bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 6279: The Severity of Nonalcoholic Fatty Liver Disease is Associated with Increased Cardiovascular Risk in a Large Cohort of Non-Obese Asian Subjects
Authors: Sung Ki C , Park Jeong B , Ryan Marno C , Wilson Andrew M , Kang Jin H , Kim Bum S , Kim Byung J 
Published: July 2021

Bcakgrounds: Non alcoholic fatty liver disease (NAFLD) has been linked independently to cardiovascular disease (CVD) but It is largely unknown if such a relationship between NAFLD and CVD risk relates to severity of liver disease or if it is independent of other potential confounding factors
Methods: This study included 30,172 subjects. Based on the presence or absence of steatosis on ultrasound and serum alanine aminotransferase (ALT), subjects were divided into controls, an increased serum ALT group without steatosis and a group with presumed nonalcoholic fatty liver disease (NAFLD), which included a steatosis alone group and a group with presumed non alcoholic steatohepatitis (NASH) with steatosis and an elevated ALT.
Results: The odds ratio for 10-year risk by total Framingham risk scores ≥10% was 5.3 times higher in NASH groups. The prevalence of diabetes, hypertension, elevated CRP and metabolic syndrome were all increased up to 15 fold over controls, independent of age, BMI, smoking and exercise habits. Overall CVD risk was significantly greater in NASH than in either steatosis or raised ALT alone.
Conclusion: Young, non-obese subjects with NAFLD are at significantly increased CVD risk, especially those with NASH. As well as specific therapy for liver disease, a diagnosis of NAFLD should lead to targeted risk assessment and risk factor modification.

Table 1.

Prevalence of Cardiovascular Risk Factors and 10- year risk

Table 2

Odds Ratios and 95% confidence intervals for Cardiovascular Risk Factors and 10- year risk
Abstract 3: Impact Of Transport To Critical Care Centers Vs. Non-critical Care Hospitals On Outcomes From Out-of-hospital Cardiac Arrest In Osaka, Japan
Authors: Kajino Kentaro , Iwami Taku , Daya Mohamud , Yonemoto Naohiro , Nishiuchi Tatuya , Hayashi Yasuyuki , Irisawa Taro , Ikeuchi Hisashi , Tanaka Hiroshi , Shimazu Takeshi , Hiraide Atushi , Sugimoto Hisashi 
Published: July 2021

Background: Recent studies suggest that specialized hospital care including hypothermia and early percutaneous coronary intervention (PCI) influences the outcome of out-of -hospital cardiac arrest (OHCA) patients. In Japan, selected hospitals are certificated as “Critical Care Centers (CCC)” based on their expertise and ability to provide these higher levels of care. We hypothesized that the outcomes of patients with OHCA who were transported to CCC is better than if they were transported to non-critical care hospitals (NCCH) in Osaka, Japan.
Materials and Methods: All adults with OHCA of presumed cardiac etiology, treated by the emergency medical services (EMS) systems, and transported to a hospital in Osaka, Japan from January 1, 2005 to December 31, 2006 were studied using a prospective Utstein style population cohort database. Primary outcome measure was one month neurologically favorable survival (CPC ≤ 2). Outcomes of patients transported to CCC were compared to patients transported to NCCH using multiple logistic regression to adjust for the following confounding variables; gender, age, witnessed status, bystander CPR, location, transport time and initial rhythm. We also performed a stratified analysis based on whether the patients achieved ROSC prior to arrival at the hospital.
Results: Of 6,943 OHCA of presumed cardiac etiology, 6,706 cases were transported. Of these, 1,780 were transported to CCC while 4,926 were transported to NCCH. Neurologically favorable survival at one-month was greater in the CCC group [103 (5.8 %) versus 119 (2.4 %), p < 0.001]. Transportation to CCC was a significant predictor [OR = 1.7, 95% CI interval (1.3 – 2.4)] of neurologically favorable survival after adjustment for confounding variables. In the stratified analysis, the impact of the CCC was not significant difference in patients transported after field ROSC. [OR = 1.4, 95% CI interval (0.92 – 2.22)] On the other hand, the impact of the CCC was even greater in patients transported prior to field ROSC. [OR = 2.4, 95% CI interval (1.3 – 4.5)]
Conclusions: The outcomes of patients with OHCA with or without field ROSC who were transported to Critical Care Centers was better than if they were transported to Non-Critical Care Hospitals.
Abstract P22: An Impedance Threshold Device Combined with an Automated Active Compression Decompression CPR Device (LUCAS) Improves the Chances For Survival in Pigs in Cardiac Arrest
Authors: Matsuura Timothy R , McKnite Scott H , Metzger Anja K , Yannopoulos Demetris , Aufderheide Tom P , Lurie Keith G 
Published: July 2021

