tbuckley/cabot-search huggingface dataset:
Evaluation of Mortality Data From the Social Security Administration Death Master File for Clinical Research
Authors: Ann Marie Navar, Eric D. Peterson, Dylan L. Steen, Daniel M. Wojdyla, Robert J. Sanchez, Irfan Khan, Xue Song, Matthew E. Gold, Michael J. Pencina
Journal: JAMA Cardiology (2019)

Despite its documented undercapture of mortality data, the US Social Security Administration Death Master File (SSDMF) is still often used to provide mortality end points in retrospective clinical studies. Changes in death data reporting to SSDMF in 2011 may have further affected the reliability of mortality end points, with varying consequences over time and by state.To evaluate the reliability of mortality rates in the SSDMF in a cohort of patients with atherosclerotic cardiovascular disease (ASCVD).This observational analysis used the IBM MarketScan Medicare and commercial insurance databases linked to mortality information from the SSDMF. Adults with ASCVD who had a clinical encounter between January 1, 2012, and December 31, 2013, at least 2 years of follow-up, and from states with 1000 or more eligible adults with ASCVD were included in the study. Data analysis was conducted between April 18 and May 21, 2018.Kaplan-Meier analyses were conducted to estimate state-level mortality rates for adults with ASCVD, stratified by database (commercial or Medicare). Constant hazards of mortality by state were tested, and individual state Kaplan-Meier curves for temporal changes were evaluated. For states in which the hazard of death was constant over time, mortality rates for adults with ASCVD were compared with state-level, age group-specific overall mortality rates in 2012, as reported by the National Center for Health Statistics (NCHS).This study of mortality data of 667 516 adults with ASCVD included 274 005 adults in the commercial insurance database cohort (171 959 male [62.8%] and median [interquartile range (IQR)] age of 58 [52-62] years) and 393 511 in the Medicare database cohort (245 366 male [62.4%] and median [IQR] age of 76 [70-83] years). Of the 41 states included, 11 states (26.8%) in the commercial cohort and 18 states (43.9%) in the Medicare cohort had a change in the hazard of death after 2012. Among states with constant hazard, state-level mortality rates using the SSDMF ranged widely, from 0.06 to 1.30 per 100 person-years (commercial cohort) and from 0.83 to 6.07 per 100 person-years (Medicare cohort). Variability between states in mortality estimates for adults with ASCVD using SSDMF data greatly exceeded variability in overall mortality from the NCHS. No correlation was found between NCHS mortality estimates and those from the SSDMF (ρ = 0.29 [P = .06] for age 55-64 years; ρ = 0.18 [P = .27] for age 65-74 years).The SSDMF appeared to markedly underestimate mortality rates, with variable undercapture among states and over time; this finding suggests that SSDMF data are not reliable and should not be used alone by researchers to estimate mortality rates.
