tbuckley/cabot-search huggingface dataset:
Abstract 470: Gata4, Mef2c and Tbx5 More Efficiently Transdifferentiate Endothelial Cells into Cardiomyocyte-like Cells Through Endothelial-Mesenchymal Transition Process
Authors: Deepthi Sanagasetti, Vivek P Singh, Jaya Pratap Pinnamaneni, Aarthi Pugazenthi, Anna Jang, Davis So, Mary Kim, Lina Yang, Kai Wang, Jianchang Yang, Megumi Mathison, Todd K Rosengart
Journal: Circulation Research (2018)

Background: The cardiac transcription factors Gata4, Mef2c, and Tbx5 (GMT) have been used to successfully reprogram cardiac fibroblasts into induced cardiomyocyte-like cells (iCMs). However their effects on other cell types remain largely unknown. Endothelial cells are an important population of the heart by Pinto et al. (2016). Given the more profound iCM induction effects observed in vivo, we have speculated that reprogramming of endogenous endothelial cells may also play an important role. Purpose: To investigate the cellular reprograming effects and mechanisms of GMT factors on cardiac endothelial cells and compare the outcomes with that from cardiac fibroblasts. Methods: Adult rat cardiac endothelial cells (REC) and cardiac fibroblasts (RCF) were purchased commercially. The cells were cultured in appropriate media and infected with GMT-expressing lentivirus and maintained with iCM media. Fourteen days later Immunofluorescence staining, FACS, and qRT-PCR were performed. Results: Both GMT treated RCFs and RECs showed positive staining of cardiac marker cTnT and αActinin-positive cells via immunofluorescence staining. FACS analysis showed GMT treated RECs had 16.7% of cTnT positive cells versus 3.3% in GMT treated RCF’s. qRT-PCR results demonstrated significant up-regulation of cTnT in GMT infected RECs (74.4±23.3 times, p&lt;0.05) as compared to the control group. Similar upregulation of cTnT was observed in RCFs but to a lesser degree (16.1±7.2 times, p=NS). Moreover, RECs presented a significant change in cell morphology from rounded cells in a cobblestone arrangement to elongated spindle-shaped cells during 14 days culture. In addition, qRT-PCR analysis demonstrated that endothelial-mesenchymal transition (EndoMT) markers such as Slug, Snail, Oct4, and αSMA were upregulated in the cells with GFP encoded virus infection and those markers were downregulated in the GMT-treated RECs (p&lt;0.01 for Snail, p&lt;0.05 for Slug, and αSMA). Conclusion: This report suggests that RECs are susceptive to GMT induced cardiac reprogramming than in RCFs. Our study also indicate that EMT and MET sequential process are involved in the reprogramming of RECs toward iCM cells. RECs could be targeted towards iCM generation for a higher reprogramming rate.
GLOBAL LONGITUDINAL STRAIN ASSESSMENT OF THE LEFT VENTRICLE BY SPECKLE TRACKING ECHOCARDIOGRAPHY DETECTS ACUTE CELLULAR REJECTION IN ORTHOTOPIC HEART TRANSPLANT RECIPIENTS: A SYSTEMATIC REVIEW AND META-ANALYSIS
Authors: Ahmed Elkaryoni, Karim Ellakany, Ahmed M. Altibi, Osama Okasha, Islam Abdelkarim, Navin Nanda
Journal: Journal of the American College of Cardiology (2019)
Abstract 279: Effects of Acute Oxidative Stress on Cardiac Proteome Dynamics
Authors: Cody T Thomas, Maggie Pui Yu Lam
Journal: Circulation Research (2018)

Introduction: Acute reactive oxygen species exposure is thought to trigger endoplasmic reticulum (ER) stress and unfolded protein response (UPR) commonly observed in pathological hearts. The pathways and molecular features impacted by acute oxidative stress are incompletely understood. To understand how proteostatic stressors impact cardiac protein dynamics, we investigate the effect of low to high doses of acute oxidant on the cardiac proteome using a paraquat-induced oxidative stress model. Methods: C57BL/6J mice were exposed to low, mid, or high doses of paraquat for up to 48 hours. Cardiac proteins were extracted and digested on-filters into tryptic peptides. The peptides were then tagged with isobaric stable isotope tandem mass tags (TMT) followed by high-pH reversed-phase (RP) fractionation. Each fraction was further separated by low-pH RP liquid chromatography and analyzed on a Q-Exactive HF Plus high-resolution mass spectrometer to obtain proteome-wide abundance levels across treatment groups. We then focused on the differential expression in the mitochondrial and ER subproteomes as well as their respective protein quality control pathways. Results: We found prominent differential expression in specific quality control proteins in response across low and high doses of oxidative stresses. The data suggest that oxidative stress activates UPR pathways including notably mitochondrial UPR (UPRmt) components in a dose-specific manner. In particular, we observed the repression of mitochondrial protein import machinery components as a specific feature of low but not high oxidative stress response. In addition, the differential expression of pyruvate metabolism proteins may constitute a link between cardiac metabolism and UPRmt, and serve as a determinant between adaptive and maladaptive responses to reactive oxygen species. Conclusion: Our results indicate that the activation of the UPRmt pathways may be an overlooked feature of acute oxidative insults that underlies stress response in cardiac cells. Future work will interrogate the molecular crosstalks between mitochondria and ER stress response pathways.
