tbuckley/cabot-search huggingface dataset:
Anthracycline treatment, cardiovascular risk factors and the cumulative incidence of cardiovascular disease in a cohort of newly diagnosed lymphoma patients from the modern treatment era
Authors: Nicholas J. Boddicker, Melissa C. Larson, Alessia Castellino, Joerg Herrmann, David J. Inwards, Gita Thanarajasingam, Matthew J. Maurer, Cristine Allmer, Thomas E. Witzig, Grzegorz S. Nowakowski, Thomas M. Habermann, Hector R. Villarraga, Susan L. Slager, James R. Cerhan, Carrie A. Thompson
Journal: American Journal of Hematology (2021)

The development of cardiovascular disease (CVD) in long-term survivors of lymphoma is of increasing importance. Here, we characterize the cumulative incidence and risk factors for CVD in lymphoma patients diagnosed in the current treatment era. From 2002-2015, newly diagnosed lymphoma patients (>18 years) were enrollment into a prospective cohort study that captured incident CVD, consisting of congestive heart failure (CHF), acute coronary syndrome (ACS), valvular heart disease (VHD), and arrhythmia. The cumulative incidence of CVD was calculated with death modeled as a competing risk. We estimated the association of treatment with anthracyclines or radiotherapy and traditional CVD risk factors with incidence of CVD using hazard ratios (HR) and 95% confidence intervals (CI) estimated from Cox regression. After excluding prevalent CVD at lymphoma diagnosis, the study consisted of 3063 patients with a median age of 59 years (range 18-95). The cumulative incidence of CVD at 10-years was 10.7% (95% CI, 9.5%-12.1%). In multivariable analysis, increasing age (HR = 1.05 per year, p < 0.001), male sex (HR = 1.36, p = 0.02), current smoker (HR = 2.10, p < 0.001), BMI > 30 kg/m
Abstract 13565: Superoxide Dismutase-loaded Nanoparticles Attenuate Myocardial Ischemia-Reperfusion Injury and Protect Against Chronic Adverse Ventricular Remodeling
Authors: Peter J Altshuler, Zhiliang J Cheng, Alexis R Schiazza, Mark R Helmers, Robin Hu, Jennifer J Chung, Samuel Kim, Jakub Jarmula, Tsourkas Andrew, Pavan Atluri
Journal: Circulation (2020)

Introduction: Revascularization relieves myocardial ischemia but induces additional reperfusion injury by oxidative stress. Superoxide dismutase (SOD) is a potent antioxidant with preclinical promise in reducing reperfusion injury but is not well retained within the myocardium. Hypothesis: Use of SOD-encapsulated nanoparticles (NP-SOD) will improve SOD retention and preserve cardiac function in a rat model of myocardial ischemia-reperfusion (I/R) injury. Methods: Ischemia was maintained for 60 minutes via occlusion of the left anterior descending artery (LAD). Immediately prior to reperfusion, intramyocardial injections of NP-SOD, free SOD or phosphate buffered saline (PBS) were administered along the border of ischemic myocardium. Acute injury was assessed 3 hours post-reperfusion (n=8 per group), and chronic injury at 4 weeks (n=12). Hemodynamics were measured by echocardiography and pressure-volume loops. Acute and chronic injury were examined histologically. Protein isolates at 3 hours measured mediators of cell-death. Intramyocardial enzyme retention analysis was performed by injecting NP or free fluorescent-tagged SOD and explanting hearts for imaging at 0, 24 and 72 hours (n=4 per group). Results: Intramyocardial SOD retention was 25% greater in NP-SOD than free SOD at 24 hours (p&lt;0.01) and 78% greater at 72 hours (p&lt;0.01). NP-SOD exhibited improved ventricular function by ejection fraction at 4 weeks (64%) compared to free SOD (51%; p&lt;0.01) and PBS (43%; p&lt;0.01). Cardiac output, stroke volume and end-systolic elastance were greater in NP-SOD. Histology at 28 days demonstrated 54% less macroscopic fibrosis and 85% less microscopic collagen deposition in NP-SOD compared to PBS, and 33/79% compared to free SOD (all p&lt;0.05). Quantifying RIPK3 protein levels in ‘at risk’ myocardium at 3 hours demonstrated 2.5-fold reduced upstream necrosome activation. Conclusions: NP-SOD provides prolonged enzyme retention within the myocardium. Intramyocardial NP-SOD administration prior to reperfusion attenuates acute myocardial injury and protects against chronic adverse ventricular remodeling. SOD acts by downregulating necrosis. These findings suggest potential for NP-SOD based therapy in mitigating myocardial I/R injury.
Abstract 16680: Endovascular Therapy of Svc Syndrome-a Systematic Review
Authors: Abdul Hussain Azizi, Irfan Shafi, Matthew Zhao, Vladimir Lakhter, Riyaz Bashir
Journal: Circulation (2020)