THE ROLE OF ATHEROSCLEROSIS AND LEFT VENTRICULAR STRUCTURE AND FUNCTION IN FRAILTY DEVELOPMENT: RESULTS FROM THE MULTI-ETHNIC STUDY OF ATHEROSCLEROSIS (MESA)
Authors: Jaclyn Sesso, Eric Xie, Jeremy Walston, Karen Bandeen-Roche, Colin Wu, Alain Bertoni, Sanjiv Shah, Joao Lima, Bharath Ambale Venkatesh
Journal: Journal of the American College of Cardiology (2019)
FROM SILOS TO PATIENTS: COMPARING A MODALITY-CENTERED TO A PATIENT-CENTERED INSTRUCTIONAL FORMAT FOR MULTIMODALITY IMAGING
Authors: Sarah Blissett, Matthew Sibbald, Christos Galatas, Annabel Chen-Tournoux, Pantelis Diamantouros, Jonathan Afilalo, Lawrence Rudski, Regina Husa, Igal Sebag
Journal: Journal of the American College of Cardiology (2019)
A DETAILED ANGIOGRAPHIC ASSESSMENT OF ANTEGRADE AND RETROGRADE PERFORATIONS DURING CHRONIC TOTAL OCCLUSION INTERVENTION
Authors: Taishi Hirai, James Sapontis, William Nicholson, Steven Marso, William Lombardi, Craig Thompson, R. Michael Wyman, Dimitrios Karmpaliotis, Jeffrey Moses, Kensey Gosch, James Grantham
Journal: Journal of the American College of Cardiology (2019)
Abstract 377: Modeling Cadmium-induced Cardiotoxicity Using Human Pluripotent Stem Cell-derived Cardiomyocytes
Authors: Jiaxi Shen, Xiaochen Wang, Danni Zhou, Tongyu Li, Ling Tang, Tingyu Gong, Jun Su, Ping Liang
Journal: Circulation Research (2018)

Cadmium, a highly ubiquitous toxic heavy metal, has been widely recognized as an environmental and industrial pollutant, which confers serious threats to human health. The molecular mechanisms of the cadmium-induced cardiotoxicity (CIC) have not been studied in human cardiomyocytes at the cellular level. Here we showed that human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) can recapitulate the CIC at the cellular level. The cadmium-treated hPSC-CMs exhibited cellular phenotype including reduced cell viability, increased apoptosis, cardiac sarcomeric disorganization, elevated reactive oxygen species, altered electrophysiology and cardiac arrhythmias. RNA-sequencing analysis revealed a differential transcriptome profile and activated MAPK signaling pathway in cadmium-treated hPSC-CMs, and suppression of P38 MAPK but not ERK MAPK or JNK MAPK rescued CIC phenotype. We further identified that suppression of PI3K/Akt signaling pathway is sufficient to reverse the CIC phenotype, which may play an important role in CIC. Taken together, our data indicate that hPSC-CMs can serve as a suitable model for the exploration of molecular mechanisms underlying CIC and for the discovery of CIC cardioprotective drugs.
ISOLATED SYSTOLIC HYPERTENSION (ISH) BY NEW ACC/AHA HYPERTENSION (HTN) GUIDELINES AND OUTCOMES IN OLDER ADULTS OVER 23 YEARS IN THE CARDIOVASCULAR HEALTH STUDY (CHS)
Authors: Samir Patel, Helen Sheriff, Cherinne Arundel, Ross Fletcher, Prakash Deedwania, Wen-Chih Wu, Wilbert Aronow, Steven Singh, Ali Ahmed
Journal: Journal of the American College of Cardiology (2019)
NOVEL BIOMARKERS FOR RISK STRATIFICATION IN ACUTE PULMONARY EMBOLISM
Authors: Yevgeniy Brailovsky, Vladimir Lakhter, Kateria Porcaro, Jeremiah Haines, Stephen Morris, Estefania Oliveros, Demetrios Doukas, Erin Mancl, Dalila Masic, John J. Lopez, Bruce Lewis, Debra Hoppensteadt, Carlos Bechara, Verghese Mathew, Jawed Fareed, Amir Darki
Journal: Journal of the American College of Cardiology (2019)