Background: By lowering intrathoracic pressure during the chest recoil phase of CPR, the impedance threshold device (ITD) increases circulation and the rate of return of spontaneous circulation (ROSC). This study evaluated the ITD combined with a new automated CPR device, the US version of the LUCAS, that compresses the chest and then pulls upwards with a 3 lb force.
Methods and Results: After 6 min of untreated ventricular fibrillation, anesthetized female pigs (40.0±0.7 kg) were randomized to 6 min of CPR (100 compressions/min with LUCAS and ventilation: 1.0 FiO2, tidal volume of 10ml/kg, rate 12/min) with an active (−10 cm H2O resistance) (n=12) or sham ITD (n=12), and then shocked once with 120 joules of direct current. Epinephrine (0.04 mg/kg) and more CPR and shocks were used if ROSC was not achieved.
Results (in mmHg) after 6 min of CPR with an active vs. sham ITD were: coronary perfusion pressure (PP) 20.8±1.2 vs. 21.0±0.9 (p=0.94); cerebral PP 8.8±1.0 vs. 10.0±0.9 (p=0.62); and end tidal CO2 38.1±1.5 and 37.1±1.3 (p=0.61). Peak and mean carotid artery blood flow (ml/min) was 323.9±15.2 vs. 256.6±21.1 (p=0.17) and 95.3±5.4 vs. 77.0±6.0 (p=0.22) with an active vs. sham ITD, respectively. Mean endotracheal pressures (mmHg) during chest recoil with an active vs. sham ITD were −2.0±0.5 vs. −0.2±0.2 (p<0.01). Arterial and venous blood gases were similar after 6 min of CPR between groups. ROSC, the primary survival endpoint for comparing the active vs. sham ITD, was 7/12 vs. 2/12 after 1 shock (p= 0.09), 12/12 vs. 5/12 after 2 shocks (p<0.01), and 12/12 vs. 7/12 after 3 shocks (p=0.04). With up to 14 shocks, 10/12 sham animals had a ROSC. All animals with ROSC lived for 30 min. There was no evidence of pulmonary edema or organ damage on autopsy with either ITD.
Conclusions: After 6 min of CPR, LUCAS and active ITD resulted in lower mean airway pressures during chest recoil versus controls but hemodynamic findings were similar. However, ROSC was significantly easier to achieve with an active ITD; with up to 3 shocks twice as many animals were resuscitated with an active ITD. This benefit is most likely explained by carotid blood flows that trended higher with the active ITD. These positive findings and lack of any adverse outcomes support the safety and efficacy of this device combination.
Abstract P26: Intra-CPR Hypothermia with and Without Volume Loading in an Ischemic Model of Cardiac Arrest
Authors: Yannopoulos Demetris , Zviman Menekhem , Kolandaivelu Aravindan , Ranjan Ravi , Dori Yoav , Castro Valeria , Resar Jon R , Brinker Jeffrey A , Wilson Robert F , Halperin Henry R 
Published: July 2021

