12 lead, 10-seconds length, 500Hz sampling frequency EKG was fed to the LUMENGT-AI STEMI detecting algorithm. Preprocessing: Detection of QRS complexes by wavelet system, segmentation of each EKG record into individual heartbeats (total dataset 27,152 beats) with fixed window of 0.4s to the left and 0.9s to the right of main QRS; Classification: A 1-D convolutional neural network was implemented, three classes were considered for individual heartbeats: “Anterior”, “Inferior” and “Lateral”, each corresponding to the heart wall affected. These individual probabilities were aggregated to generate the final label for each of the 12 leads. Training & Testing: 90% and 10% of the dataset was used respectively. Experiments: Intel PC i7 8750H processor at 2.21GHz, 16GB RAM, Windows 10 OS with a NVidia GTX 1070 GPU, 8GB RAM.

Results
Accuracy – Lead V2 (91.7%); Sensitivity Anterior wall – Lead V2 (97.4%); Sensitivity for Lateral wall – Lead I (10.0%); and Sensitivity for Inferior wall – Lead V2 (93.6%).

Conclusions
AI algorithms merged with a Single lead approach detect and localize STEMI within any setting. The V2 lead yields superior results for mapping of ischemic areas of the heart among the anterior and inferior walls. In contrast, diagnosis remains suboptimal for identifying the lateral wall. The usage of synergistic technologies facilitates easy, fast and early STEMI triage and management.
3041Wall shear stress measurement by ultrafast vector flow imaging for atherosclerotic carotid stenosis
Authors: Goudot G , Khider L , Pedreira O , Poree J M , Julia P , Alsac J M , Mirault T , Pernot M , Messas E 
Published: October 2019

Abstract

Background
Carotid plaque vulnerability assessment is an important factor in guiding the decision to treat significant carotid stenosis. Ultrafast Ultrasound Imaging (UF) offers the possibility of evaluating local flow velocities over an entire 2D image, allowing access to velocity measurements in contact with the arterial wall and to measure the wall shear stress (WSS).

Purpose
To evaluate the feasibility of WSS measurement in a prospective series of patients with carotid stenosis.

Methods
A 7.5 MHz linear probe of an Aixplorer scanner was used. UF acquisitions had 3 tilted plane waves transmits (−10; 0; 10°) and an effective frame rate of 5000Hz. We evaluated the flow velocity in 5 areas of the carotid wall: common carotid artery (1), plaque ascent (2), plaque peak (3), plaque descent (4), internal carotid artery (5) (Figure). WSS was computed with the vector field speed using the following formula, WSS=μ·δn·v with v the blood velocity, n the normal vector to the vessel wall and μ, the blood viscosity, calculated from the hematocrit value for each patient. WSS measurement method was first validated using a laminar flow phantom and known viscosity. And then, 33 patients were then prospectively evaluated, with a median carotid stenosis degree of 80% [75–85].

Results
Significant correlation was found between in vitro measurement and the theoretical WSS values (R2=0.95; p<0.001).In patients,the maximum WSS value over the cardiac cycle follows the shape of the plaque with an increase during the ascend, reaching its maximum value of 3.57 Pa [2.47–4.45] at the peak of the plaque, and a fall after passing the peak (0.99 Pa [0.8–1.32]) lower than the WSS values in the non-stenotic areas (1.55 Pa [1.13–1.90] for the common carotid artery) (Table).
Table 1 Wall's area Wall shear stress (Pa) Min Max Delta 1. Common carotid artery 0.14 [0.05–0.27] 1.55 [1.13–1.90] 0.73 [0.55–0.96] 2. Plaque's ascent 0.39 [0.24–0.59] 2.63 [1.89–3.28] 1.20 [0.89–1.79] 3. Plaque's peak 0.60 [0.32–0.89] 3.57 [2.47–4.45] 1.78 [1.44–2.46] 4. Plaque's descent 0.16 [0.13–0.22] 0.99 [0.80–1.32] 0.52 [0.34–0.73] 5. Internal carotid artery 0.17 [0.13–0.35] 1.37 [1.04–1.75] 0.72 [0.50–0.87] Results are median [25th–75th percentile].
Figure 1

Conclusion
UF provide reliable WSS values. High WSS was present at the peak of the plaque, whereas lowest WSS values were found at the post-stenotic zone. WSS evaluation may help to better characterize the carotid plaque vulnerability.
3045Role of osteogenic circulating endothelial progenitor cells in dissemination of large arterial calcification in rheumatoid arthritis
Authors: Chan Y.-H , Ngai M C , Chen Y , Wu M Z , Yu Y J , Zhen Z , Lai K , Cheung T T , Ho L M , Chung H Y , Lau C S , Tse H F , Yiu K H 
Published: October 2019

Abstract

Background
Rheumatoid arthritis is associated with both abnormal bone metabolism and atherogenesis but mechanistic links were missing.