PATIENTS WITH ACUTE CHEST PAIN IN THE EMERGENCY ROOM: EARLY AND LATE OUTCOMES AFTER NEGATIVE CORONARY COMPUTED TOMOGRAPHY ANGIOGRAPHY-DERIVED FRACTIONAL FLOW RESERVE
Authors: Jason Schott, Adam Hafeez, Kavitha Chinnaiyan, Gilbert Raff, Michael Gallagher, A. Neil Bilolikar, Robert Safian
Journal: Journal of the American College of Cardiology (2019)
Abstract 303: Fast Skeletal Myosin Binding Protein-c Expression in Heart Failure
Authors: James W McNamara, Thomas L Lynch, Taejong Song, Jack L Rubinstein, Sakthivel Sadayappan
Journal: Circulation Research (2018)

Background: Heart failure is a devastating disease affecting nearly 5 million Americans. We recently identified the upregulation of fast skeletal myosin binding protein-C (fsMyBP-C) in models of heart failure. fsMyBP-C is a homologue of cardiac MyBP-C, which is normally expressed in the heart. This family of proteins regulate contractility by modulating thick and thin filament interactions. However, the functional role(s) of fsMyBP-C expression in the heart is unknown. Methods: To understand the role of fsMyBP-C expression in the heart, we generated cardiac specific transgenic mice expressing fsMyBP-C under the control of the alpha myosin heavy chain promoter. Mice underwent serial echocardiography to monitor cardiac function. Western blotting and qRT-PCR were performed to determine transgene expression levels. Additionally, fsMyBP-C localization in cardiomyocytes was established by immunofluorescence. Furthermore, to understand the temporal expression profiles of the MyBP-C homologues, we performed qRT-PCR on 9 muscle groups at different developmental stages in healthy mice. Results: qRT-PCR demonstrated an upregulation of the slow MyBP-C transcript in the developing heart, while fsMyBP-C transcript levels increased steadily following birth in WT mice. At 3 months of age, transgenic mice displayed a significant increase in ventricular dimensions compared to NTG littermates by echocardiography (LVID d : 3.72 ± 0.07 vs. 4.17 ± 0.09 mm, p&lt;0.01; LVID s : 2.44 ± 0.09 vs. 2.81 ± 0.09, p&lt;0.05), with no changes in wall thickness. This was accompanied by a 25% increase in stroke volume (p&lt;0.01) and a 30% increase in cardiac output (p&lt;0.05). fsMyBP-C correctly localized to the C-zone of the sarcomere. Furthermore, protein levels showed mild expression of fsMyBP-C, in line with the small upregulation seen in diseased hearts, while qRT-PCR confirmed overexpression of fsMyBP-C in the ventricles. Conclusion: Mice expressing fsMyBP-C in the heart display a mild hypertrophic phenotype at 3 months, with preserved function, possibly indicating compensated hypertrophy. Ongoing studies investigate cardiac function at later stages and cardiac specific conditional knockout of fsMyBP-C to determine the long-term effect of fsMyBP-C regulation in the heart.
CIRCULATING EXTRACELLULAR RNA, MYOCARDIAL REMODELING, AND HEART FAILURE
Authors: Khanh-Van Tran, David McManus, Kahraman Tanriverdi, Gerard Aurigemma, Darleen Lessard, Selim Tanriverdi, Olga Vitseva, Bruce Barton, John Keaney, Catarina Kiefe, Jane Freedman
Journal: Journal of the American College of Cardiology (2019)
Histology and stage at presentation among patients with rare pancreatic tumors: An exploratory analysis of the SEER database.
