tbuckley/cabot-search huggingface dataset:
RANOLAZINE EXHIBITS ANTI-ISCHEMIC PROPERTIES BY INCREASING CARDIAC ENDOTHELIAL CELL ADENOSINE LEVELS
Authors: Dai-Trang Elizabeth Le, Catherine Davis, Shanthi Nagarajan, Kristin L. Lyon Scott, Zhiping Cao, Helen Liu, Alkayed Nabil, Sanjiv Kaul
Journal: Journal of the American College of Cardiology (2019)
USE OF TRANSCATHETER PULMONARY VALVE REPLACEMENT ACROSS THE AGE SPAN OF PATIENTS WITH CONGENITAL HEART DISEASE: A REPORT FROM THE NCDR IMPACT REGISTRY
Authors: Ada C. Stefanescu Schmidt, Aimee Armstrong, Jamil Aboulhosn, Kevin Kennedy, Thomas Jones, Daniel Levi, Doff B. McElhinney, Ami Bhatt
Journal: Journal of the American College of Cardiology (2019)
SEX DIFFERENCES IN PLASMA CONCENTRATIONS AND PROGNOSTIC VALUE OF NT-PROBNP IN CHRONIC HEART FAILURE
Authors: Alberto Aimo, James Januzzi, Giuseppe Vergaro, Andrea Ripoli, Roberto Latini, Jennifer Meessen, Inder S. Anand, Jay Cohn, Jørgen Gravning, Thor Ueland, Ståle H. Nymo, Hans-Peter Brunner-La Rocca, Antoni Bayes-Genis, Josep Lupon, Rudolf De Boer, Akiomi Yoshihisa, Yasuchika Takeishi, Michael Egstrup, Ida Gustafsson, Hanna Gaggin, Kai Eggers, Kurt Huber, Ioannis Tentzeris, Claudio Passino, Michele Emdin
Journal: Journal of the American College of Cardiology (2019)
Low-Dose Amitriptyline for Chronic Low Back Pain
Authors: Chung-Wei Christine Lin, Andrew J. McLachlan, Chris G. Maher
Journal: JAMA Internal Medicine (2019)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal
EFFECTS OF PULMONARY HYPERTENSION IN PATIENTS UNDERGOING TRANSCATHETER AORTIC VALVE REPLACEMENT: AN INSIGHT FROM THE MOST RECENT NATIONAL INPATIENT SAMPLE
Authors: Dhrubajyoti Bandyopadhyay, Vivek Modi, Adrija Hajra, Karan Sud, Faris Haddadin, Alba Munoz Estrella, Hassan Beydoun, Ashish Kumar, Raktim Ghosh, Eyal Herzog
Journal: Journal of the American College of Cardiology (2019)
Abstract 332: Dissecting Mechanisms for Hand2-Dependent Pacemaker Cell Reprogramming
Authors: Antonio Fernandez-Perez, MInoti Bhakta, Nikhil V Munshi
Journal: Circulation Research (2018)

Direct reprogramming of one cell type into another has recently emerged as a powerful paradigm for regenerative medicine, disease modeling, and lineage specification. Currently, the conversion of fibroblasts into induced cardiomyocyte-like myocytes (iCLMs) by Gata4, Mef2c, and Tbx5 (GMT) represents an important avenue for generating de novo cardiac myocytes, in both in vitro and in vivo applications. Recent evidence suggests that the supplementation of GMT with Hand2 (GHMT) can enhance this process. We previously showed that iCLM derived from GHMT are complex and heterogeneous, consisting of atrial (iALMs), ventricular (iVLMs), and pacemaker-like myocytes (iPLMs), thus underscoring the need for a systematic approach for conducting additional studies. Although chromatin and single-cell studies have explored GMT-iCLM cell fate determination in great detail, little is known about how Hand2 enhances iCLM induction, and in particular, iPLM specification. Before direct reprogramming can be used as a therapeutic strategy, the mechanistic underpinnings of specific cardiac lineage conversion must be understood. In the present study, we characterize the molecular mechanisms by which Hand2 regulates iCLM induction and iPLM diversification. We compare the transcriptional and genomic accessibility landscape of GMT and GHMT iCLMs to uncover common and distinct gene regulatory networks that drive iCLM determination. In parallel, using a series of Hand2 deletions, in combination with quantitative mass spectrometry, we identify a Hand2 interactome in reprogrammed cells enriched for iPLMs. Taken together, these complementary approaches have begun to elucidate the molecular details of GHMT-mediated cardiac reprogramming and iPLM specification.
