bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 98: The Assessment and Value of Bystander Cardio Pulmonary Resuscitation (by-CPR)
Authors: Hasselqvist-Ax Ingela , Herlitz Johan , Rosenqvist Mårten , Hollenberg Jacob , Nordberg Per , Ringh Mattias , Jonsson Martin , Axelsson Christer , Lindqvist Jonny , Svensson Leif 
Published: April 2024

Background:
3 million people in Sweden are educated in CPR and the value of this has been questioned if this leads to increased By-CPR and survival.

Aim:
To describe different aspects and effect on survival after OHCA depending if bystander CPR (By-CPR) was performed or not, and if the bystander was Lay or Medical educated. Also to explore the effects from CPR training on times to CPR, alarm and on outcome, when a medical educated bystander perform CPR versus when a Lay person act.

Methods:
Patients in the Swedish Cardiac Arrest Registry receiving bystander CPR 1990-2011 were included and divided into:
No-ByCPR
, and
By-CPR
. By-CPR was further divided in
Lay-ByCPR
and
Med-ByCPR
when CPR was performed by professionals in terms of medical educated bystanders. Crew witnessed cases were excluded.

Results:
In all 61 704 patients are included in the registry, and among them 30 188 bystander witnessed cases (49 %) were included in this survey. By-CPR have over the years continuously increased from 40% to 68% and 30 days survival increased from 3.8% 1990 to 10.7% 2011. Survival was 4.0% in No-ByCPR, 10.6% in By-CPR, 9.4% in Lay-ByCPR and 13.7% in Med-ByCPR.

Various aspects on delay to treatment were independently associated with survival to one month: Collapse-call for EMS (OR 0.70;95% CI 0.64-0.77); collapse-start of CPR (OR 0.72;95% CI 0.68-0.76); call for arrival of EMS (OR 0.41;95% CI 0.36-0.46). (Adjusted for age, gender, place and etiology)
Lay-ByCPR was significant better than No-ByCPR (OR 2.49) in all patients. Med-ByCPR had even better outcome compared to No-ByCPR (OR 2.84). When comparing Med-ByCPR vs. Lay-ByCPR bystanders, there were non- significant differences, OR 1.18 (CI:0.98-1.41).

Conclusion:
Increased By-CPR correlate to increased survival and can more than double survival rate compared to No-ByCPR.

Collapse to call, start of CPR, call-arrival EMS were independently associated with survival to one month. Lay-ByCPR were better than no ByCPR and as good as Med-ByCPR.
Abstract 9814: Nf-?B Inhibition Prevents Vascular Obliteration and Improves Immune Regulation in Severe Pulmonary Arterial Hypertension
Authors: Farkas Daniela , Alhussaini Aysar A , Kraskauskas Donatas , Kraskauskiene Vita , Nicolls Mark R , Voelkel Norbert F , Natarajan Ramesh , Farkas Laszlo 
Published: April 2024

Nuclear factor-κB (NF-κB) and interleukin-6 (IL-6), a NF-κB downstream mediator, play a central role in inflammatory response and vascular cell growth. Inflammation and a dysregulated immune response are found in many forms of severe pulmonary arterial hypertension (PAH), but how the NF-κB pathway contributes to PAH development is unclear. The SU5416 and chronic hypoxia (Su/Hx) rat PAH model is, like severe human PAH, characterized by obliterative pulmonary vascular lesions and right ventricular failure. We hypothesized that activation of the classical NF-κB pathway in severe PAH promotes ongoing vascular lesion cell apoptosis and proliferation, as well as dysregulation of the immune system.
We aimed to determine the role of NF-κB in severe PAH induced by Su/Hx in rats.
PAH was induced by a single injection of SU5416 and exposure to chronic hypoxia. Su/Hx rats were treated from day 1-21 with the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) and/or anti-IL-6 antibody. After hemodynamic assessment at day 21, cytokine/chemokine expression, NF-κB activation, lymphocyte accumulation, as well as pulmonary arterial cell apoptosis and proliferation were evaluated by Western blot, Flow cytometry and immunohistochemistry.