Authors: Jay Subramoney, David J. Delgado, Victoria Nguyen, Rachel Gray Denneny, Brandon George, Edith P. Mitchell
Journal: Journal of Clinical Oncology (2019)

e15774 Background: Rare pancreatic tumors account for approximately 15% of all pancreatic cancers (PCs) and 8,300 new cases diagnosed within the United States annually, while 85% of PCs diagnosed are classified as adenocarcinomas. Comparatively little research exists to analyze differences in diagnosis between rare PCs and the more common adenocarcinoma given greater clinical interest in the latter. The purpose of this study was to analyze the relationship between PC histology and stage at presentation with a focus on rare histologies. Methods: This study employed a retrospective cohort model using the NCI’s Surveillance, Epidemiology, and End Results (SEER) 1990-2015 database. We included patients diagnosed with PC aged 18+, with the comparator group being patients diagnosed with adenocarcinoma, and “rare” tumors defined as one of the following histologies: ductal, carcinoid, mucinous adenocarcinoma, and undetermined neoplasm. Stage was dichotomized (locoregional versus distant). Multivariable logistic regression was used to describe the association between tumor histology with initial stage at diagnosis, controlling for patient and tumor characteristics. Results: 90,764 PC patients were analyzed: 66.3% adenocarcinoma, 9.6% ductal carcinomas, 4.5% carcinoid, 3.8% mucinous, and 15.8% undetermined neoplasm. 54.7% of all cases were distantly metastasized at diagnosis. In multivariable analysis, pancreatic cancer patients with mucinous histology had greater odds of presenting at late-stage compared to those with adenocarcinoma: OR = 1.41, 95% CI = [1.31, 1.52]. Carcinoid and undetermined neoplasm odds for late stage presentation were not significant compared to adenocarcinoma: OR = 0.99, 95% CI = [0.92, 1.07] and OR = 1.01, 95% Cl = [0.97, 1.05] respectively. Ductal carcinoma was less likely than adenocarcinoma to present with late stage: OR = 0.38, CI = [0.36, 0.40]. Conclusions: We observed that mucinous histology had greater odds of late-stage diagnosis compared to those with adenocarcinoma. Patients with ductal carcinoma was less likely than those with adenocarcinoma to present with late stage. Further investigation is needed to explore the reasons for these differences.
PULMONARY EMBOLISM HOSPITALIZATIONS AND USE OF INFERIOR VENA CAVAL FILTERS IN OLDER ADULTS: NATIONAL STUDY OF MEDICARE BENEFICIARIES
Authors: Behnood Bikdeli, Yun Wang, David Jimenez, Joseph Ross, Mayur Desai, Sahil Parikh, Manuel Monreal, Samuel Goldhaber, Harlan M. Krumholz
Journal: Journal of the American College of Cardiology (2019)
Inconsistencies in Reporting Studies of Lactic Acidosis—Reply
Authors: Benjamin Lazarus, Morgan E. Grams
Journal: JAMA Internal Medicine (2019)

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CORONARY ARTERY CALCIUM IS ASSOCIATED WITH 90-DAY MACE AT ANY LEVEL OF ISCHEMIC BURDEN IN PATIENTS REFERRED FOR PET/CT
Authors: Viet T. Le, Stacey Knight, Raymond McCubrey, Benjamin Horne, Kurt Jensen, Kent Meredith, Donald Lappe, Steve Mason, David Min, Jeffrey Anderson, J. Muhlestein, Kirk Knowlton
Journal: Journal of the American College of Cardiology (2019)
Characterization of Hematopoietic Differentiation Profiles of MPN Patient-Derived Inducible Pluripotent Stem Cells Harboring Homozygous Vs Heterozygous Calreticulin Mutations
Authors: Lijuan Han, Marcelo A. Szymanski Toledo, Alexandre Theocharides, Angela Maurer, Tim H. Brümmendorf, Martin Zenke, Nicolas Chatain, Steffen Koschmieder
Journal: Blood (2018)
Prostate Radiotherapy for Metastatic Hormone-sensitive Prostate Cancer: A STOPCAP Systematic Review and Meta-analysis
Authors: Sarah Burdett, Liselotte M. Boevé, Fiona C. Ingleby, David J. Fisher, Larysa H. Rydzewska, Claire L. Vale, George van Andel, Noel W. Clarke, Maarten C. Hulshof, Nicholas D. James, Christopher C. Parker, Mahesh K. Parmar, Christopher J. Sweeney, Matthew R. Sydes, Bertrand Tombal, Paul C. Verhagen, Jayne F. Tierney
Journal: European Urology (2019)