Background: Coronary occlusive ischemic events are responsible for 50 –70% of cardiac arrests in adults. We investigated the effects of intra-CPR mild hypothermia (HTM) (target 32–33°C) with and without volume loading on return to spontaneous circulation (ROSC) and infarction size in a severe, mid-LAD occlusion model of cardiac arrest.
Methods: 46 (27±2.3kg) pigs had their mid LAD balloon occluded and were divided in 5 groups. After 15 minutes, ventricular fibrillation (VF) was electrically induced and 5 minutes of untreated VF were followed by 5 minutes of pneumatic vest CPR with a set compression pressure (250mmHg). If ROSC was obtained, animals were followed for another 95 minutes for a total LAD occlusion time of 120 min. Subsequently the balloon was deflated and 90 min of reperfusion were followed by myocardial staining to define area at risk (AAR) and myocardial infarct size. Group A had no additional intervention. Group B received immediately post ROSC surface cooling with cooling blankets and ice. Group C received intra-CPR 680±23ml of 28°C 0.9% NS via a central femoral venous catheter. Group D received during CPR 673±26 of 4°C NS followed by post ROSC surface cooling as in group B. Group E received intra-CPR and post ROSC volume-sparing HTM with an Endovascular Therapeutic Hypothermia System (ETHS) placed into the right atrium and set at a target of 32°C.

Results: During CPR, coronary perfusion pressure was significantly decreased in groups C and D compared to groups A, B and E but groups D and E had significantly reduced infarct size. Group E had significantly improved EF compared to all other groups. Table

.

Conclusions: Intra-CPR HTM significantly reduces myocardial infarction size. Volume loading during CPR is detrimental for ROSC due to reduction of coronary perfusion pressure. ETHS intra-CPR application improves ROSC and post-resuscitation LV function and minimizes infarction in this ischemia-reperfusion cardiac arrest model.

Results
Abstract P65: Community Based Application of Therapeutic Hypothermia for Survivors of Cardiac Arrest
Authors: Getts Roger , Fedor David , Vanston Vincent J , Triano Mary , Prior John 
Published: July 2021

Objectives: To demonstrate that the application of therapeutic hypothermia is technically feasible in a community-based setting.
Background: Implementation of therapeutic hypothermia for survivors of cardiac arrest in the US has been slow, at least partially because of the perception that this therapy is technically difficult, especially at the community level. Scranton, Pennsylvania is a just such a community. It has 75,000 people served by 3 hospitals with 700 acute care beds.
Methods: At three community hospitals, after return of spontaneous circulation (ROSC) survivors of cardiac arrest were treated with mild therapeutic hypothermia using ice and cooling blankets or suits in order to achieve a goal temperature of 32 to34 degrees C for 24 hours. After ROSC, the timing goals of therapeutic hypothermia were to cool patients within 4 hours, to achieve goal temperature within 8 hours, and to maintain goal temperature for 24 hours.
Results: Beginning in 2004, 27 survivors of cardiac arrest were managed with therapeutic hypothermia. The mean time from ROSC to initiation of therapeutic hypothermia was 2.8 hours (range, 0.4 – 6.3 hours), the mean time from ROSC to goal temperature was 6.9 hours (range, 1.9 –15 hours), and the mean time maintained at goal temperature was 26.7 hours (range, 12–39 hours). Once patients achieved goal temperature, 4.3% of the temperature readings were above 34 degrees C, reflecting undercooling, while 13.4% of the readings were below 32 degrees C, indicative of overcooling. Overall survival until hospital discharge with good neurologic outcome was 52%, compared to only 12% (p < 0.001) among historical controls with cardiac arrest. There were no major complications attributable to the procedure.
Conclusion: A simple protocol of mild therapeutic hypothermia using locally-available resources is technically feasible and safe in a community-based setting.
Abstract P123: Vasopressin, but not Norepinephrine, causes Ventriculoarterial Mismatch in Experimental Post Ischemic Cardiogenic Shock
Authors: How Ole-Jakob , Røsner Assami , Gjessing Petter , Hermansen Stig E , Myrmel Truls 
Published: July 2021