Estimating glomerular filtration rate at the transition from pediatric to adult care
Authors: Hans Pottel, Jonas Björk, Arend Bökenkamp, Ulla Berg, Kajsa Åsling-Monemi, Luciano Selistre, Laurence Dubourg, Magnus Hansson, Karin Littmann, Ian Jones, Per Sjöström, Ulf Nyman, Pierre Delanaye
Journal: Kidney International (2019)
REPRODUCIBILITY AND OPTIMIZATION OF 18-FLUORO-DEOXYGLUCOSE POSITRON EMISSION TOMOGRAPHY FOR EVALUATION OF CARDIAC SARCOIDOSIS
Authors: Raza M. Alvi, Bryan D. Young, Zartashia Shahab, Hongyi Pan, Julia Winkler, Erica Herzog, Edward J. Miller
Journal: Journal of the American College of Cardiology (2019)
Abstract 406: Loss of Sigmar1 Leads to Impaired Mitochondrial Respiration, Altered Mitochondrial Dynamics and Development of Cardiac Contractile Dysfunction
Authors: Chowdhury S Abdullah, Shafiul Alam, Richa Aishwarya, Sumitra Miriyala, Manikandan Panchatcharam, Anthony W Orr, Jeanne James, Jeffrey Robbins, John N Lorenz, Md. Shenuarin Bhuiyan
Journal: Circulation Research (2018)

Rationale: Studies involving different neuronal and cancer cell lines indicated that Sigma 1 receptor (Sigmar1) function as an inter-organelle signaling molecule and elicit cytoprotective functions. Though the presence of Sigmar1 in the heart was reported using ligand binding assay, all studies to date have been limited to pharmacological approaches using less selective ligands for Sigmar1. Despite all these studies, the physiological function of Sigmar1 in the heart remains unknown. Objective: We investigated the physiological function of Sigmar1 in the heart in regulating mitochondrial respiration, mitochondrial dynamics and cardiac contractility using the Sigmar1 knockout mouse (Sigmar1 -/- ). Methods and Results: Sigmar1 -/- hearts showed significantly increased hemodynamic parameters assessed by left ventricular (LV) catheterization both under basal conditions and after stimulation with increasing doses of the β 1 -adrenoceptor agonist. Noninvasive echocardiographic measurements showed the development of cardiac functional decline in Sigmar1 –/– hearts over aging indicated by decreased LV percent fraction shortening and percent ejection fraction. Histochemistry also showed significant cardiac fibrosis and increased expression of periostin in the Sigmar1 –/– hearts compared to wildtype (Wt) hearts. Ultrastructural analysis of Sigmar1 -/- cardiomyocytes showed irregularly shaped, highly fused mitochondrial network, and exhibited abnormal cristae. Mitochondrial size distribution in Sigmar1 -/- hearts showed an increased number of large mitochondria resulting in decreased numbers of mitochondria per microscopic field and also showed altered expression of mitochondrial dynamics regulatory proteins. Real-time oxygen consumption rates in isolated mitochondria showed reduced respiratory function in Sigmar1 -/- hearts compared with Wt hearts. Conclusions: All these data demonstrate a potential function of Sigmar1 in regulating normal mitochondrial organization and size in the heart. Knockdown of Sigmar1 evoked mitochondrial dysfunction, accumulation of abnormal mitochondria, enhanced adverse cardiac remodeling and resulting in cardiac contractile dysfunction.