The classical NF-κB pathway was activated in pulmonary arterial lesions SuHx rats. NF-κB inhibition with PDTC prevented the development of pulmonary arterial obliteration and in part PAH without reducing muscularization. However, the elevated lung levels of IL-6 were not reduced in PDTC-treated SuHx animals. Apoptosis of pulmonary artery wall cells and pulmonary arterial obliteration was prevented by PDTC or by PDTC+IL-6 inhibition and partially by IL-6 inhibition alone. Pulmonary arterial media wall thickness was not affected by any of these treatments. In Su/Hx rats, CD4
+
T cells were reduced and perivascular CD8
+
T lymphocytes and CD45RA
+
B lymphocytes were increased. NF-κB inhibition promoted immune regulation by increasing the number of perivascular CD4
+
T cells and reducing the number of perivascular CD8
+
T lymphocytes and CD45RA
+
B lymphocytes.

Inhibition of NF-κB may represent a therapeutic option for pulmonary arterial obliteration
via
reduced vessel wall cell apoptosis and improved immune regulation.
Abstract 9852: T Lymphocyte Depletion Following Primary Percutaneous Coronary Intervention Predicts Infarct Size and Ischemia Reperfusion Injury
Authors: Boag Stephen , Shmeleva Evgeniya , Das Rajiv , Egred Mohaned , Zaman Azfar , Bagnall Alan , Owens Andrew , Keavney Bernard , Spyridopoulos Ioakim 
Published: April 2024

Background:
We have previously demonstrated acute changes in lymphocyte numbers in peripheral blood following reperfusion with primary percutaneous coronary intervention (PPCI) for STEMI. The goal of this study was to investigate a potential role for T cells in ischemia reperfusion (I/R) injury.

Methods:
We analyzed blood from 22 STEMI patients undergoing PPCI. Blood was taken at the start of the procedure, and at 15, 30, 90 minutes, and 24 hours post reperfusion. In 5 patients with infarcts due to LAD occlusion, coronary sinus (CS) blood was also obtained 30-60min after reperfusion along with simultaneous aortic blood. 8-colour flow cytometric analysis was performed on the fresh blood to quantify lymphocyte populations. Cardiac MRI was performed at 1-7 days, and left ventricular ejection fraction, infarct size (measured by late gadolinium enhancement), microvascular obstruction (MVO), area at risk and salvage index quantified.

Results:
T-lymphocytes dropped between 0 and 90 minutes by a mean of 42% (0min mean 1767/μl, 90min 931/μl), CD4 T-helper cells by 31%, and CD8 cytotoxic T-cells by 55%. The change in total T-cells correlated with infarct size (r=-0.78, p<0.001), as did that of CD4 (r=-0.66, p<0.01) and CD8 T cells (r=-0.76, p<0.001).

The T cell drop between 0 and 90 minutes also correlated strongly with MVO (r=-0.72, p<0.01), as did the CD4 (r=-0.66, p<0.01) and CD8 T cell drop (r=-0.77, p<0.001). Myocardial salvage index correlated strongly with the change in T cells (r=0.85, p<0.001), CD4 T cells (r=0.76, p<0.01) and CD8 T cells (r=0.76, p<0.01) between 30 and 90 minutes.
Prior to reperfusion 6.4% of CD8 T cells were activated (CD69+), with progressive loss of CD69+ cells after 90 minutes (4.3%) and 24 hours (2.6%, 0min vs 24hr p<0.01). However, CS sampling showed an increase in CD69 expression between aortic and CS blood, suggesting activation of T cells as they pass through the myocardial vascular bed.