Many trials are evaluating therapies for men with metastatic hormone-sensitive prostate cancer (mHSPC). To systematically review trials of prostate radiotherapy. Using a prospective framework (framework for adaptive meta-analysis [FAME]), we prespecified methods before any trial results were known. We searched extensively for eligible trials and asked investigators when results would be available. We could then anticipate that a definitive meta-analysis of the effects of prostate radiotherapy was possible. We obtained prepublication, unpublished, and harmonised results from investigators. We included trials that randomised men to prostate radiotherapy and androgen deprivation therapy (ADT) or ADT only. Hazard ratios (HRs) for the effects of prostate radiotherapy on survival, progression-free survival (PFS), failure-free survival (FFS), biochemical progression, and subgroup interactions were combined using fixed-effect meta-analysis. We identified one ongoing (PEACE-1) and two completed (HORRAD and STAMPEDE) eligible trials. Pooled results of the latter (2126 men; 90% of those eligible) showed no overall improvement in survival (HR = 0.92, 95% confidence interval [CI] 0.81–1.04, p = 0.195) or PFS (HR = 0.94, 95% CI 0.84–1.05, p = 0.238) with prostate radiotherapy. There was an overall improvement in biochemical progression (HR = 0.74, 95% CI 0.67–0.82, p = 0.94 × 10−8) and FFS (HR = 0.76, 95% CI 0.69–0.84, p = 0.64 × 10−7), equivalent to ∼10% benefit at 3 yr. The effect of prostate radiotherapy varied by metastatic burden—a pattern consistent across trials and outcome measures, including survival (<5, ≥5; interaction HR = 1.47, 95% CI 1.11–1.94, p = 0.007). There was 7% improvement in 3-yr survival in men with fewer than five bone metastases. Prostate radiotherapy should be considered for men with mHSPC with a low metastatic burden. Prostate cancer that has spread to other parts of the body (metastases) is usually treated with hormone therapy. In men with fewer than five bone metastases, addition of prostate radiotherapy helped them live longer and should be considered.
Abstract 116: <i>Mybphl</i> is a Novel Myofilament Component Implicated in Arrhythmia and Dilated Cardiomyopathy
Authors: David Y Barefield, Jordan J Sell, Megan J Puckelwartz, Lisa D Wilsbacher, Glenn I Fishman, Elizabeth M McNally
Journal: Circulation Research (2018)

Dilated cardiomyopathy is under significant genetic influence. Using whole-genome sequencing, we found a premature stop variant (R255X) in the MYBPHL gene in a family with DCM and conduction system disease. A Mybphl null mouse model revealed systolic dysfunction with atrial and ventricular conduction system (VCS) abnormalities. We found MyBP-HL protein highly expressed in both human and mouse atria and in a subset of ventricular cardiomyocytes. We hypothesize that MyBP-HL regulates VCS function and loss of MyBP-HL causes ventricular arrhythmia and cardiac dysfunction. We now examined hearts and isolated VCMs from Mybphl WT, het, and null mice using immunofluorescence microscopy (IFM). Clusters of MyBP-HL+ ventricular cardiomyocytes were evident in WT hearts (~1/200,000), with only 10% as many MyBP-HL+ cardiomyocytes in het samples. In WT hearts, MyBP-HL+ cells localized in the right ventricular free wall, with significantly fewer MyBP-HL+ cells in the right ventricular free wall in het hearts. The VCS marker contactin-2 (Cntn2) was used to assess MyBP-HL co-localization in the VCS. MyBP-HL co-localized with Cntn2+ cardiomyocytes in the transition zone between the atria and ventricle near the AV node, as well as in a subset of Cntn2+ Purkinje fibers. MyBP-HL+ ventricular cardiomyocytes were also found outside the VCS, suggesting other roles for those cells in regulating ventricular function. To discern MyBP-HL myofilament localization, we used super-resolution structured illumination microscopy on atrial cardiomyocytes. MyBP-HL co-localized with cMyBP-C in the C-zone of the A-band but also occupied space in the inner portion of the A-band near the M-line. This localization was not altered in het mice; however, the ratio of MyBP-HL in the inner portion of the A-band was diminished in het mice compared to WT. This suggests that MyBP-HL may bind the light meromyosin coiled-coil tail that originates from the M-line. Following the discovery that loss of MyBP-HL is associated with DCM and arrhythmia, we identified that MyBP-HL associates with the VCS and reduced MyBP-HL levels reduce the amount of MyBP-HL positive VCMs. These data suggest that loss of MyBP-HL may impair the development and function of the VCS, resulting in arrhythmias.
