tbuckley/cabot-search huggingface dataset:
Improving Research on Screen Media, Autism, and Families of Young Children—Reply
Authors: Karen Frankel Heffler, David S. Bennett, Keshab Subedi
Journal: JAMA Pediatrics (2020)

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Abstract 13298: The Association Between Coronary Artery Calcium and Atherosclerotic Cardiovascular Disease Risk in Women With Early Menopause: The Multi-Ethnic Study of Atherosclerosis
Authors: Jian Chu, Erin D Michos, Pamela Ouyang, Dhananjay Vaidya, Roger S Blumenthal, Matthew J Budoff, Michael J Blaha, Seamus P Whelton
Journal: Circulation (2020)

Background: Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of mortality among women, and early menopause (EM) is associated with an increased risk for ASCVD. Coronary artery calcium (CAC) is a non-invasive measurement of an individual’s subclinical atherosclerotic burden that is used to refine ASCVD risk estimation, and the absence of CAC is a robust predictor of low 10-year ASCVD risk. However, it is unknown whether there is a difference in the long-term association between the absence of CAC and ASCVD risk between women with and without EM. Objectives: To compare the prevalence of CAC and its association with incident ASCVD between women with and without EM. Methods: We performed Kaplan-Meier survival analysis and multivariable Cox proportional hazards modeling using data from 2,456 postmenopausal women in the Multi-Ethnic Study of Atherosclerosis (MESA) with or without EM, defined as occurring at &lt;45 years of age. Results: Participants had a mean age of 64.1 years, 39% were White, and 28% (n=688) experienced EM. There were 291 ASCVD events over a mean follow-up of 12.5 years. Women with EM had a slightly lower prevalence of CAC=0 (55.1%) than women without EM (59.7%) (p=0.04) despite no difference in mean age. Among women with CAC=0, the cumulative incidence of ASCVD was slightly higher at 10-year follow-up for women with vs. without EM (5.4% vs. 3.2%, p=0.06) and significantly higher at 15-years (11.4% vs. 6.4%, p&lt;0.01) (Figure). In multivariable Cox models, compared to women with CAC=0, those with CAC 1-99 and ≥100 had progressively increased ASCVD risk that did not significantly differ by EM status. Conclusions: More than half of postmenopausal women with EM had CAC=0 and an associated low-to-borderline 10-year risk of ASCVD. When CAC&gt;0, the risk of ASCVD was similar for women with and without EM. Additional research is needed to better understand very long-term differences in ASCVD risk between women with and without EM who have CAC=0.
Abstract 14310: Elephant Sitting on My Chest: A Tale of Two Vessels
Authors: Anudeep K Dodeja, Patrick I McConnell, Elisa A Bradley, Curt Daniels, Laxmi S Mehta, Aarthi Sabanayagam
Journal: Circulation (2020)

Introduction: A dilated main pulmonary artery (MPA) seen in congenital heart disease (CHD) or pulmonary arterial hypertension (PAH) is a rare cause of angina due to left main coronary artery (LMCA) compression. Case: A 49 year old male with no prior cardiac history presented with substernal chest pain. He reported exercise intolerance for several years. On exam he had an oxygen saturation of 85%, loud P2, fixed split second heart sound and ejection click. Electrocardiogram showed right ventricular (RV) hypertrophy and no significant ST changes. Laboratory data revealed a negative troponin. An enlarged main and right pulmonary artery (RPA) (Figure 1A) was seen on computed tomography (CT) chest angiography for pulmonary embolism (CTPE) and on echocardiography he had a severely dilated RV with decreased function (Figure 1B,1C). Cardiac catheterization showed a step up in saturations from 56 to 71%, Qp:Qs of 1.5 mean MPA pressure of 53 mmHg, pulmonary capillary wedge pressure of 11mmHg and pulmonary vascular resistance (PVR) of 7WU. A slit-like narrowing of LMCA ostium was seen on coronary angiography and intravascular ultrasound (Figure 1D). He was diagnosed with a sinus venosus defect, anomalous right upper pulmonary venous drainage and suspicion for extrinsic compression of LMCA by the dilated RPA that was confirmed on cardiac CT (Figure 1E-I). He was started on triple therapy for PAH with a significant reduction in PA pressures (mean 36 mmHg and PVR 2.1 WU). Percutaneous stenting of the LMCA was deferred and he underwent successful sinus venosus defect repair with a 5mm fenestrated patch, baffling of the anomalous pulmonary veins and a 32 mm interposition graft in the MPA with reduction plasty of MPA/RPA. Conclusion: This is an unusual presentation of unrepaired CHD with angina due to a compressed LMCA from a dilated pulmonary artery. Treatment of the underlying PAH as well as repair of the defect including reduction plasty of the MPA is a consideration for symptomatic relief.
Abstract 15092: The Yin-yang of Bmpr2 and Ces1 in the Pulmonary Endothelium Aad Its Role in Pulmonary Arterial Hypertension
Authors: Stuti Agarwal, Ananya Chakraborty, David Condon, Salvador Tello, Karthik Suresh, Bruce D Hammock, Marlene RABINOVITCH, Mark Nicolls, Flora Huang, Vinicio A De Jesus Perez
Journal: Circulation (2020)