Abstract 388: Small GTPase Rnd3 Fine-tunes Inflammatory Response in Myocardial Infarction
Authors: Wenjiao Li, Weijia Luo, Kelsey Andrade, Jiang Chang
Journal: Circulation Research (2018)

Introduction: Myocardial infarction (MI) is a severe clinical condition caused by coronary artery thrombotic occlusion. According to the 2017 update from the American Heart Association, about 790,000 Americans have MI each year and 114,000 of those will die. Acute inflammation is developed post MI to clear necrotic myocardium and to guide the upcoming healing processes. A well-balanced and tightly-controlled inflammation, therefore, is critical for the post-MI cardiac recovery. We have previously demonstrated the essential roles of small GTPase Rnd3 in cardiac remodeling, calcium handling and angiogenesis. In the present study, we aimed to investigate Rnd3’s regulation of post-MI inflammation. Methods and results: Cardiac-specific Rnd3-deficient mice were subjected to MI operation and the hearts were dissected 3 days post MI. Rnd3-deficient hearts showed significantly enlarged infarct size and excessive inflammation than wild-type hearts. Importantly, we found that MI patients with lower Rnd3 expression levels exhibit a worse prognosis in cardiac function recovery. In the mechanistic study, hyperactivation of NF-kB signaling was observed in Rnd3-deficient cardiomyocytes and hearts post MI. Rnd3 blocks NF-kB nuclear translocation by disrupting the heterodimerization between p65 and p50. Finally, we generated transgenic mice with cardiac-specific overexpression of Rnd3. The mouse exhibited significantly preserved cardiac function and restrained inflammation post MI. Conclusions: This study identified Rnd3 as a fine-tuning factor mediating post-MI inflammation. Cardiac Rnd3 expression level positively correlates with MI patient prognosis. Thus, Rnd3 may serve as a potential therapeutic target for MI.
USING DOBUTAMINE STRESS ECHOCARDIOGRAPHY TO PREDICT THE RECOVERY OF LEFT VENTRICULAR FUNCTION IN CANCER PATIENTS RECEIVING CHEMOTHERAPY
Authors: Laura McDermott, Rida Laeeq, Nicolas Palaskas, Rohit Moudgil, Peter Kim, Syed Yusuf, Saamir Hassan, Jose Banchs, Teodora Donisan, Dinu V. Balanescu, Cezar Iliescu, Jean-Bernard Durand, Juan Lopez-Mattei
Journal: Journal of the American College of Cardiology (2019)
PRESENCE OF HEART FAILURE WITH REDUCED EJECTION FRACTION IS ASSOCIATED WITH INCREASED MORTALITY AND MORBIDITY IN PATIENTS UNDERGOING TRANSCATHATER AORTIC VALVE REPLACEMENT: AN INSIGHT FROM MOST RECENT NATIONAL INPATIENT DATABASE (2016)
Authors: Vivek Modi, Dhrubajyoti Bandyopadhyay, Hassan Beydoun, Faris Haddadin, Alba Munoz Estrella, Ruchit Shah, Eyal Herzog
Journal: Journal of the American College of Cardiology (2019)
Abstract 435: Post-transcriptional Regulation of Tropomyosin Isoforms Altered in Human Heart Diseases
Authors: Jun Cao, KarryAnne Belanger, Curtis Nutter, Ping Ji, Ela Jaworski, Nathan Elrod, Sunil Verma, Eric Wagner, Andrew Routh, Muge N. Kuyumcu-Martinez
Journal: Circulation Research (2018)

Background: Tropomyosin 1 (TPM1) is a coiled coil protein that forms polymers along with the actin filament, and it is required for myofibril organization, myocardial contraction, and cardiac development. TPM1 has cardiac muscle and non-muscle specific protein isoforms that dictate its function in cardiac muscle contraction or in cytoskeleton. TPM1 mutations in exon 2b, 5, 6b or 8 are associated with cardiovascular diseases including familial hypertrophic cardiomyopathy, dilated cardiomyopathy and left ventricular non-compaction. Thus, it is of great importance to investigate the mechanisms that control tropomyosin isoforms in order to identify novel therapeutic targets for cardiovascular diseases in which TPM1 is mutated. Method: We used nanopore sequencing technology using MinION and poly(A)click seq (PAC-seq) to identify different TPM1 transcripts generated in rat heart derived H9c2 cells. RT-PCR and western blotting were conducted to measure mRNA and protein levels of TPM1 respectively. Results: We identified 10 different isoforms of TPM1 using nanopore sequencing and determined several exons that are extensively spliced and favored in cardiac cells. We further identified an RNA binding protein that controls cardiac specific isoforms of TPM1 via alternative splicing and polyadenylation. Importantly, we found that this RNA binding protein regulates alternative splicing of exon 6b of TPM1, which is mutated in patients with cardiomyopathies. Conclusions: We identified an RNA binding protein, which controls expression of cardiac specific TPM1 isoforms by alternative polyadenylation and alternative splicing.