CORONARY ANGIOGRAPHY AMONG CANCER PATIENTS: DETERMINING A SAFE PLATELET THRESHOLD
Authors: Ali Agha, Clarence Gill, Dinu Balanescu, Teodora Donisan, David Boone, Juhee Song, Gloria Iliescu, Nicolas Palaskas, Juan Lopez-Mattei, Peter Kim, David Doundoua, Konstantinos Marmagkiolis, Jean-Bernard Durand, Cezar Iliescu
Journal: Journal of the American College of Cardiology (2019)
DIASTOLIC FUNCTION IN MYOSIN-BINDING PROTEIN C FOUNDER MUTATION CARRIERS WITH AND WITHOUT CLINICAL EVIDENCE OF HYPERTROPHIC CARDIOMYOPATHY
Authors: Berglind Adalsteinsdottir, Carolyn Ho, Michael Burke, Ragnar Danielsen, Barry Maron, Jonathan Seidman, Christine Seidman, Gunnar Gunnarsson
Journal: Journal of the American College of Cardiology (2019)
Abstract 434: A Diet Rich in Oleic Acid, as Primary Lipid Source, Attenuates the Progressive Functional Decline in Hypertrophied Hearts During Pathological Stress
Authors: Andrew N Carley, E. Douglas Lewandowski
Journal: Circulation Research (2018)

Two major dietary long chain fatty acids (LCFA), oleate and palmitate, display differing capacities to induce transcriptional activation of metabolic genes, lipid trafficking, substrate metabolism, and contractile function in the failing heart. Perfusing isolated failing rat hearts with the unsaturated LCFA, oleate, improves contractile function and restores intracellular lipid dynamics vs. failing rat hearts perfused with the saturated LCFA, palmitate. We therefore investigated whether chronically feeding rats a diet of either high-oleate (as triolein) or high-palmitate (as tripalmitin) could alter the development of heart failure in response to chronic pressure overload induced by transverse aortic constriction (TAC). Following TAC or sham surgery rats were randomized to a diet rich in either triolein or tripalmitin as primary fat source (65% carbohydrate, 20% protein and 15% fat (210 Kcal/kg)). TAC induced similar increases in LV mass independent of diet, however rats fed tripalmitin showed a significant reduction in survival and a decline in ejection fraction and fractional shortening as well as LV dilation, evident at 6 and 10 weeks post TAC (Figure). In contrast, triolein diet attenuated declining systolic function and LV dilation (Figure) and eliminated the otherwise expected elevation of plasma BNP, as seen with tripalmitin diet (50%, P&lt;0.05) after 14 weeks of TAC, indicating differential effects of these fats on both the heart and whole body metabolism and physiology during cardiac stress. The results suggest that a diet rich in oleic acid affords benefits in attenuating the development of cardiac decompensation independent of changes in hypertrophic growth.