Background/Hypothesis: Pulmonary Arterial Hypertension (PAH) is a life-threatening disease characterized by loss of pulmonary microvessels and vascular remodeling. Loss of function BMPR2 mutations contribute to pulmonary endothelial cell (EC) apoptosis and oxidative stress, but their reduced penetrance suggests need for additional modifiers. Carboxylesterase1 (CES1) is endoplasmic reticulum (ER) enzyme responsible for detoxification, proteostasis, and redox balance. Similar to BMPR2 mutations, we found that loss of CES1 is associated with oxidative stress and apoptosis. In this study, we explore a plausible link between BMPR2 pathway and CES1 regulation in promoting EC survival and angiogenesis. Methods: PECs &amp; lung tissue from healthy donors and PAH patients were obtained from PHBI. To induce oxidative stress, we used H 2 O 2 (100 μM) &amp; methamphetamine HCl (METH, 0.5-2mM). Both siRNA and pharmacological approaches were used to inhibit BMPR2, Nrf2, and CES1 expression. Caspase and Matrigel assays were used to assess PEC survival and tube formation, respectively. Results: RNAseq of BMPR2-mutant PECs showed significantly less CES1 expression, which correlated with reduced protein expression in PEC lysates and within lung vascular lesions. In healthy PECs, BMP9 stimulation led to increase in CES1 expression that was absent post BMPR2 knockdown. CES1 gene transcription was by BMPR2-dependent activation of Nrf2, a transcription factor responsible for antioxidant gene expression and mitochondrial biogenesis. Inhibition of Nrf2 activation by ML385 (5μM) abrogates BMP9 induced CES1 mRNA levels similar to BMPR2 knockdown. The connection between BMPR2 and CES1 was further strengthened by CES1 knockdown studies in PECs that demonstrated reduction in BMPR2 protein synthesis associated with ER stress and reduced autophagy. Finally, lung examination in CRISPR generated CES1 +/- mice demonstrated increased microvascular muscularization at normoxia compared to wild type mice. Conclusion: BMPR2 and CES1 are part of common signaling pathway that protects PECs against oxidative stress and mitochondrial damage through a positive feedback loop. Interventions that restore CES1 activity could rescue BMPR2 signaling and serve as novel PAH therapeutics.
Abstract 20423: Prognostic Impact of the Minute Ventilation Carbon Dioxide Production Slope in Patients With Acute Myocardial Infarction With Preserved Left Ventricular Ejection Fraction
Authors: Chikara T Urabe, Masashi Fujino, Kazuhiro Nakao, Shuichi Yoneda, Fumiyuki Otsuka, Tetsuo Arakawa, Shigefumi Fukui, Takuya Hasegawa, Michio Nakanishi, Teruo Noguchi, Satoshi Yasuda
Journal: Circulation (2017)

Background: Ventilatory efficiency, commonly assessed by the minute ventilation (VE)-carbon dioxide production (VCO2) slope, is proven to be a good predictor in the heart failure (HF) population. H...
Ebola-negative neonates born to Ebola-infected mothers after monoclonal antibody therapy: a case series
Authors: Maria Paula Ottoni, James D Ricciardone, Adi Nadimpalli, Saschveen Singh, Anne Marie Katsomya, Landry Mavita Pokoso, Roberta Petrucci
Journal: The Lancet Child & Adolescent Health (2020)
Abstract 15471: Structural Valve Degeneration of Transcatheter Aortic Valve Replacement in a Veterans Affairs Population
Authors: Rachel Yang, Vimala Ponna, Kendrick A Shunk, Jeffrey Zimmet, Liang Ge, Elaine E Tseng
Journal: Circulation (2020)