Conclusion:
Acute changes in T lymphocyte numbers following reperfusion after PPCI predict infarct size, MVO, and salvage index. The drop in these cells following reperfusion, and the dynamics of CD69 expression, suggest a potential role for CD69+ activated T cells in I/R injury. This requires further investigation and may represent a novel therapeutic target.
Abstract 12624: Therapeutic Lymphangiogenesis Improves Diastolic Function by Limiting Cardiac Edema and Fibrosis After Myocardial Infarction
Authors: Henri Orianne , Houssari Mahmoud , Pouehe Chris , Galas Ludovic , Nicol Lionel , Edwards-Lévy Florence , Henry Jean-Paul , Dumesnil Anais , Schapman Damien , Thuillez Christian , Richard Vincent , Mulder Paul , Brakenhielm Ebba 
Published: April 2024

Little knowledge exists on how cardiac lymphatics respond to myocardial infarction (MI). We investigated the impact of MI on cardiac lymphatic structure and function during the development of chronic heart failure (CHF).
We hypothesized that 1) insufficient cardiac lymph drainage may contribute to the deleterious cardiac remodeling post-MI; and 2) therapeutic stimulation of lymphatic growth, or lymphangiogenesis, may reduce chronic myocardial edema and inflammation in this setting.
MI was modeled in Wistar rats by coronary occlusion (45 min) followed by reperfusion. Lymphangiogenesis-selective VEGF-C was delivered intramyocardially using slow-release albumin-alginate microparticles. Animals were divided into: sham (n=19), control MI (n=64), and treated MI, receiving low (1.5 μg; n= 54) or high (5 μg; n=26) dose of VEGF-C upon reperfusion. Cardiac function, lymphatics, edema, and levels of infiltrating immune cells were evaluated at 3 and 8 weeks post-MI.

We found that control rats displayed lymphatic remodeling with increased lymphatic capillary density but rarefaction of epicardial pre-collector and collector vessels, leading to cardiac lymphatic dysfunction. In accordance with insufficient lymph drainage, chronic myocardial edema and low grade inflammation were found at both 3 and 8 weeks post-MI as determined by gravimetry, MRI T2 imaging, and immunohistochemistry, respectively. VEGF-C treatment led to a dose-dependent increase in lymphatic capillary density (sham, 255±16; con, 267±25; VEGF-C, 362±22 lymphatics/mm
2
; p<0.05) and reduced rarefaction of pre-collectors and collector vessels. As a consequence, myocardial edema (sham, 75.5±0.1; con, 77.9±0.2; VEGF-C, 77.3±0.1% water content; p<0.05) and macrophage infiltration levels were both significantly reduced. Further, cardiac interstitial fibrosis was completely prevented by 8 weeks, even by low dose VEGF-C (con, 6.0±0.6; VEGF-C, 3.3±0.1% fibrosis; p<0.001), leading to reduced diastolic dysfunction (LVDPVR, LV end-diastolic pressure-volume relation: sham, 0.8±0.1; con, 2.0±0.2; VEGF-C, 1.1±0.1; p<0.001).

In conclusion, our data suggest that therapeutic lymphangiogenesis may represent a new therapeutic target in CHF.
Abstract 14764: Left Atrial Appendage Function and Risk of Stroke After Left Atrial Appendage Electrical Isolation in Patients With Long-Standing Persistent AF: Results From the BELIEF Randomized Trial
Authors: Di Biase Luigi , Burkhardt J. David , Mohanty Prasant , Mohanty Sanghamitra , Sanchez Javier , Trivedi Chintan , Gunes Mahmut , Gökoglan Yalçin , Gianni Carola , Horton Rodney , Gallinghouse G. Joseph , Bailey Shane , Zagrodzky Jason , Hao Steven , Hongo Richard , Beheiry Salwa , Santangeli Pasquale , Casella Michela , Dello Russo Antonio , Al-Ahmad Amin , Hranitzky Patrick , Lakkireddy Dhanujaya , Tondo Claudio , Natale Andrea 
Published: April 2024

Introduction:
The Belief Randomized trial sought to assess whether the empirical isolation of the left atrial appendage (LAA) in addition to an extensive ablation could improve success at follow up in patients with long standing persistent (LSP) atrial fibrillation (AF). The aim of this sub-analysis of the trial aimed to evaluate the LAA contraction at the 6 month repeat Trans-esophageal echocardiogram (TEE).