Aim
This study aimed to investigate the role of osteocalcin (OCN)-expressing circulating endothelial progenitor cells (EPC)s in the severity and dissemination of systemic arterial calcifications in rheumatoid arthritis.

Methods
We performed flow cytometry studies in 145 consecutive patients with rheumatoid arthritis to determine osteogenic circulating levels of OCN-positive (OCN+) CD34+KDR+ and OCN+CD34+, versus conventional early EPC CD34+CD133+KDR+. Total calcium load of the thoracic aorta (ascending plus descending) and the carotid arteries were assessed by non-contrast computed tomography (CT) and contrast CT angiography.

Results
Osteogenic EPCs OCN+CD34+KDR+ (P=0.002) and OCN+CD34+ were strikingly associated with the clustered presence of aortic and carotid calcification (P=0.002 and 0.001 respectively, Figure). Multivariable analyses revealed that circulating OCN+CD34+KDR+ (B=14.4 [95% CI 4.0 to 24.8], P=0.007) and OCN+CD34+ (B=9.6 [95% CI 4.9 to 14.3], P<0.001) remained independently associated with increased aortic calcium load. OCN+CD34+ EPC (B=0.8 [95% CI 0.1 to 1.5], P=0.023), but not OCN+CD34+KDR+ EPC (B=1.2 [95% CI −0.2 to 2.6], P=0.09) was further independently associated with carotid calcium load. In comparison, conventional early EPC CD34+CD133+KDR+ had no significant association with aortic or carotid calcium load (P=0.46 and 0.88, respectively).

Conclusions
Circulating level of osteogenic EPC is associated with promulgated aortic and carotid calcification in patients with rheumatoid arthritis, suggesting a potential mechanistic role of the bone-vascular axis in pro-atherogenicity of rheumatic diseases.

Acknowledgement/Funding
General Research Fund, Hong Kong Research Grants Council
3047Long-term changes after carotid stenting assessed by intravascular ultrasound and near-infrared spectroscopy
Authors: Stechovsky C , Hajek P , Horvath M , Veselka J 
Published: October 2019

Abstract

Background/Introduction
Long-term effect of carotid stenting (CAS) on the stabilization of the plaque is not well described. The interaction among the late stent expansion, neointimal hyperplasia, and lipid core might explain stabilization of the plaque and low long-term incidence of stroke after CAS.

Purpose
To assess long-term change in the lipid signal, stent, and luminal dimensions and restenosis after CAS with the multimodality intravascular ultrasound (IVUS) and near-infrared spectroscopy (NIRS) imaging.

Methods
We performed follow-up NIRS-IVUS imaging in patients who underwent CAS at our institution. Of the 112 patients (120 carotid arteries) who had NIRS-IVUS during CAS, 96 were alive at the time of the study, and 52 (58 carotid arteries) agreed to participate on the study. The lipid signal of the stented segment was calculated from the NIRS-derived chemogram (a spectroscopic map) as the lipid core burden index (LCBI, a dimensionless number from 0 to 1000). Volumetric calculations were performed using dedicated software with the automated lumen and stent detection and manual corrections. Median time from CAS to the follow-up examination was 31 months (range 5–56).

Results
The mean (± SD) LCBI significantly decreased from 32±56 to 17±27 (p=0,002). The mean stent volume significantly increased from 717±302 mm3 to 1019±429 mm3 (p<0,001) with mean stent expansion 43±24%. The mean luminal volume increased from 717±302 mm3 to 760±359 mm3 (p=0,025) due to the mean in-stent restenosis (ISR) 26±15% of the stent volume. Significant increase in the mean minimal stent area (MSA) (from 11,1±3,0 mm2 to 15,0±3,5 mm2, p<0,001) was not observed in the minimal luminal area (MLA) (from 11,1±3,0 mm2 to 11,4±4,4 mm2, p=0,098) due to the ISR. Significant restenosis (reduction of MLA ≥50% from baseline) was present in 7 stents.