Introduction In agreement with existing guidelines, inotropic and vasopressor support is given routinely in cardiogenic shock (CS). However, there is a lack of scientific evidence supporting the efficacy and safety of such treatment.
Hypothesis Vasoconstrictors given in cardiogenic shock will increase the ventriculoarterial mismatch and thus lead to reduced cardiac output
Methods In a closed chest pig model we tested the inodilator (dobutamine, Dobut) alone and combined with either an inoconstrictor (norepinephrine, NE) or a pure vasopressor (arginine vasopressin, AVP). In anesthetized animals, CS was induced by coronary microembolization under fluoroscopic guidance. Hemodynamic indices were obtained by Swan-Ganz catheters, left ventricular pressure-volume catheters and echocardiography, and the ventriculoarterial coupling calculated.
Results In the normal heart, Dobut (2ug/kg/min) enhanced ventriculoarterial energy transfer, shown as a decreased Ea/Ees (ratio of arterial and ventricular elastance), 1.0 ± 0.1 to 0.8 ± 0.1, and an increased preload recruitable stroke work (PRSW), 53 ± 5 to 63 ± 2. This was further enhanced by NE (100 ng/kg/min) to 0.7 ± 0.1 and 79 ± 6. In contrast, adding AVP (0.001 u/kg/min) resulted in an increased Ea/Ees (1.0 ± 0.1) and decreased PRSW (56 ± 8) compared to Dobut alone (a two fold increase in systemic vascular resistance (SVR), concomitant with no elevation in contractility). In post ischemic CS, energy transfer from the ventricle to the arterial system (Ea/Ees 1.8 ± 0.2, PRSW 26 ± 2 and Ejection fraction 42 ± 6 %) was partly restored by Dobut (1.4 ± 0.2, 46 ± 2 and 47 ± 6%) unaffected by further adding NE (1.5 ± 0.2, 53 ± 2 and 45 ± 5%), but impaired after adding AVP (2.0 ± 0.1, 43 ± 1 and 34 ± 4%). Consequently, Dobut improved the shock by increasing cardiac output (CO) and SVO2 from 74 ± 3 ml/kg and 37 ± 2% to 103 ± 8 ml/kg and 49 ± 3%. Adding NE resulted in a further improvement of CO (125 ± 9 ml/kg) and SVO2 (59 ± 4%). In contrast AVP further worsened the shock state by decreasing CO (70 ± 6 ml/kg) and SVO2 (45 ± 5%) compared to Dobut alone.
Conclusion A pure afterload increasing substance in acute ischemic hearts with cardiogenic shock aggravate the shock state by causing a ventriculoarterial mismatch.
Abstract P144: Bioinformatic Profiling of the Transcriptional Response of Adult Porcine Bone Marrow Stem Cell during Exposure to Hypoxia
Authors: Wang Suna , Zhou Yifu , Xu Xiuli , Hunt Timothy , Hoyt Robert F , Horvath Keith A 
Published: July 2021