Methods:
Patients with LSP AF undergoing ablation were enrolled and randomly assigned to undergo empirical LAA isolation along with an extensive ablation or extensive ablation alone.

All patients undergoing LAA isolation received a TEE at the 6 months follow up, irrespective of their underlying rhythm. We evaluated TEE parameters and compared thromboembolic complication between groups.

Results:
We enrolled 173 pts with average age of 63.8 ± 8.5 years and 85.5% male pts.

LAA isolation was performed in 101 pts. LAA was not isolated in 72 pts. Follow-up TEE was performed in all pts with LAA isolation. The peak flow velocity in the appendage was low (<0.4 m/s) in 56.4% (57/101) patients. The doppler across the mitral valve demonstrated E-wave to A-wave ratio (E/A) of 2.64 ± 1.4. All patients had E/A >1, out of which 55.4 %( 56/101) had E/A > 2 (p=0.16). One (1.2%) LAA thrombus [Oral anticoagulant warfarin INR subtherapeutic] and 1 (1.2%) LAA smoke [Oral anticoagulant warfarin, INR : 2.24] were detected in the LAA isolation group as an incidental finding at TEE before redo ablation procedure.
One patient (0.99%) had stroke in the LAA isolation group after warfarin discontinuation due to a surgical procedure, while 3 (4.2%) stoke/TIA occurred (p=0.31) in the no LAA isolation group (2 pts on warfarin, 1 pt on aspirin).

Conclusion:
The results of this study show that LAA isolation does not increase the risk of tia/stroke at follow up. This risk appears to be related to the compliance to oral anticoagulation.
Abstract 15800: Identification of a Novel Transcript and Regulatory Mechanism for Microsomal Triglyceride Transfer Protein
Authors: Suzuki Takashi , Brown Judy J , Swift Larry L 
Published: April 2024

Microsomal triglyceride transfer protein (MTP) is heterodimeric protein complex consisting of a unique 97 kDa protein with lipid transfer activity and the ubiquitous 58 kDa protein disulfide isomerase. The complex is essential for assembly of triglyceride-rich apolipoprotein (apo) B-containing lipoproteins. In tissues that do not synthesize apoB nor assemble lipoproteins, it is presumed to serve specialized needs in lipid trafficking, such as in the lipidation of CD1d in antigen presenting cells, including adipocytes.
Previous studies in our laboratory identified a novel isoform of MTP in mice that we named MTP-B. MTP-B has an alternative first exon (Ex1B) located 2.7 kbp upstream of the first exon (Ex1A) of MTP-A, the canonical isoform of MTP. The two mature isoforms, though nearly identical in sequence and function, have different tissue expression patterns.
In this study, we have identified another splice variant, MTP-C, that contains both exons Ex1B and Ex1A. PCR analysis revealed that MTP-C mRNA is expressed in a number of tissues including liver, ovary, heart, kidney, brain and testis. In CHO and HEK 293 cells transfected with MTP-C, protein expression was less than 15% of that found when the cells were transfected with MTP-A or MTP-B. In silico analysis of the 5’ untranslated region (UTR) of MTP-C revealed six ATGs (uATGs) upstream of the translation initiation site for MTP-A, which is the only viable start site in frame with the main open reading frame (ORF), and three potential upstream ORFs (uORFs). Since uATGs and uORFs are generally associated with repressed translational efficiency, we inserted the 5’ UTR of MTP-C into a pGL3 vector between the SV40 promoter and luciferase reporter gene and transfected it into CHO cells. Luciferase activity was significantly reduced (45.5 ± 6.4%) compared to pGL3-Control vector transfected cells. This suggests the reduced protein expression observed in MTP-C transfected cells resulted in part from decreased translation efficiency.
We conclude that uORFs in the 5’ UTR of MTP-C repress translation, providing a mechanism to fine tune MTP levels to meet the needs of the cell. uORFs in human MTP-C could represent novel therapeutic targets for regulation of MTP expression and plasma lipid levels.
Abstract 11912: Glycocalyx Shedding is Markedly Increased During Acute Phase of Takotsubo Cardiomyopathy
Authors: Nguyen Thanh H , Liu Saifei , Ong Gao , Stafford Irene , Frenneaux Michael , Horowitz John D 
Published: April 2024