METASTATIC PERICARDIAL MESOTHELIOMA: A RARE CASE OF CONSTRICTIVE PERICARDITIS
Authors: Ilya Karagodin, Kathleen Nagle, Brooke Scheidemantle, Jonathan Chung, Jonathan D. Paul, Paul Larsen, Rohan Kalathiya, Tae Song, Jeanne M. DeCara, Karima Addetia, Corey Tabit, Matthew J. Sorrentino, R. Parker Ward
Journal: Journal of the American College of Cardiology (2019)
Tumor stem-like cell-derived exosomal RNAs prime neutrophils for facilitating tumorigenesis of colon cancer
Authors: Wei-Lun Hwang, Hsin-Yi Lan, Wei-Chung Cheng, Shih-Ching Huang, Muh-Hwa Yang
Journal: Journal of Hematology & Oncology (2019)

Cell-cell interactions maintain tissue homeostasis and contribute to dynamic alteration of the tumor microenvironment (TME). Communication between cancer and host cells not only promotes advanced disease aggression but also determines therapeutic response in cancer patients. Despite accumulating evidence supporting the role of tumor-infiltrating immunocytes in modulating tumor immunity, the interplay between heterogeneous tumor subpopulations and immunocytes is elusive. We expanded colorectal cancer stem cells (CRCSCs) as cancer spheroids from the murine colorectal cancer (CRC) cell line CT26 to interrogate tumor-host interactions using a syngeneic tumor model. RNA-sequencing analysis of host cells and tumor exosomes was performed to identify molecular determinants that mediate the crosstalk between CRCSCs and immunocytes. The Cancer Genome Atlas (TCGA) database was used to validate the clinical significance in CRC patients. The expanded CT26 cancer spheroids showed increased stemness gene expression, enhanced spheroid and clonogenicity potential, and an elevated tumor-initiating ability, characteristic of CRCSCs. By examining immune cell composition in syngeneic tumor-bearing mice, a systemic increase in CD11b+/Ly6GHigh/Ly6CLow neutrophils was observed in mice bearing CRCSC-derived tumors. An increased secretion of CRCSC exosomes was observed in vitro, and through in vivo tracking, CRCSC exosomes were found to be transported to the bone marrow. Moreover, CRCSC exosomes prolonged the survival of bone marrow-derived neutrophils and engendered a protumoral phenotype in neutrophils. Mechanistically, tumor exosomal tri-phosphate RNAs induced the expression of interleukin-1β (IL-1β) through a pattern recognition-NF-κB signaling axis to sustain neutrophil survival. CRCSC-secreted CXCL1 and CXCL2 then attracted CRCSC-primed neutrophils to promote tumorigenesis of CRC cells via IL-1β. Moreover, neutrophil depletion using a Ly6G-specific antibody (clone 1A8) attenuated the tumorigenicity of CRCSCs. In human specimens, CRC patients exhibiting an active CRCSC signal (Snail+IL8+) showed elevated tumor infiltration of MPO+ neutrophils, and high (in the top 10%) MPO expression predicted poor survival of CRC patients. This study elucidates a multistep CRCSC-neutrophil interaction during advanced cancer progression. Strategies targeting aberrant neutrophil activation may be developed for combating CSC-related malignancy.