Background: Cell-based transplantation therapy in a large animal model has been shown to improve angiogenesis and function of ischemic myocardium. These improvements may be due to the endothelial progenitor cells from bone marrow derived stem cells (BMC) generated under ischemic or hypoxic conditions. However the molecular activities of porcine BMC (PBMC) are largely unknown. Thus, a comprehensive gene expression pattern for PBMC is needed to advance the preclinical work necessary for future human treatment.
Methods: Fifteen PBMC were cultured in the medium of EGM 2 for 4 weeks, and then incubated either in a monitored hypoxic chamber (1% O2, 5% CO2) (H) or in normal culture conditions (normoxia, N) for 6, 12, 24 and 48 hrs. Twenty RNAs comprising 5 Ns and 15 Hs (6, 12 and 24hr) were hybridized to Affymetrix Porcine arrays. An additional 40 samples were prepared for data confirmation by qRTPCR and Western blot. Data normalization and pattern recognition in each of these subgroups were achieved using R package 2.4 and GeneSpringGX. Homologous gene search and functional classification based on NCBI Pig Genomic Resources and DAVID Bioinformatics Resources 2007.
Results: Significant gene expression levels among the four groups were identified. The patterns of three hypoxia (H) groups were clearly distinct from that of normoxia (N) group. However, the expression pattern of 12hr H was more similar to 24hr H than that of 6hr H. Of 23,928 probes, 394 genes were statistically regulated rapidly in 6hr Hs vs. Ns, including HIF2alpha, VEGFA, PDGFA, ANGPT2, CXCL14 and PGD. Only 182 genes were modulated in 12hr Hs, but 84% (152/182) of the genes appeared either with 6hr or 24hr H groups. 227 genes were significantly over- or down- regulated in 24hr Hs, among the 94 genes were overlapped with 6hr and 12hr Hs. Notably, the 94 genes were the most differentially modulated in all three H groups, some of the genes were known involving in the processes of hypoxic stress, response to inflammatory, wounding, apoptosis and angiogenesis. The 94 genes are considered as hypoxic targets for further study.
Conclusions: Our results confirmed the role of several genes involved in hypoxic or ischemic states, and captured a set of genes that associated the PBMC response to hypoxic or ischemic surroundings.
Abstract P182: Usefulness of Mobile Telemedicine System in Real-time Transmission of Out-of-hospital 12-lead ECG
Authors: Nonogi Hiroshi , Yokoyama Hiroyuki , Otsuka Yoritaka , Kasahara Yoichiro , Kataoka Yu , Kokubu Nobuaki , Sase Kazuhiro 
Published: July 2021

[Purpose] AHA/ACC guidelines recommend routine use of 12-lead ECG and advance notification for patients with acute coronary syndrome. However, transmission of out-of-hospital 12-lead ECG to emergency department is still not spread and ECG interpretation on the prehospital and emergency department is not established. Therefore, we have developed and tested the clinical usefulness of the mobile telemedicine system to transmit 12-lead ECG between moving ambulances and physicians in cardiovascular emergency.
[Method] We set up the mobile telemedicine using the third-generation digital mobile phone to promote communications between an ambulance and diverse hospital. Compatibility issue among device vendors was solved by the implementation of open-standard medical waveform encoding rule with motion noise-reduction system. Real time 12-lead ECG was transferred together with vital signs and live video during transfer the patient by an ambulance. The performance of the mobile telemedicine system in the field-test was checked to transfer 12-lead ECG in different scenarios such as transferred ECG from a volunteer moving hand or leg, coughing or twisting body in an ambulance driving on common road or highway. In the next step, we set up the mobile telemedicine on an ambulance to promote communications between moving 5 ambulances in Suita-city and National Cardiovascular Center since 2008 June 2. To establish the efficacy of real-time transmission of out-of-hospital 12-lead ECG, the time-line from the onset of acute myocardial infarction to reperfusion is analyzed.
[Results] Totally 36 patters of 12-lead ECG were checked in the field test and all of them were comparable than those original one in the ambulance. Time-delay for transmission of 12 lead ECG was within 10seconds and for one-lead ECG monitoring and vital signs including BP, HR and oxygen saturation was 1 second without the difficulties for the interpretation.
[Conclusion] Those results indicate the usefulness and reliability of transmission of 12-lead ECG using the mobile telemedicine system from the ambulance. Further investigation is on-going to determine the efficacy in clinical conditions to reduce the treatment delay for acute myocardial infarction.
Abstract 310: Thrombospondin 2 Protects Against Uncontrolled Cardiac Inflammation and Injury During Viral Myocarditis
Authors: Swinnen Melissa , Vanhoutte Davy , Pinto Yigal , Carmeliet Peter , Heymans Stephane 
Published: July 2021