Introduction:
Acute myocardial infarction (AMI) and other forms of myocardial acute oxidative stress are associated with variable “shedding” of vascular and other glycocalyx. This glycocalyx shedding (GCS) can be quantitated by release into plasma of glycocalyx components such as Syndecan-1 (SD1), which is the most prevalent proteoglycan. Previous in vitro studies have implicated both catecholamines and BNP release as potential accentuating factors in GCS: since these are prominent aspects of the pathogenesis of Takotsubo cardiomyopathy (TTC), we hypothesised that TTC (i) would be associated with increased GCS both acutely and during subsequent 3 months of continued myocardial inflammation and (ii) extent of GCS would be predictable on the basis of NT-proBNP and catecholamine releases.

Methods:
SD1 concentrations were measured in 49 TTC patients acutely and after 3 months in comparison with 12 normal age-matched controls and 10 myocardial infarct patients. Correlations between SD1 and (i) acute LV function, (ii) lowest BP on admission, (iii) peak catecholamine release, and (iv) extent of systemic and myocardial inflammatory activation [measured by high sensitive C-reactive protein (hsCRP), NT-proBNP concentrations, and myocardial T2 signal intensity on cardiac MRI] were sought.

Results:
Acute SD1 concentrations in TTC patients were significantly elevated compared to 3 month and control values (2-way ANOVA) (Figure). However, there was no significant difference between acute TTC and MI levels. In addition, there were no correlations between SD1 concentrations and extent of severity of acute episode.

Conclusions:
1. TTC, despite minimal associated myocardial necrosis, is associated with marked increase in GCS.

2. Extent of GCS in TTC is not closely related to either release of NT-proBNP or normetanephrine.
We postulate that GCS may contribute to some of the clinical features of TTC, such as development of pulmonary oedema without marked increases in PCWP.
Abstract 13510: No-reflow in Reperfused Myocardium Does Not Contribute to Final Infarct Size in Pigs
Authors: Skyschally Andreas , Kleinbongard Petra , Heusch Gerd 
Published: April 2024

The no-reflow phenomenon is a frequent complication in patients with reperfused acute myocardial infarction and associated with a worse prognosis. It is unclear whether cardioprotection, apart from infarct size (IS) reduction, has also a beneficial impact on the extent of no-reflow.
In an anesthetized pig model of myocardial ischemia/reperfusion, we have now used established conditioning maneuvers as a tool to distinguish damage and protection from it in the myocardium, expressed as final IS, and in the coronary microcirculation, expressed as area of no-reflow (ANR).
Myocardial ischemia was induced by transient occlusion of the left anterior descending coronary artery (LAD). Myocardial blood flow was measured with microspheres. Cardioprotection was induced by local ischemic preconditioning (IPC; n=10; 2 x 3 min LAD occlusion/2 min reperfusion 15 min prior to 60 min LAD occlusion), remote ischemic preconditioning (RIPC; n=10; 4x5 min hindlimb occlusion/reperfusion 90 min prior to 60 min LAD occlusion), or ischemic postconditioning (POCO; n=6; 4x1 min LAD re-occlusion/reperfusion at 1 min reperfusion after 60 min LAD occlusion). Pigs without protection (PLA; n=10) served as controls. After 180 min reperfusion, the ANR (intra-atrial injection of thioflavin S) and the area at risk (AAR; intra-atrial injection of blue dye with re-occluded LAD) were demarcated. IS was determined by post-mortem triphenyl-tretrazolium chloride (TTC) staining.
The AAR and myocardial blood flow during ischemia were not different among groups. IS reduction was similar with IPC, RIPC, and POCO (PLA: 37±3% of AAR; IPC*: 21±3%; RIPC*: 17±2; POCO*: 24±5%; mean±SEM; *p<0.05 vs. PLA). Only IPC and RIPC reduced the ANR (PLA: 28±4% of AAR; IPC*: 4±3%; RIPC* 9±2%), whereas POCO did not (24±5%).
All conditioning maneuvers protected the myocardium, but the microcirculation was only protected by conditioning maneuvers applied prior to LAD occlusion. POCO’s protection of myocardium, but not coronary microcirculation might be related to different time frames or to different underlying mechanisms of injury and/or protection in the two compartments. Nevertheless, the remaining no-reflow observed with POCO did not result in greater infarction.
Abstract 14271: TLR3 as a Potential Target to Prevent Aortic Valve Stenosis
Authors: Willemsen Nicola , Niepmann Sven , Boucher Ann Sophie , Zimmer Sebastian , Nickenig Georg 
Published: April 2024