Conclusions
During nearly three years of the follow-up after CAS the lipid signal decreased suggesting stabilization of the plaque. Significant late stent expansion was balanced with substantial neointimal hyperplasia therefore the late luminal gain was only modest in volume and nonsignificant at the site of MLA. There was a major variability in the rate of the late stent expansion and restenosis.
3051Effectiveness and safety of apixaban, dabigatran and warfarin compared to rivaroxaban in non-valvular atrial fibrillation; a Norwegian nationwide cohort study
Authors: Rutherford O.-C.W , Jonasson C J , Ghanima W G , Halvorsen S H 
Published: October 2019

Abstract

Introduction
Non-vitamin K oral anticoagulants (NOACs) are increasingly used for stroke prevention in patients with non-valvular atrial fibrillation (NVAF). Although proven effective and safe, there is limited knowledge of the comparative effectiveness and safety of the different NOACs in real life. Norway has nationwide registries of good quality, being suitable for doing such a comparison.

Purpose
The aim of this nationwide cohort study was to compare the risk of stroke/systemic embolism (SE) and major bleeding in patients with NVAF treated with dabigatran, apixaban and warfarin compared with patients treated with rivaroxaban.

Methods
By merging nationwide registries (the Norwegian Patient Registry and the Norwegian Prescription Database), a cohort was created including all oral anticoagulant (OAC)-naïve adult NVAF patients initiating OAC in the study period 1 Jan 2013 to 31 Dec 2017. The patients were followed until switching of OAC type, discontinuation, death, or end of study-period. Cox proportional-hazards regression was used to estimate adjusted hazard ratios (HRs) for the risk of stroke/SE or bleeding in patients using dabigatran, apixaban and warfarin compared to rivaroxaban.

Results
A total of 65 563 new users of OAC were included; 10,413 initiated dabigatran, 28,363 apixaban, 13,087 warfarin and 13,700 rivaroxaban. The median age was 71 yrs for dabigatran, 74 yrs for apixaban, 75 yrs for warfarin, and 73 yrs for rivaroxaban; 58.3% were men. Dabigatran-users were younger and had less comorbidities than all other OAC-users; the greatest difference was in the proportion with chronic kidney disease (2.4% in the dabigatran-group versus 7.0%, 12.5%, and 4.6% in the apixaban, warfarin and rivaroxaban groups, respectively). During a median follow-up time of 14.7 months (IQR 4.9–30.6), 2 361 (3.6%) patients suffered a stroke/SE, 2,051 (3.1%) had a major bleeding, and 4 250 (6.5%) died. Adjusted HRs for stroke/SE and major bleeding are presented in the figure. When the risk of stroke/SE and major bleeding was assessed solely in patients that received the standard dose of OAC (73% of NOAC users), the results were similar to the results for the entire population.
OACs compared to rivaroxaban

Conclusion
In this nationwide cohort study of patients with NVAF being new users of OAC, we found no significant differences in risk of stroke/SE between different OACs and rivaroxaban, whereas dabigatran and apixaban were associated with significantly lower risk of major bleeding.

Acknowledgement/Funding
The study was funded by the South-Eastern Norway Regional Health Authority, and by BMS/Pfizer through the ERISTA program.
3055Interactions between metabolism regulator adiponectin and intrinsic cardiac autonomic nervous system: a potential treatment target for atrial fibrillation
Authors: Yu L , Zhou Z , Jiang H 
Published: October 2019

Abstract

Background
Previous studies indicated that inhibiting the cardiac autonomic nervous system (CANS) suppressed atrial fibrillation (AF). Clinical research revealed that high levels of serum adiponectin (APN) could exert a beneficial influence on sympathetic and vagal tone in patients with type 2 diabetes. The aim of this study was to elucidate whether APN could regulate CANS and subsequently suppress rapid atrial pacing (RAP)-induced AF.

Methods
Eighteen anesthetized male beagles were randomly divided into three groups: the control group (saline plus sham RAP, N=6), the RAP group (saline plus 3 h RAP, N=6) and the APN + RAP group (APN plus 3 h RAP, N=6). Multielectrode catheters were attached to all atria and pulmonary veins. After bilateral thoracotomy, APN (10 μg, 0.1 μg/μL) or saline was microinjected into 4 fat pads, each containing one of the major atrial ganglionated plexi (GP), prior to RAP. Electrophysiological parameters including atrial effective refractory period (ERP), cumulative window of vulnerability (ΣWOV), anterior right GP (ARGP) function and neural activity were measured at baseline and 3 h after pacing. The fat pads containing the GP were excised for molecular biological testing and pathological staining at the end of the protocol.