Background: Superior vena cava (SVC) syndrome is caused by the occlusion of the SVC and can result in significant morbidity and mortality. Recently, endovascular therapy (ET) has become the standard of care for majority of these patients. We performed a systematic review of available literature to assess the contemporary technical success rate, restenosis rate, and recurrence rate of SVC syndrome following endovascular intervention. Methods: We searched PubMed, Cochrane Library, and Embase databases from 1988 to 2019 for studies on Endovascular Therapy for SVC syndrome. After screening 709 records, 13 studies were included. Screening was conducted using Rayyan QCRI software for systemic reviews. Studies included full-length journal articles on SVC syndrome and ET among adults (18+ years). Case reports, or case series with &lt;20 patients were excluded. Data analysis was performed using OpenMeta software. Proportions and 95% confidence intervals (CIs) were calculated using random effects models. Heterogeneity among studies was assessed using Q and I 2 statistics. We evaluated the end-points of the technical success, restenosis rate and recurrence rates in SVC syndrome patients after endovascular stenting Results: A meta-analysis of 13 studies included a total of 1024 patients. The results of our meta-analysis show a weighted technical success rate of 98.6% (95% CI 0.97 – 0.99) (Fig. 1A), restenosis rate of 11.8% (95 CI 0.08-0.14) (Fig 1B) and recurrence rate of 9.9% (95% CI 0.06-0.13) (Fig 1C). Our studies had a substantial heterogeneity (I 2 ) of 52-80%. Figures:Figure 1A Figure 1B Figure 1C Conclusions: Our systematic review revealed high technical success rate, low restenosis, and recurrence rates after endovascular therapy supporting the paradigm of endovascular therapy as first line treatment for patients with SVC syndrome. Disclosures: Dr. Bashir has equity interest in Thrombolex Inc.
The Chinese Society of Hepatology position statement on the redefinition of fatty liver disease
Authors: Yuemin Nan, Jihong An, Jianfeng Bao, Hongsong Chen, Yu Chen, Huiguo Ding, Xiaoguang Dou, Zhongping Duan, Jiangao Fan, Yanhang Gao, Tao Han, Ying Han, Peng Hu, Yan Huang, Yuan Huang, Jidong Jia, Jiaji Jiang, Ying’an Jiang, Jie Li, Jun Li, Rongkuan Li, Shuchen Li, Wengang Li, Yufang Li, Shumei Lin, Jingfeng Liu, Shourong Liu, Lungen Lu, Qinghua Lu, Xinhua Luo, Xiong Ma, Huiying Rao, Hong Ren, Wanhua Ren, Jia Shang, Li Shi, Minghua Su, Bingyuan Wang, Rongqi Wang, Lai Wei, Zhili Wen, Biao Wu, Jing Wu, Shaojie Xin, Huichun Xing, Jinghang Xu, Ming Yan, Jiming Yang, Jinhui Yang, Li Yang, Yongfeng Yang, Yanyan Yu, Liaoyun Zhang, Lingyi Zhang, Xinxin Zhang, Yuguo Zhang, Yuexin Zhang, Jingmin Zhao, Shousong Zhao, Huanwei Zheng, Yongjian Zhou, Yongning Zhou, Hui Zhuang, Weize Zuo, Xiaoyuan Xu, Liang Qiao
Journal: Journal of Hepatology (2021)
Abstract 12975: A New Systemic Inflammation-nutrition Index Provides the Additional Long-term Prognostic Information to Ahead Score in Patients With Admitted for Acute Decompensated Heart Failure
Authors: Takahisa Yamada, Testuya Watanabe, Takashi Morita, Yoshio Furukawa, Shunsuke Tamaki, Masato Kawasaki, Atsushi Kikuchi, Tsutomu Kawai, Masahiro Seo, Jun Nakamura, Kiyomi Kayama, Masatsugu Kawahira, Kumpei Ueda, Takanari Kumura, Masatake Fukunami
Journal: Circulation (2020)