DAMAGING GENETIC VARIANTS IN PRO-ANGIOGENIC GENES IMPAIR GROWTH IN FETUSES WITH CRITICAL CONGENITAL CARDIAC DEFECTS
Authors: Mark W. Russell, Julie S. Moldenhauer, Jack Rychik, Nancy Burnham, Samuel I. Parry, Rebecca Simmons, Michal Elovitz, Susan Nicolson, Rebecca Linn, Mark P. Johnson, Sunkyung Yu, Matthew Sampson, Hakon Hakonarson, J. William Gaynor
Journal: Journal of the American College of Cardiology (2019)
LIFETIME INCIDENCE OF CORONARY ARTERY CALCIUM FOR ASYMPTOMATIC INDIVIDUALS WITH AND WITHOUT DIABETES: INSIGHTS FROM THE MULTI-ETHNIC STUDY OF ATHEROSCLEROSIS
Authors: Bart Ferket, M.G. Myriam Hunink, Umesh Masharani, Wendy Max, Kirsten Fleischmann
Journal: Journal of the American College of Cardiology (2019)
THE HEART SCORE IN BLACKS WITH EMERGENCY PRESENTATION OF CHEST PAIN: A PERFORMANCE TEST AND RISK ANALYSIS
Authors: Olusayo Fadiran, Vishnu Priya Mallipeddi, Sumon Mahbubur, Adebayo Atanda, Emmanuel Mbey, Basharat Ahmad, Henry Janna, Julius Ngwa, Daniel A. Larbi
Journal: Journal of the American College of Cardiology (2019)
Abstract 18117: Epicardial Adipose Tissue Produces Proinflammatory Cytokines and Influences the Pathogenesis of Atrial Fibrillation
Authors: Takeshi Soeki, Tomomi Matsuura, Etsuko Uematsu, Takeshi Tobiume, Kenya Kusunose, Takayuki Ise, Koji Yamaguchi, Shusuke Yagi, Daiju Fukuda, Hirotsugu Yamada, Tetsuzo Wakatsuki, Masataka Sata
Journal: Circulation (2017)

Background: Several studies have shown that epicardial adipose tissue (EAT) is not only an anatomic depot of fat, but also may serve as a local source of proinflammatory cytokines related to coronary artery disease (CAD). Although there are several studies reporting an association between EAT and CAD, the evidence concerning the association between EAT and arrhythmias is relatively limited. A recent study has shown that EAT locations are in excellent agreement with high dominant frequency sites, suggesting that EAT may be involved in the maintenance of atrial fibrillation (AF). Purpose: In the present study, we studied whether adjoining atrial EAT may produce proinflammatory cytokines and influence the pathogenesis of AF. Methods: Samples were obtained from periventricular EAT, periatrial EAT, and subcutaneous adipose tissue in patients without CAD during elective cardiac surgery (aortic valve replacements or aortic vascular surgery). Cytokine expression was evaluated using a quantitative real-time polyme...
Highly Efficient Editing of the Beta-Globin Gene in Patient Derived Hematopoietic Stem and Progenitor Cells to Treat Sickle Cell Disease
Authors: So Hyun Park, Ciaran M Lee, Daniel P. Dever, Timothy H Davis, Joab Camarena, Yankai Zhang, Matthew Porteus, Vivian A Sheehan, Gang Bao
Journal: Blood (2018)
ASSOCIATION OF THROMBOCYTOPENIA AND ADVERSE EVENTS AMONG PATIENTS UNDERGOING FIBRINOLYTIC THERAPY FOR ACUTE PULMONARY EMBOLISM
Authors: Gbolahan Ogunbayo, Robert Pecha, Elliott Goodwin, Karam Ayoub, Naoki Misumida, Ayman Elbadawi, Ahmed Abdel-Latif, Samy-Claude Elayi, Susan Smyth, Adrian Messerli
Journal: Journal of the American College of Cardiology (2019)
Abstract 500: Low Aldehyde Dehydrogenase 2 (ALDH2) Potentiates Obesity in Leptin Receptor Mutant Mice
Authors: Guodong Pan
Journal: Circulation Research (2018)

Obesity aggravates type 2 diabetes and thus cardiometabolic complications. Aldehyde dehydrogenase 2 (ALDH2), a cardiac mitochondrial enzyme is known to be cardioprotective. ALDH2*2 is the most common genetic mutation in East Asians (~800 million carriers), which causes a low ALDH2 activity. We hypothesize that ALDH2*2 mutation aggravates obesity and diabetes in leptin receptor deficient db/db mice and consequentially cardiometabolic complications. To test our hypothesis, we cross db/db mice with ALDH2*2 knock-in mutant mice. We obtained a new breed of mice which had leptin receptor mutation and ALDH2*2 mutant gene. We termed this mice as ALDH2*2-Fat. The body weight gain of ALDH2*2-Fat mice was extremely faster than their non-obesity littermates (ALDH2*2-Lean, the mice only carrying ALDH2*2 mutant gene). At 30 weeks old, the body weights of ALDH2*2-fat mice (84.15±6.75 g) was 2.88 folds higher than ALDH2*2-Lean mice (29.32±3.75 g, p&lt;0.001). Fasting blood glucose and serum insulin concentration were higher in ALDH2*2-Fat mice than ALDH2*2-Lean mice (blood glucose: 506.20±88.27 vs. 192.83±21.32 mg/dl, p&lt;0.001; insulin: 13.94±6.28 vs. 2.46±0.58 ng/ml, p&lt;0.001 respectively). Echocardiographic measurements revealed a progressive cardiac dysfunction in ALDH2*2-Fat mice (Fractional shortening, 48.00±3.17 vs. 56.90±3.11 % at 6 months, p&lt;0.05, and 39.11±7.50 vs. 56.98±1.55 % at 9 months, p&lt;0.01). Body temperatures were significantly lower in ALDH2*2-Fat mice (35.5±0.94 vs. 38.86±0.49 °C, p&lt;0.01). The interscapular brown adipose tissues in ALDH2*2 fat mice were shrunk to invisible at 9 months old. Western-blotting found a decreased PGC-1 α and increased PPAR-γ expression in white adipose tissues from ALDH2*2-fat mice. Cultured primary bone marrow cells showed a significantly decrease in colony forming units in ALDH2*2-Fat mice (7.67±4.50 vs., 26.33±3.33 p&lt;0.05). Under adipogenic medium, the adipocytes differentiation was increased in ALDH2*2 fat mice. In conclusion, low ALDH2 activity aggravates obesity and consequentially cardiometabolic complications in leptin receptor deficiency-induced obesity and diabetes.
COMPARISON OF ESTABLISHED RISK SCORES FOR PREDICTION OF CORONARY ARTERY DISEASE AND STROKE IN ESSENTIAL HYPERTENSION: DATA FROM A GREEK 8-YEAR-FOLLOW-UP STUDY
Authors: Konstantinos P. Tsioufis, Kyriakos Dimitriadis, Costas Michas, Panagiotis Iliakis, Alexandros Kasiakogias, Ioannis Leontsinis, Niki Kakouri, Mairh Kourementi, Dimitris Tousoulis
Journal: Journal of the American College of Cardiology (2019)
Long-term trends in child maltreatment in England and Wales, 1858–2016: an observational, time-series analysis
Authors: Michelle Degli Esposti, David K Humphreys, Benjamin M Jenkins, Antonio Gasparrini, Siân Pooley, Manuel Eisner, Lucy Bowes
Journal: The Lancet Public Health (2019)

BackgroundIt is unclear whether child maltreatment is increasing or decreasing in England and Wales. More evidence is needed, from multiple sources and over longer periods of time, to explore trends in child maltreatment. We investigated whether the annual incidence of child maltreatment has changed over time, using official record data and time-series methods to establish long-term trends.MethodsIn this observational time-series analysis, we used six data sources (Government records for child mortality, police-recorded child homicides, crimes against children, child protection, and children in care; and NSPCC data) to estimate the incidence of child maltreatment in England and Wales and examine long-term trends. We included nationally representative data that could estimate the incidence of child maltreatment for more than 25 years. Our primary outcomes were the number of victims (age <20 years) or perpetrators (age >16 years) of child maltreatment per 12-month period in England, including or excluding Wales. We fitted Poisson regression models with year as the exposure and the number of victims or perpetrators of child maltreatment as the outcome (adjusted for population age-structure and size). When a linear trend was not appropriate, we fitted generalised additive models with penalised splines to visualise trends.FindingsThe incidence of child mortality by homicide or assault decreased by 90% (2·7 per 100 000 children) between 1858 and 2016 and the incidence of people guilty of child cruelty or neglect decreased by 83% (6·7 per 100 000 adults) between 1893 and 2016, whereas child protection registrations increased by 182% (328·7 per 100 000 children) between 1988 and 2016. Crimes against children and children entering care increased between 2000 and 2016. In 2016, 40 children died by homicide, with twice as many adolescent (15–19 years) deaths than infant (age <1 year) deaths. In 2016, 67 700 children were placed on the child protection register and neglect and emotional abuse were the most common reasons.InterpretationAlthough long-term trends have decreased, child maltreatment remains a major public health problem in England and Wales. Further research is needed to establish whether adolescents are a particularly vulnerable age group and whether neglect and emotional abuse are increasing. Future child protection policies and practices should respond to these areas of growing need.FundingAndrew W Mellon Foundation and Clarendon through The Oxford Research Centre in the Humanities, Oxford.