Results
Compared with the control treatment, RAP markedly shortened ERP values at all tested sites and increased ΣWOV, ARGP function and neural activity, whereas APN injection into the GP reversed these changes. Mechanistically, APN treatment ameliorated the increased inflammatory response induced by RAP. In addition, the APN receptors AdipoR1 and AdipoR2 were detected both in neurons and in non-neuronal cells. Downstream of the AdipoRs, AMPK signaling was significantly activated and NF-κB signaling was significantly inhibited. More importantly, binding between APN and AdipoRs promoted macrophage phenotype switching from proinflammatory to anti-inflammatory.
Figures

Conclusion
This study demonstrates that local administration of APN into atrial GP suppress RAP-induced AF by regulating the activity of the CANS. AMPK activation and macrophage phenotype switching may contribute to the attenuation of GP inflammation after APN injection. Therefore, APN signaling may provide a potential therapeutic target to AF.
3077Load dependency of left ventricular longitudinal strain by 2D-speckle tracking echocardiography: myth or reality?
Authors: Nobre De Matos Pereira Vieira M J , Ribeiro D , Craveiro N , Teixeira R , Pitta L , Alves M , Martins V 
Published: October 2019

Abstract

Background
2D-speckle tracking echocardiography (2D-STE) derived strain measurements has been proposed as a non-invasive measure of myocardial deformation and function. However, the effects of left ventricular (LV) loading conditions on 2D-STE derived LV longitudinal strain (GLS) have not been totally elucidated and the results of some studies regarding the load dependency of GLS are controversial.

Purpose
To characterize the effects of acute load change (preload increase) on LV GLS.

Methods and results
We evaluated the variation of LV GLS by 2D-STE, in response to a preload increasing maneuver (leg lifting maneuver – LLM), in a population of 30 healthy individuals. Clinical, demographic and echocardiographic parameters (including LV longitudinal mechanics obtained with 2D-STE before and after LLM) were described. The population had a mean age of 27±4 years and 73% were women. Increased preload to the heart with LLM was confirmed by an increase in the maximal diameter of the inferior vena cava (16±3.5 vs 22±3.3 mm, p<0.01). No significant changes in left atrial volume, LV ejection volume and LV ejection fraction were observed in response to the LLM. There was a significant variation of global LV GLS (−21.9±2.3 vs −23.2±1.6%, p<0.001, Δ 1.25%, 95% CI 0.5–1.91) – figure. An increase in right ventricular longitudinal function with LLM (TAPSE 22.5±5.4 vs 25.5±0.5 mm, p=0.005, Δ 2.9, 95% CI 0.9–4.8) was also observed.

Conclusion
To our knowledge this is the first study performed to assess the effect of preload increase in GLS using the LLM in healthy individuals. In this study, the absolute LV GLS value increased significantly in response to preload increase (LLM). The dependence of GLS on preload is in accordance with the Frank-Starling Law, in which an increase in preload in a healthy individual lead to an increase in myocardial contractility. These findings suggest that LV GLS is a sensitive parameter for detecting subtle changes in LV longitudinal function.
3079Subclinical progression of biventricular cardiomyopathy in patients with systemic sclerosis
Authors: Stronati G , Guerra F , Zuliani L , Manfredi L , Ferrarini A , Fischetti C , Danieli M G , Gabrielli A , Capucci A 
Published: October 2019

Abstract

Background
Systemic sclerosis (SSc) is a progressive autoimmune disease which has been proven to affect the heart. While it is widely known that the disease can cause pulmonary artery hypertension and therefore secondary right heart impairment, new studies have detected a subclinical heart involvement of both the left and right ventricles. The similar changes in myocardial deformation of both chambers assessed by speckle tracking imaging are consistent with the definition of SSc-related cardiomyopathy as a standalone entity with peculiar characteristics.

Purpose
The aim of the present study is to describe the progression of myocardial deformation as assessed through speckle tracking in patients with SSc and no pulmonary hypertension.