Introduction: Transcatheter aortic valve replacement (TAVR), previously reserved for intermediate to prohibitive surgical risk, has now expanded to patients with severe aortic stenosis of any surgical risk. However, bioprostheses are prone to structural valve degeneration (SVD), a progressive process that limits valve durability. As the population undergoing TAVR shifts toward a lower-risk and younger profile, long-term durability is a crucial determinant for patient outcomes. Our objective was to report the characteristics of and assess risk factors for SVD in a veteran TAVR population. Methods: Patients undergoing TAVR at our Veterans Affairs Medical Center were retrospectively evaluated for SVD and other endpoints using recently standardized consensus criteria. Multivariate Cox proportional hazards analysis was performed to evaluate risk factors for SVD. Results: From 2013 to 2020, 312 patients (median age 79.0) underwent TAVR. Survival from all-cause mortality was 90.8% at 1 year, 76.1% at 3 years, and 64.0% at 5 years (Figure 1). Cumulative freedom from SVD was 98.0% at 1 year, 95.7% at 3 years, and 91.8% at 5 years. The 13 patients who met criteria for SVD were classified as moderate hemodynamic, and 2 required intervention. Median time to SVD was 1.04 years. Independent predictors of SVD include age (HR=0.92, CI:0.86-0.99) and valve size (HR=0.16, CI:0.03-0.81). Conclusions: SVD was evident at a low but detectable rate in 5 year follow-up, and associated with risk factors of patient age and implanted valve size. Further understanding of TAVR biomechanics will be essential to inform patient-specific risk of SVD. Figure 1: Kaplan-Meier curves of survival and freedom from SVD
Rates of increase of antibiotic resistance and ambient temperature in Europe: a cross-national analysis of 28 countries between 2000 and 2016
Authors: Sarah F McGough, Derek R MacFadden, Mohammad W Hattab, Kåre Mølbak, Mauricio Santillana
Journal: Eurosurveillance (2020)

BackgroundThe rapid increase of bacterial antibiotic resistance could soon render our most effective method to address infections obsolete. Factors influencing pathogen resistance prevalence in human populations remain poorly described, though temperature is known to contribute to mechanisms of spread.AimTo quantify the role of temperature, spatially and temporally, as a mechanistic modulator of transmission of antibiotic resistant microbes.MethodsAn ecologic analysis was performed on country-level antibiotic resistance prevalence in three common bacterial pathogens across 28 European countries, collectively representing over 4 million tested isolates. Associations of minimum temperature and other predictors with change in antibiotic resistance rates over 17 years (2000-2016) were evaluated with multivariable models. The effects of predictors on the antibiotic resistance rate change across geographies were quantified.ResultsDuring 2000-2016, for Escherichia coli and Klebsiella pneumoniae, European countries with 10°C warmer ambient minimum temperatures compared to others, experienced more rapid resistance increases across all antibiotic classes. Increases ranged between 0.33%/year (95% CI: 0.2 to 0.5) and 1.2%/year (95% CI: 0.4 to 1.9), even after accounting for recognised resistance drivers including antibiotic consumption and population density. For Staphylococcus aureus a decreasing relationship of -0.4%/year (95% CI: -0.7 to 0.0) was found for meticillin resistance, reflecting widespread declines in meticillin-resistant S. aureus across Europe over the study period.ConclusionWe found evidence of a long-term effect of ambient minimum temperature on antibiotic resistance rate increases in Europe. Ambient temperature might considerably influence antibiotic resistance growth rates, and explain geographic differences observed in cross-sectional studies. Rising temperatures globally may hasten resistance spread, complicating mitigation efforts.
Abstract 13717: Autologous Skeletal Myoblast Patch Remodeled Swine Pressure-overloaded Right Heart by Amelioration in Myocardial Ischemia
Authors: Kanta Araki, Shigeru Miyagawa, Takuji Kawamura, Ryo Ishii, Akima Harada, Takayoshi Ueno, Koichi Toda, Yoshiki Sawa
Journal: Circulation (2020)