Abstract 15429: A Comparison of Left Atrial Appendage Closure to Warfarin and NOACs in Routine Clinical Practice
Authors: Xiaoxi Yao, Bernard J Gersh, Lindsey R Sangaralingham, Nilay D Shah, David R Holmes, Peter A Noseworthy
Journal: Circulation (2017)

Introduction: In clinical trials, left atrial appendage closure (LAAC) demonstrated a lower risk of hemorrhagic stroke and cardiovascular death, but a trend toward higher risk of ischemic stroke or...
ANGIOTENSIN CONVERTING ENZYME INHIBITOR THERAPY IS ASSOCIATED WITH REDUCED SURVIVAL IN PATIENTS WITH SEVERE AORTIC REGURGITATION: A 20 YEAR FOLLOW UP IN 756 PATIENTS
Authors: Mandira Patel, Padmini Varadarajan, Asbat Hasan, Aditya Goud, Ramdas Pai
Journal: Journal of the American College of Cardiology (2019)
PLANNING HIGH RISK VAGINAL DELIVERY IN A PATIENT WITH NON-COMPACTION CARDIOMYOPATHY: A MULTIDISCIPLINARY APPROACH
Authors: Sayf Altabaqchali, Ahmed Bakhit, Fady Marmoush, Ramses Thabet, Nirmal Kaur, Michelle Hadley, Luigi Pacifico
Journal: Journal of the American College of Cardiology (2019)
Identification of platelet-derived growth factor C as a mediator of both renal fibrosis and hypertension
Authors: Claudia R.C. van Roeyen, Ina V. Martin, Ana Drescher, Katharina A. Schuett, Daniela Hermert, Ute Raffetseder, Stephanie Otten, Eva M. Buhl, Gerald S. Braun, Christoph Kuppe, Elisa Liehn, Peter Boor, Ralf Weiskirchen, Ulf Eriksson, Oliver Gross, Frank Eitner, Jürgen Floege, Tammo Ostendorf
Journal: Kidney International (2019)
PAI-1 augments mucosal damage in colitis
Authors: Gerard E. Kaiko, Feidi Chen, Chin-Wen Lai, I-Ling Chiang, Jacqueline Perrigoue, Aleksandar Stojmirović, Katherine Li, Brian D. Muegge, Umang Jain, Kelli L. VanDussen, Bridie J. Goggins, Simon Keely, Jessica Weaver, Paul S. Foster, Daniel A. Lawrence, Ta-Chiang Liu, Thaddeus S. Stappenbeck
Journal: Science Translational Medicine (2019)

SERPINE1/PAI-1 is elevated in the colon tissue of the most difficult-to-treat patients with IBD and leads to worsening of experimental colitis.
SAFETY PROFILES OF LEADLESS PACEMAKERS (MICRA) DEVICES: AN ANALYSIS OF THE FOOD AND DRUG ADMINISTRATION MANUFACTURER AND USER FACILITY DEVICE EXPERIENCE (MAUDE) DATABASE
Authors: Geetanjali Dang, Mohammed Saleh, Maria Del Carmen Perez, Wilmary Garcia Flete, Raviteja Guddeti, Hussam Abuissa, Venkata Alla
Journal: Journal of the American College of Cardiology (2019)
Abstract 211: Modified Endothelial Progenitor Cell (EPC) Transplantation Improves Diabetic Kidney Disease
Authors: Sabyasachi Sen, Nabanita Kundu, Laureano Asico, Cleyton Domingues, Pedro Jose
Journal: Circulation Research (2018)

DKD is a major vascular complication of diabetes, which is associated with glomerulosclerosis and poor perfusion. Therefore, improving the renal perfusion may help to treat the sclerotic kidney disease. EPCs have been shown to improve tissue perfusion. Here, we investigated whether transplanting apoptosis resistant genetically modified mouse EPCs (p53 gene silenced, transiently, using Adenovirus ex-vivo), could improve angiogenesis and renal perfusion, in a hyperglycemic type 1 diabetes milieu. Mesenchymal stromal cells (MSC) transplantation has also been used in DKD however concern for epithelial to mesenchymal transformation remains. Methods: We compared the efficacy of p53shEPC with MSC, Null-EPC and saline in STZ-induced type 1 diabetic C57BL/6J mouse model. 8 weeks after STZ delivery stable hyperglycemia, polyuria and proteinuria was confirmed followed by transplantation of 0.3 million EPC/ MSC bilaterally, under each kidney capsule. We compared our results with non-STZ normal C57Bl6J mouse. Urine was collected weekly for volume, protein and creatinine estimation. Blood creatine and renal blood flow was measured by laser Doppler, at sacrifice. qRT-PCR on harvested kidneys were performed focusing on genes associated with angiogenesis. Results: Polyuria was reduced in p53shEPC transplanted animals with urine volume close to non DM animals and half the volume compared to saline and MSC group at week 4 and 6. Protenuria levels were the lowest in p53shEPC group. Plasma creatinine was lowest in p53shEPC group (3-fold lower) compared to Null EPC group Enhanced blood flow by laser doppler was also noted with delivery of p53sh-EPCs vs controls, such as null EPC (1.2 fold), saline (3 folds) at wk4&amp;6. Markers for angiogenesis, such as eNOS mRNA (4.5 fold, p=0.002) and VEGF-A mRNA (1.5 fold, p=0.03) upregulated significantly post p53 silenced EPC transplantation compared to null EPC group. Capillary density staining is pending. Conclusion: Apoptosis resistant EPCs help to improve proteinuria, plasma creatinine, polyuria and renal perfusion most likely by helping to increase angiogenesis and may have a prominent therapeutic role in DKD. MSC transplantation results were consistently less efficacious compared to p53silenced EPC transplantation.