Aortic stenosis (AS) is the most common valvular disease in the western world and is associated with severe morbidity and mortality. Our current concept of disease development suggests that local chronic inflammation drives fibrosis and calcification of the valve cups. It has recently been proposed that activation of pattern recognition receptors may be critical in this context. In a preliminary screening, we found Toll-like receptor 3 expression increased in human AS samples.
Aim of this study was to investigate the role of TLR3 in the pathogenesis of AS.
Isolated human valvular interstitial cells (VICs) were cultured and stimulated with the TLR3 agonist Poly I:C. To inhibit TLR-3 activation, a knockdown was performed using TLR3 small interfering RNA (siRNA) as well as the TLR3/ RNA Complex inhibitor C4a. Calcification was induced by changing the culturing media. RNA was isolated for gene expression analysis. Calcification was visualized by alizarin red staining. Wild type as well as TLR3 knockout mice underwent an ultrasound guided wire injury. After surgery, C4a was injected in WT mice to suppress TLR3 signaling. Valves were explanted and stained with hematoxylin/eosin or anti CD68. Upon stimulation of TLR3 with PolyI:C, TLR3 expression was consistently upregulated in VICs while incubation of VICs with the TLR3/ RNA complex inhibitor C4a resulted in a downregulation of TLR3. These results suggest that TLR3 may be subject to a potential detrimental positive feedback loop in these cells. Importantly, activation of TLR3 led to a marked increase in expression of the pro-osteogenic markers BMP-2 and RUNX2. TLR3 inhibition or knockdown blunted this response.TLR3 deficient mice revealed a significantly smaller aortic valve leaflet area as well as a reduced intravalvular infiltration with monocytes compared to WT. C4a treatment resulted in lower trans-aortic valve peak velocity levels. Further, C4a mice failed to develop AS upon injury.
These findings not only support the endogenous role of TLR3 in the development of AS but suggest that specific TLR3 inhibition might be beneficial for the treatment or prevention of AS. Further studies are required to test this hypothesis and to decipher the exact mechanisms how TLR3 contributes to AS.
Ibn Taymiyya and his Circle on samāʿ: a means to Purify Sufism? (with an Arabic edition of al-Wāsiṭī’s (d. 711/1311) Bulgha)
Authors: Post Arjan , Van Eyken Sarah 
Published: April 2024

Abstract
By examining polemical treatises on Sufi samāʿ or ‘spiritual audition’, written by scholars with a Ḥanbalī or traditionalist orientation, we assess the strategies and rhetorical devices that they used to discuss the status of samāʿ within their tradition. Our exploration reveals a clear difference in approach between pre-Taymiyyan scholars, on the one hand, and ‘Taymiyyan’ scholars, including Ibn Taymiyya (d. 728/1328) himself, on the other. Unlike their predecessors, the latter systematically refer to the legacy of esteemed figures from the formative period of Sufism, such as al-Junayd (d. 289/910) and some of his contemporaries, invoking his spiritual authority to consolidate the relation between Ahl al-Ḥadīth traditionalism and what they considered to be Sufism in its ‘true’ form.