Introduction: Myocardial ischemia (MI) is majorly seen in the right ventricular (RV) dysfunction in patients with congenital heart disease secondary to residual hemodynamic stressors in form of pressure-overloaded, suggesting therapeutic target for RV dysfunction may be how to control MI. Autologous skeletal myoblast patch showed the angiogenetic effect for left ventricular dysfunction by cytokine paracrine effects, which are expected to be sufficiently effective against pressure-overloaded RV dysfunction. Hypothesis: An autologous skeletal myoblast patch alleviates the MI in a pressure-overloaded right heart in swine model, leading to amelioration of metabolic and functional dysfunction. Methods: Five-month-old mini-pigs underwent pulmonary artery banding. Two months after banding, myoblast patch derived from autologous skeletal muscles were placed on the epicardium of RV free wall. Groups were as follows: control (C, n=6), sheet implantation (S, n=6). Two months after sheet implantation, cardiac function exam and C11-Acetate positron emission tomography (PET) were done, and hearts were dissected for histologic and real-time polymerase chain reaction (RT-PCR) analysis. Results: Two months after sheet implantation, RV dysfunction was significantly ameliorated in group S than group C (RVEF; S 44.9+/-2.2 vs C 31.9+/-2.1 % [p=0.0042]). PET revealed the deterioration of myocardial blood flow (Rest/Stress; S 3.22+/-0.39 vs C 2.13+/-0.92 min -1 [p=0.0421]) and myocardial oxidative metabolism (K mono -Rest/Stress: S 3.17+/-0.69 vs C 2.03+/-0.65 min -1 [p=0.0421]) were suppressed in group S than group C. In histologic analysis, group S presented more angiogenesis in CD31 expression (S 18.3+/-1.5 vs C 10.7+/-2.8 units/cells [p=0.0122]). In RT-PCR analysis, mRNA expression of vascular endothelial growth factor (S 1.28+/-0.35 vs C 0.75+/-0.17 folds [p=0.030]), hepatocyte growth factor (S 1.70+/-0.79 vs C 0.74+/-0.10 folds [p=0.030]), and chemokine stromal cell-derived factor-1 (S 1.49+/-0.97 vs C 0.35+/-0.20 folds [p=0.030]) were upregulated in group S than group C. Conclusions: Autologous skeletal myoblast patch ameliorated metabolic and functional dysfunction in a swine model of pressure-overloaded right heart by alleviation of MI.
Abstract 15063: The Atf6-inducible Selenoprotein, Vimp, Regulates Proteostasis and Pressure Overload-induced Heart Failure
Authors: Erik Blackwood, Donna Thuerauf, Lauren MacDonnell, Alina S Bilal, Chris C Glembotski
Journal: Circulation (2020)

Introduction: Cardiac hypertrophy is associated with an increase in protein synthesis, which must coordinate with protein folding and degradation to allow for homeostatic growth without affecting the functional integrity of cardiac myocytes (i.e. proteostasis). There is a gap in our understanding of how proteostasis becomes imbalanced during chronic pathological hypertrophy. Hypothesis: The objective of this study to examine the mechanisms regulating the protein degradation aspect of proteostasis, ER associated degradation (ERAD), by focusing on the role in cardiac hypertrophy of the unique selenoprotein and functional initiator of the ERAD molecular machinery, VIMP, which is induced in cardiac pathology by the nodal proteostasis transcription factor, ATF6. Methods and Results: VIMP was increased in failing human and in mouse hearts subjected to TAC-induced heart failure in an ATF6-dependent manner. AAV9-shRNA-mediated VIMP knockdown in the heart dramatically suppressed cardiac hypertrophy and staved off decompensation and heart failure, while AAV9-mediated VIMP overexpression exacerbated cardiac decompensation in response to TAC, an effect not observed with overexpression of an ERAD-null mutant of VIMP. Unexpectedly, VIMP knockdown enhanced ERAD-mediated degradation of the cytosolic pro-hypertrophic kinase, serum/glucocorticoid-regulated kinase 1, SGK1. Furthermore, AAV9-mediated overexpression of SGK1 negated the beneficial effects of VIMP knockdown; knockdown of the SGK1-binding protein, GILZ enhanced ERAD-mediated degradation of SGK1 and blunted cardiac hypertrophy. A peptide inhibiting the SGK1-GILZ interaction enhanced the ERAD-mediated degradation of SGK1 and ameliorated agonist-induced cardiac myocyte hypertrophy. Conclusions: Here we studied ERAD for the first time in any organ, in vivo , finding that an ATF6-inducible selenoprotein, VIMP, regulates the ERAD-dependent degradation of SGK1, thus accelerating TAC-induced cardiac decompensation and heart failure.
Abstract 15492: The Prognostic Role of Education Attainment Level in Individuals With Ischemic Heart Disease: Analysis From the Endocrine Vascular Approach Study
Authors: Valeria Raparelli, Claudia Tucci, Marco Proietti, Floriana Santonemma, Andrea Lenzi, Nicola Viceconte, Bernadette Corica, Gaetano Tanzilli, Giulio Francesco Romiti, Stefania Basili
Journal: Circulation (2020)