ATRIAL CONDUCTION DELAY IN SERIALLY STACKED OBSTRUCTIVE SLEEP APNEA EPISODES
Authors: Krishan Patel, Pavan Reddy, Hussain Basrawala, Shamili Allam, Edwin Valladares, Vincent Grbach, Michael Khoo, Vladimir Konecny, Rahul Doshi, Terese Hammond, Virend Somers, Tomas Konecny
Journal: Journal of the American College of Cardiology (2019)
The withdrawal of replacement therapy and outcomes in alpha-1 antitrypsin deficiency lung transplant recipients
Authors: Jana Kleinerova, Patricia Ging, Colin Rutherford, Iain Lawrie, Sara Winward, Donna Eaton, Karen C. Redmond, Jim J. Egan
Journal: European Respiratory Journal (2019)

Alpha-1 antitrypsin deficiency (AATD) accounts for 5% of lung transplants performed worldwide. Ireland has a high frequency of 1 in 25 for the Z allele and 1 in 10 for the S allele [1]. These variants are associated with decreased production of alpha-1 antitrypsin (AAT), which predisposes to unprotected proteolytic activity of neutrophil elastase (NE) and proteinase 3 (PR3), linked to an increased risk of emphysema and hepatic disease. Associated inflammatory conditions such as vasculitis, panniculitis and inflammatory bowel disease are also suspected to be caused by uncontrolled neutrophil proteinase activity [2–4]. Vascular problems, including aortic aneurysm, in AATD patients are more severe and may reflect abnormal elastic tissue properties potentially impacting on wound healing [5]. Our study suggests an association between timing of withdrawal of replacement therapy and bronchial anastomotic complications after lung transplantation <http://ow.ly/jhuP30o9dSS>
EARLY VASCULAR RESPONSE AFTER BIODEGRADABLE-POLYMER SIROLIMUS-ELUTING STENT IMPLANTATION IN ST ELEVATION MYOCARDIAL INFARCTION: SUB-ANALYSIS OF MECHANISM-ULTIMASTER TRIAL
Authors: Takumi Kimura, Tomonori Itoh, Masaru Ishida, Hiromasa Otake, Yoshihiro Morino
Journal: Journal of the American College of Cardiology (2019)
COMPARISON OF CLINICAL TRIALS AND ADMINISTRATIVE CLAIMS TO IDENTIFY STROKE: FINDINGS FROM THE NHLBI-SPONSORED EXTEND-COREVALVE STUDY
Authors: Jordan B. Strom, Yuansong Zhao, Jeffrey Popma, J. Matthew Brennan, Mike Boulware, Changyu Shen, Robert Yeh
Journal: Journal of the American College of Cardiology (2019)
IMPACT OF MICROVASCULAR DISEASE ON CARDIORENAL OUTCOMES IN TYPE 2 DIABETES: AN ANALYSIS FROM THE LEADER AND SUSTAIN-6 CLINICAL TRIALS
Authors: Subodh Verma, Stephen C. Bain, Julie Broe Honore, Johannes F.E. Mann, Michael A. Nauck, Richard E. Pratley, Soren Rasmussen, Maria Sejersten Ripa, Bernard Zinman, John Buse
Journal: Journal of the American College of Cardiology (2019)