Background: Comorbidities are associated with poor clinical outcome in heart failure patients. AHEAD (A: atrial fibrillation; H: hemoglobin; E: elderly; A: abnormal renal parameters; D: diabetes mellitus) score has been related to clinical outcomes in patients with acute decompensated heart failure (ADHF). On the other hand, systemic inflammation plays a critical role in the outcomes of heart failure. Malnutrition is also associated with poor outcome in heart failure patients. It has been recently reported that advanced lung cancer inflammation index (ALI), which is calculated as body mass index х serum albumin / neutrophil to lymphocyte ratio, is an independent prognostic marker in several types of cancer. We sought to investigate the prognostic value of the combination of AHEAD score and ALI in ADHF patients. Methods and Results: We studied 263 patients admitted for ADHF and discharged with survival. At the discharge, we obtained ALI and AHEAD score (range 0-5, atrial fibrillation, hemoglobin &lt;13 mg/dL for men and 12 mg/dL for women, age &gt;70 years, creatinine &gt;130 μmol/L, and diabetes mellitus). During a follow-up period of 5.0±4.2 yrs, 67 patients had cardiovascular death (CVD). At multivariate Cox analysis, AHEAD score and ALI were significantly independently associated with CVD, independently of prior heart failure hospitalization, systolic blood pressure and serum sodium level. The patients with both greater AHEAD score (≥median value=3) and lower ALI (≤median value=42.3) had a significantly increased risk of CVD than those with either and none of them (45% vs 24% vs 13%, p&lt;0.0001, respectively). Conclusion: ALI would provide the additional long-term prognostic information to AHEAD score in patients with ADHF.
Abstract 16554: Sphingosine-1-Phosphate Activates the Mitochondrial Unfolded Protein Response in the Pulmonary Vasculature
Authors: Angelia D Lockett, Grace Vlasak, Viswanathan Natarajan, Roberto F MacHado
Journal: Circulation (2020)

Introduction: Aberrant activation of pathways that promote pulmonary arterial smooth muscle (PASMC) and endothelial cell (PAEC) proliferation causes vascular remodeling and increased vascular resistance that leads to the deadly disease Pulmonary Arterial Hypertension (PAH). Sphingosine-1-phosphate (S1P) induces PASMCs proliferation and disruption of its signaling mitigates vascular remodeling and PAH. Mitochondria regulate proliferation and can promote or inhibit it in a signal dependent manner. The mitochondrial unfolded protein response (UPR mt ) is a mechanism by which mitochondria preserve cell survival due to stress. Mitochondria are important mediators of PASMC proliferation and PAH development as both mitochondrial (mt) fission and aerobic glycolysis contribute to disease progression. Studies in C. elegans suggest a link between regulation of mt fission and activation of the UPR mt as suppression of fission leads to S1P dependent activation of the UPR mt . Hypothesis: We hypothesized that S1P stimulation leads to activation of the UPR mt to promote proliferation of hPASMCs and hPAECs. Methods: hPASMCs were stimulated with S1P (1 μM) for up to 24h. Cell extracts were analyzed by immunoblotting for proteins (eIF2α, ATF-5, HSP70 and Lonp1) that regulate the UPR mt . Mitochondrial dynamics was assessed by immunoblotting or immunofluorescence for mediators of fission (Drp-1) and fusion (mitofusin-2). SPHK1, the lipid kinase that catalyzes S1P generation, was overexpressed in hPAECs followed by immunoblotting for UPR mt and mt fission activation. PCNA expression was assessed to measure cell proliferation. Results: S1P stimulation of hPASMCs enhanced proliferation and caused rapid and sustained activation of the UPR mt as phosphorylation of eIF2α and expression of ATF-5 and HSP70 were increased. S1P also enhanced mt fission in hPASMCs as Drp-1 phosphorylation was increased concomitant with decreased mitofusin-2 expression. Overexpression of SPHK1 in hPAECs increased proliferation and activation of both the UPR mt and mt fission. Conclusions: S1P promotes functional and phenotypic changes of mitochondria that leads to activation of pathways that promote PASMC and PAEC proliferation which could contribute to vascular remodeling in PAH.
Errors in Numbers in the Text and Tables in a Secondary Analysis of the ISCHEMIA Randomized Clinical Trial
Authors: Harmony R. Reynolds
Journal: JAMA Cardiology (2021)