Methods
Prospective, longitudinal study on 48 patients affected by SSc. Patients with a history of heart failure, known structural heart disease, atrial fibrillation, and pulmonary hypertension were excluded. For every patient, standard echocardiographical and speckle-tracking derived variables for the systolic and diastolic function of the left ventricle (LV) and right ventricle (RV) were acquired at baseline and after 15±6 months.

Results
While common parameters of systolic function (Simpons's left ventricular ejection fraction, right ventricular fractional area change, TAPSE, tricuspidal S') did not change during follow-up, mean global longitudinal strain (GLS) significantly worsened for both left (from −19.1%±4.2% to −17.2%±5.0%) and right ventricle (from −17.9%±5.2% to −15.9%±4.8%) over 15 months. The increased impairment seen in SSc patients was homogeneous across endocardial layers (LV: from −21.8%±4.8% to −18.8%±5.2%; RV: from −20.6%±4.5% to −19.4%±4.9%), midventricular layers (LV: from −19.2%±4.5% to −17.7%±4.9%; RV: from −17.7%±4.7% to −16.7%±4.6%) and epicardial layers (LV: from −16.3%±4.7% to −16.0%±4.3%; RV: from −15.4%±5.0% to −14.6%±4.1%), as well as across myocardial segments (Figure 1). No difference in progression rate was seen between the diffuse and limited version of SSc, nor between different serotypes.
Figure 1

Conclusions
While traditional echocardiographical parameters are useless in order to follow the natural history of SSc-related cardiomyopathy during its early stages, GLS impairment progresses during a 15-month follow-up and involves similarly both the left and right ventricle. Whether, how, and how much the altered myocardial deformation contributes to the incidence of pulmonary arterial hypertension in these patients is still to be assessed.

Acknowledgement/Funding
Marche Polytechnic University
3149Regional strain patterns according to hypertension and left ventricular hypertrophy in the general population
Authors: Frimodt-Moeller K E , Olsen F J , Biering-Soerensen S R , Moegelvang R , Jespersen T , Schnohr P , Gislason G , Biering-Soerensen T 
Published: October 2019

Abstract

Background
A pattern of reduced basal longitudinal strain (BLS) is often observed in hypertension (HT) and with altered left ventricular (LV) geometry. Whether this pattern is associated with poor outcome is unclear. We hypothesized that BLS becomes incrementally more impaired in the transition from HT to LV hypertrophy (LVH) and is a predictor of outcome.

Methods
We investigated 1,096 participants from a community-based cohort study who had an echocardiogram with speckle tracking performed. Regional strain was calculated as: BLS, midventricular and apical strain. The participants were stratified by LV geometry: LVH vs. non-LVH (LVH defined as left ventricular mass index >116 g/m2 for men and >96g/m2 for women). Outcome was major adverse cardiovascular events (MACE) defined as incident myocardial infarction, heart failure, and cardiovascular death.

Results
BLS and midventricular strain were significantly reduced when comparing normal participants without HT to participants with HT, whereas only BLS was reduced when comparing participants with HT to those with LVH (figure). Overall, patients with LVH showed both reduced BLS and midventricular strain (BLS: −17.5 vs −19.2%, p<0.001; midventricular strain: −19.2 vs. −19.9%, p=0.007 for LVH and non-LVH, respectively) compared to non-LVH, whereas apical strain was similar between groups.
During a median follow-up of 12.9 years (13.5; 14.9 years) there were 139 events. Only BLS was reduced in patients with MACE (BLS: −18.0 vs −19.1%, p=0.002) compared to patients without outcome. Both BLS and midventricular strain were univariable predictors of MACE in patients with LVH (BLS: HR=1.20 [1.04; 1.20], p=0.002; midventricular strain: HR=1.08 [1.00; 1.17], p=0.049) but not in patients without LVH (BLS: HR=1.02 [0.97; 1.08], p=0.46; midventricular strain: HR=1.01 [0.94; 1.07], p=0.88). Both measures were independent predictors after multivariable adjustment for clinical risk factors: age, gender, smoking, hypertension, and cholesterol (BLS: HR=1.08 [1.00; 1.16, p=0.048; midventricular strain: HR=1.10 [1.00; 1.20], p=0.049).
Regional strain by HT and LV geometry

Conclusion
BLS and midventricular strain, but not apical strain, becomes incrementally impaired in the transition from normal to LVH, and is associated with poor outcome. In regional strain analyses, BLS provides the highest predictive value for outcome in patients with LVH.

Acknowledgement/Funding
None