Background-The matricellular protein thrombospondin 2 (TSP2), a secreted extracellular matrix (ECM) glycoprotein, plays a crucial role in controlling cell-matrix interaction in tissue repair and cancer biology. Our previous data revealed that increased TSP2 reinforces the matrix and protects the against heart failure during hypertension. The present study investigated whether TSP2 may protects against exaggerated cardiac inflammation, injury and dysfunction during viral myocarditis.
Methods and Results-Therefore, mortality, cardiac inflammation and function were investigated in TSP2-null (KO) and wild type (WT) mice, and after adeno-associated virus (AAV)-9 mediated TSP-2 overexpression in WT, in a mouse model of coxsackievirus B3 (CVB3)-induced (106 CCID50 ip CBV3, 14 days) myocarditis. Absence of TSP2 resulted in an increased mortality in TSP2-null as compared with WT mice in both viral myocarditis (KO: 37,5% vs WT: 0%; n=8 per group). Histological analysis revealed increased cardiac inflammation (60 % increase of CD3-positive T-lymphocytes), necrosis and injury in TSP2-null compared to WT mice at 14 days of viral myocarditis. Ultrastructural analysis showed increased inflammation, matrix disruption and myocyte injury in absence of TSP2, together resulting in depressed systolic function (% FS; 40.1 ± 2.3 in WT vs. 24.6 ± 1.7 in KO mice, P<0.05) and increased cardiac dilatation (end-diastolic dimensions, mm; 2.6 ± 0.18 in WT vs. 3.6 ± 0.06 in KO mice, P<0.05) at 14 days at echocardiography. In concordance, AAV9-gene transfer of TSP2, with 50 % increase in cardiac TSP-2 expression, significantly reduced cardiac inflammation (60% reduction) and injury at 14 days as compared to control AAV9-GFP.
Conclusion-Together, these data clearly point towards a novel protective role for TSP2 against uncontrolled inflammation, myocardial injury and dysfunction in acute viral myocarditis.
Abstract 311: Poly(ADP-ribose) Polymerase-1 Inhibition Prevents High Fat Diet-induced Cardiac Hypertrophy by Modulating Matrix-destabilizing Proteases and Oxidative Stress
Authors: Hans Chetan P , Feng Yumei , Naura Amarjit , Zerfaoui Mourad , Troxclair Dana , Matrougui Khalid , Lazartigues Eric , Boulares Hamid 
Published: July 2021

Background: We recently showed that PARP-1 is activated within atherosclerotic plaques and that inhibition of this enzyme, exerts protective effects against high fat diet-induced atherogenesis. Given the tight association between atherosclerosis and cardiac pathologies, we examined, whether PARP-1 is an active participant in high fat diet-induced cardiac hypertrophy and whether PARP-1 gene knockout prevents such pathological abnormalities.
Methods: Apolipoprotein (ApoE)−/− mice fed a high-fat diet were used as a model of atherosclerosis. C57BL/6 ApoE−/− mice that are deficient in PARP-1 (ApoE-PARP-1d−/−) were generated in our laboratory. Hemodynamic parameters were obtained by a small animal-adapted ultrasound imaging system.
Results: Hemodynamic parameters revealed that ApoE−/− mice on regular diet exhibited markers of cardiac hypertrophy. PARP-1 gene knockout markedly protected against dyslipidemia-induced cardiac hypertrophy. An increase in dyslipidemia burden further exacerbated the latter parameters in ApoE−/− mice. Inhibition of PARP-1 by gene deletion provided a significant protection against the parameters of cardiac hypertrophy. Histology showed enlarged hypertrophied cardiac myocytes in ApoE−/− mice with typical “boxcar-shaped” nuclei and high-fat diet caused separation of the myocardial fibers suggestive of dilated cardiomyopathy in these mice. PARP-1 gene deletion maintained the structural integrity of cardiac myocytes. MMP activity, measured by zymography, was dramatically increased in heart and aorta of ApoE−/− mice on high-fat diet compared to ApoE-PARP-1d−/− mice on similar diet regimen, which was accompanied by increased collagen degradation and mast cell degranulation. PARP-1 gene knockout was associated with increased TIMP-2 expression in various cells of vascular origin which seemed to neutralize the degenerative effects of MMP activity.
Discussion: Our results demonstrate that PARP-1 gene deletion protects against dyslipidemia-induced cardiac hypertrophy and dilatations. We also provide evidence that PARP-1 inhibition protects against these pathologies by increasing expression of TIMP-2 and subsequent inhibition of tissue-degrading proteases in a mouse model of atherosclerosis.