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Abstract 15292: Acute Coronary Syndrome in Patients With Severe Aortic Stenosis Undergoing TAVR: A Retrospective Analysis
Authors: Saad M Amin, Harsh Mehta, AKHTAR AMIN
Journal: Circulation (2020)

Introduction: Transcatheter aortic valve replacement (TAVR) has been increasingly utilized in patients with Aortic Stenosis (AS). The purpose of this study is to document the incidence of acute coronary syndrome (ACS) in patients with a history of severe Aortic Stenosis (AS) undergoing TAVR. Methods: Using the Nationwide Inpatient Sample (NIS) for years 2015 to 2017, we performed a retrospective analysis of adults over 18 years of age who underwent TAVR and their inpatient course was complicated by ACS. We further analyzed the comorbidities and complications associated with patients who developed ACS during the same hospitalization. Results: We divided a total of 69,584 patients with ACS, who underwent TAVR into two groups: patients with ACS (2.11%) and patients without ACS (97.89%). From 2015 to 2017 there was a decline in the incidence of ACS in patients undergoing TAVR from 2.62% to 1.93%. There were no demographic differences between the two groups. Comorbidities like diabetes, peripheral vascular disease, end-stage renal disease and chronic liver disease were more prevalent in ACS group (Table 1). Patients with ACS had a higher history of previous PCI (4.42% vs 2.64% p-0.08). Complications like cardiogenic shock (11.9% vs 1.29% p-&lt;0.05), acute respiratory failure (25.17% vs 4.1% p &lt;0.05), acute kidney injury requiring dialysis (1.7% vs 0.46% p&lt;0.05) and cardiac arrest (4.08% vs 0.78% p&lt;0.05) were more prevalent in the ACS group. Overall, in-hospital mortality (3.41% vs 1.42% p&lt; 0.05) and length of stay (12.22 days vs 4.20 days p&lt;0.05) was higher in the ACS group. Conclusions: A steady decline was noted in the number of cases complicated by ACS undergoing for TAVR over 3 years. ACS in TAVR cases was associated with higher rates of complications, prolonged hospitalizations and higher mortality.
Sports and exercise medicine in Europe and the advances in the last decade
Authors: Daniel Neunhaeuserer, Josef Niebauer, Gino Degano, Veronica Baioccato, Mats Borjesson, Maurizio Casasco, Norbert Bachl, Nicolas Christodoulou, Juergen Michael Steinacker, Theodora Papadopoulou, Fabio Pigozzi, Andrea Ermolao
Journal: British Journal of Sports Medicine (2021)

Sports and exercise medicine (SEM) is a professional qualification for physicians responsible for the health and care of athletes, but also for the functional evaluation and exercise prescription in patients with chronic diseases. SEM clinicians are involved in health promotion, screening and illness prevention for public health purposes.1 These medical specialists provide preparticipation evaluations in sports as well as comprehensive support and counselling for all those who engage in physical activity and exercise training. Although the exact role may vary in different settings and countries, key competencies of SEM-specialists have been identified including2 3:

Scientific evidence clearly shows that physical exercise is one of the most important prevention strategies and cost-effective/cost-saving medical treatment options for multiple chronic diseases.4 5 Surprisingly, abilities regarding the prescription of this exercise ‘poly-pill’ is not adequately taught in medical schools or during postgraduate specialisations. Athletes from different sports and performance levels will also seek SEM specialists for medical care. We, here, report the current state of the SEM specialisation in Europe and reflect on both our advances over the last decade and contemporary challenges.