ASSESSING THE ACCURACY OF THE SIMPLE RISK PREDICTION MODEL FOR ACUTE TYPE A AORTIC DISSECTION OVER TIME
Authors: Delaney A. Smith, Derek Brinster, Arturo Evangelista-Masip, Santi Trimarchi, Kevin Harris, Eduardo Bossone, Alan Braverman, Patrick O'Gara, G. Chad Hughes, Toru Suzuki, Amit Korach, Daniel Montgomery, Firas F. Mussa, Nilto De Oliveira, George Arnaoutakis, Christoph Nienaber, Eric Isselbacher, Kim Eagle
Journal: Journal of the American College of Cardiology (2019)
Genotypic Groups As Risk Factor for Cardiac MR Abnormalities and Complications in Thalassemia Major
Authors: Alessia Pepe, Antonella Meloni, Stefano Salvadori, Silvia Macchi, Angelantonio Vitucci, Mauro Murgia, Aurelio Maggio, Maria Flavia Fiorenza, Francesco Massei, Francesca Valeria Commendatore, Pietro Giuliano, Vincenzo Positano, Laura Pistoia
Journal: Blood (2018)
Abstract 220: Adipocyte-Derived Exosome-Containing miRNAs Exacerbated Cardiac Ischemia/Reperfusion Injury in Diabetic Mice
Authors: Lu Gan, Dina Xie, Dajun Zhao, Erhe Gao, Walter J. Koch, Yajing Wang, Xinliang Ma
Journal: Circulation Research (2018)

Objective: Diabetes significantly exacerbates myocardial ischemia/reperfusion (MI/R) injury. However, the molecules mediate the crosstalk between adipose tissue and heart is unclear. The current study investigated whether exosomes released by adipose tissue, the primary source for circulating exosomes, are responsible for aggravating myocardial ischemia/reperfusion injury in diabetic mice. Methods and results: 6-8 week-old male C57B6/J mice were fed with normal diet (ND) or high fat diet (HFD) for 12 weeks to induce diabetes (characterized by abnormal glucose tolerance and insulin resistance). Exosomes were purified from ND or HFD murine serum and from culture medium of ND or HFD primary adipocytes. Equal amount of exosomes were intramyocardially injected to non-diabetic mice prior to MI/R. Myocardial functional assay showed that the exosomes purified from ND serum and culture medium of ND primary adipocytes attenuates MI/R injury (p&lt;0.05 vs. MI/R). In contrary, the exosomes from HFD serum and culture medium of HFD primary adipocytes markedly depressed cardiac function, enlarged myocardial infarction size and increased cardiomyocyte apoptosis (p&lt;0.05 vs. MI/R). To identify the specific molecules in exosomes that mediate cardiac injury, we performed Venn diagraph assay via combining the two databases (the adipocyte relevant miRNAs; serum exosomal miRNAs sequencing database in diabetic and nondiabetic mice). Candidate miRNAs were selected and validated. RT-qPCR assay confirmed that miR-17-3p, miR-127b-3p, miR-130b-3p, miR-345-5p and miR-532-5p were significantly elevated in exosomes isolated from HFD serum and culture medium of HFD primary adipocytes. Most importantly, these miRNAs were markedly elevated in heart tissue when exosomes isolated from HFD mice serum and culture medium of HFD primary adipocyte were injected. Conclusion: Our finding suggests that adipose-derived and exosome-carrying miRNAs are the likely molecules mediating the adipocyte-cardiomyocyte communication, thereby aggravating myocardial ischemia/reperfusion injury in diabetic mice.