Introduction: Although adverse outcomes from cardiovascular disease (CVD) have been on a linear decline, the burden remains high. Addressing the social determinants of health in the care of CVD patients is emerging as a strategy for improving outcomes. Educational attainment level (EAL), a proxy of socioeconomic status, has been associated with both cardiovascular risk and patient’s ability to self-manage the complex cardiovascular treatment. Objective: To assess the impact of EAL on major adverse cardiovascular events (MACE) and all-cause death in patients with ischemic heart disease (IHD). Methods: Endocrine Vascular disease Approach (EVA) is a prospective observational study recruiting hospitalized patients with IHD undergoing coronary angiography and/or percutaneous coronary interventions. Socio-demographics and clinical data, including the level of multimorbidity defined by a Charlson Comorbidity Index≥ 4, were collected. A low-EAL, assessed through a self-reported questionnaire, was defined if at least elementary/middle school education was completed. The primary outcome was the occurrence of MACE (i.e. cardiovascular death, non-fatal myocardial infarction, non-fatal stroke) and a secondary composite endpoint (i.e. all-cause death, non-fatal myocardial infarction, non-fatal stroke) was also analyzed. Results: Among 460 individuals (mean age 67±11, 30% women) with IHD, 252 (55%) had a low-EAL. Individuals with low-EAL were younger and more likely to have heart failure, vascular encephalopathy, and high multimorbidity. A low-EAL was associated with a higher risk of MACE compared with higher EAL (Log-rank=12.29, p&lt;0.001) with similar results for the secondary outcome (Log-rank=9.45, p=0.002). In the adjusted multivariate regression analysis, low EAL was independently associated with MACE [Hazard Ration (HR): 2.31, 95% Confidence Interval (CI): 1.23-4.34, p=0.010] and secondary outcome [HR: 1.73, 95%CI 1.02-2.92, p=0.042] compared to high-EAL. Conclusion: Individuals with IHD and low-EAL had a higher risk of MACE and all-cause death. Interventions that specifically address health literacy and cognition should be tested among these high-risk patients to improve outcomes.
Abstract 14715: Diabetes and Relative Rates of Cardiovascular Events in Women Compared With Men
Authors: Denis Angoulvant, Pierre Henri Ducluzeau, Peggy Renoult Pierre, Gregoire Fauchier, Julien Herbert, Pascal Spiesser, Alexandre Bodin, Arnaud Bisson, Laurent Fauchier
Journal: Circulation (2020)

Data are inconsistent regarding sex-differences in the relative rates of cardiovascular events associated with diabetes. We aimed to investigate whether diabetes confers higher relative rates of cardiovascular events in women compared with men using contemporary data, and whether these sex-differences depend on age. Methods: All patients seen in French hospitals in 2013 with at least 5 years or follow-up (or dying earlier) without a history major adverse cardiovascular event, were identified and characterized by individual-level linkage of French nationwide administrative registers. They were categorized by diabetes-status and followed-up until 31 December 2019. Using Cox models, we calculated overall and age-dependent incidence rates, incidence rate ratios, and women-to-men ratios for myocardial infarction, heart failure, ischemic stroke, or cardiovascular death (MACE-HF). Results: The study included 3,381,472 individuals among whom 482,848 (14.3%) had diabetes (88.1% with type 2 diabetes). Among 482,848 (45% women) patients with diabetes, the absolute rate of MACE-HF was higher in men than in women (9.7 vs. 7.4 per 100 person-years). Corresponding absolute rates in men and women without diabetes were 4.9 vs. 3.1 per 100 person-years. Comparing individuals with and without diabetes, women had higher incidence rate ratio (IRR) of MACE-HF than men (IRR 2.42 95% confidence interval [CI] 2.40-2.44) in women vs. 1.99, 95% CI 1.98-2.01 in men) with a women-to-men ratio (WMR) of 1.22 (CI 1.20-1.23, p&lt;0.001). The IRRs of MACE-HF for diabetes vs no diabetes were highest in women aged 45 and in the youngest men and decreased with advancing age for both men and women, but the IRRs were higher in women across all ages, with the highest WMR between age 45 and 70 years. This effect was more apparent for myocardial infarction (women-to-men ratio 1.43, 95%CI 1.39-1.47 after adjustment) than for ischemic stroke (WMR 1.10, 95%CI 1.07-1.13 after adjustment) or overall MACE-HF (WMR 1.16, 95%CI 1.15-1.18 after adjustment). Conclusion: Although men have higher absolute rates of cardiovascular complications, the relative rates of cardiovascular complications associated with diabetes are higher in women than in men across all ages in recent years.