Specialisation in SEM varies largely and a formal European Union (EU)-wide recognition as well as a defined role within healthcare settings have not yet been reached in many European countries. This is illustrated by the fact that a common curriculum has not yet been implemented, even though it has been recently proposed by the …
Bystander effects in FUS1-nanoparticle-mediated human lung cancer gene therapy
Authors: Gitanjali Jayachandran, Wuguo Deng, Jack Roth, Lin Ji
Journal: Cancer Research (2008)

2408  Restoration of tumor suppressor FUS1 function in FUS1-deficient lung cancer cells by DOTAP:cholesterol nanoparticle-mediated gene transfer significantly suppressed tumor cell growth by induction of apoptosis in vitro. Systemic treatment with FUS1-nanoparticles demonstrated a potent antitumor efficacy in preclinical lung cancer animal models and showed promising clinical benefits in advanced lung cancer patients. However, the currently available gene transfer protocols and techniques for cancer gene therapy are capable of transducing only a fraction of tumor cells in vivo, thus, relying on a bystander effect (killing of non-transduced cells by products of transduced cells) to achieve clinically-meaningful therapeutic efficacy. Based on observations that FUS1 protein could interact extensively with various receptor tyrosine kinases and cellular proteins and demonstrates a potent pro-apoptotic activity, we hypothesized that cancer cells transduced by FUS1-nanoparticles would kill their neighboring cells through a bystander effect. To test whether ectopic expression of FUS1 in tumor cells can cause neighboring cell killing by triggering the release of cytotoxic soluble factors, we collected conditioned medium (CM) from FUS1-nanoparticle-transduced H1299 cells. CM was collected after 48 h in cell culture either containing or free of bovine fetal serum and concentrated by lyophilization. The CMs from untransduced, or empty vector (EV), and dysfunctional mutant FUS1-transduced cells were used as controls. A marked inhibition of tumor cell growth and induction of apoptosis were detected in H1299 cells treated by concentrated CMs from wt-FUS1-transduced cells compared with those of controls. In addition, distinct soluble protein/peptide species were clearly detected in the serum-free wt-FUS1-CM on protein mass spectra by a ProteinChip array-based SELDI-TOF-MS analysis, compared to those of control CMs, suggesting release of specific soluble peptides. To further test the potential bystander effects of FUS1 on lung cancer cells, we used the wt-FUS1-nanoparticles-transfected H1299 cells as effector cells and mixed them with the Ad-GFP-transduced H1299 target cells, which do not express FUS1, at a ratio of 1:1. The EV-transfected H1299 effectors were used as the control. The mixed cells were cultured for 48 hr. The dead/apoptotic cells in both effector and target (GFP) cell populations were determined by flow cytometry with TUNEL-reaction. A significantly increased population of dead/apoptotic cells was detected in the GFP-expressing target cells mixed with wt-FUS1-transfected H1299 effecter cells, compared with that of target cells mixed with EV-transfected effectors. These results strongly suggest the presence of bystander effects induced by FUS1-nanoparticle-mediated gene transfer in lung cancer cells. This abstract is supported by grants of NIH NCI (SPORE P50CA70907 and RO1CA116322).
Abstract 15120: Mechanistic Determinants of Atrial Functional Mitral Regurgitation
Authors: Milad Matta, Ossama K. Abou Hassan, Chadi Ayoub, Serge C. Harb
Journal: Circulation (2020)

Introduction: Atrial functional mitral regurgitation (AFMR) is an increasingly recognized entity that is defined as MR in the absence of primary leaflet pathology and left ventricular dysfunction. Objectives: Identify the mechanistic determinants of AFMR by cardiac computed tomography (CT). Methods: We reviewed all consecutive CTs performed in atrial fibrillation (Afib) patients pre/post-ablation and appendage occlusion procedures starting in February 2017. We identified the first 50 patients with significant MR (≥2+) then 50 controls without MR that were age and gender-matched. Clinical and echo data were collected. A dedicated CT software (Aquarius, TeraRecon) was used to perform detailed annular measurements Results; The median age was 70.7 years, and 39% were females. There were no significant differences in baseline clinical comorbidities, including type and duration of Afib, and medication use, including rate control agents and antiarrhythmics (Table 1). On echo, patients with significant MR had larger LA volumes (mean +/- SD, 47.63 ml/m2 +/- 17.21 vs. 35.53 +/- 14.22, p&lt;0.001) higher estimated RVSP (40.77 +/- 13.88 mmHg vs. 33.54 +/-6.92, p 0.004), and more frequent concomitant significant TR (32% vs 8%, p=0.006). On CT analysis, there were significant differences (all p&lt;0.001) in the mitral annular measurements, including larger area, perimeter, and septo-lateral and inter-commissural distances in the MR group (Figure 1). Conclusion: Patients with Afib who develop significant AFMR have significantly larger annular and atrial sizes, higher RVSP, and more concomitant significant TR. The type and duration of Afib do not appear to be significant predictors.