Abstract 20856: Effects of Niacin on Glucose Levels in Patients With Normal Glucose (<100mg/dl): A Combined Analysis of the Familial Atherosclerosis Treatment Study (FATS), the HDL-Atherosclerosis Treatment Study (HATS), the Armed Forces Regression Study (AFREGS), the Carotid Plaque Composition by MRI During Lipid-Lowering Study (CPC), and the Familial Atherosclerosis Treatment Study-Observational Study (FATS-OS)
Authors: Luis Munoz, Peymon Shadzi, Daniel Isquith, Michael Triller, B. Greg Brown, Xue-Qiao Zhao
Journal: Circulation (2010)

Introduction: Effect of niacin on glucose levels in subjects with diabetes has been investigated; however, the magnitude of niacin's effect on glucose in subjects with normal glucose levels has not...
Underutilization of Cardiac Rehabilitation for Type 2 Myocardial Infarction
Authors: Cian P. McCarthy, Sean Murphy, Joshua A. Cohen, Saad Rehman, Maeve Jones-O’Connor, David S. Olshan, Avinainder Singh, Muthiah Vaduganathan, James L. Januzzi, Jason H. Wasfy
Journal: Journal of the American College of Cardiology (2019)
CARDIOTOXICITY PHENOTYPES IN WOMEN TREATED WITH ANTHRACYCLINES AND TRASTUZUMAB FOR EARLY STAGE BREAST CANCER
Authors: Mark T. Nolan, Mustafa Abdul Selam, Eitan Amir, Anne Koch, Paul Yip, Maria Michalowska, Bernd Wintersperger, Paaladinesh Thavendiranathan
Journal: Journal of the American College of Cardiology (2019)
TIME TO THINK BEYOND DOOR TO BALLOON TIME: SIGNIFICANCE OF TOTAL ISCHEMIC TIME IN PATIENTS WITH ST ELEVATION MYOCARDIAL INFARCTION
Authors: Sanam Khowaja, Salik Ahmed, Naveed Ullah Khan, Tahir Saghir, Syed Nadeem, Nadeem Qamar, Musa Karim
Journal: Journal of the American College of Cardiology (2019)
Abstract 579: Beta-blockers Regulate Hypoxia Sensing of Beta Adrenergic Receptors
Authors: Yu Sun, Manveen K Gupta, Sathyamangla V Prasad
Journal: Circulation Research (2018)

Beta adrenergic receptors (βARs) are one of the most powerful regulators of cardiac function. Activation of βAR leads to phosphorylation by G-protein coupled receptor kinase 2 and β-arrestin binding resulting in desensitization. The phosphorylated βARs are resensitized by dephosphorylation by PP2A. Besides classical agonist activation, increasing evidence shows that βARs can be regulated by inflammation and oxidative stress. In this regard, we have shown that βARs can be regulated by hypoxia wherein hypoxia increases the β2AR phosphorylation and HIFα accumulation (Cheong et. al., 2016). However, the mechanisms of βARs regulation in hypoxia are not well understood and we postulated that shift in homeostasis existing between kinase and phosphatase driven mechanisms may underlie βAR dysfunction. To test this hypothesis, β2AR HEK 293 cells were exposed to hypoxia (2% O 2 ) and assessed the mechanisms underlying desensitization (kinases) and resensitization (PP2A). Our studies showed that 6 hours of hypoxia treatment resulted in increase of βAR phosphorylation and GRK2 expression. Assessment of βAR phosphorylation in the plasma membrane and endosomal fractions surprisingly, shoed marked increase in β2AR phosphorylation in the endosomal fraction. Furthermore, we also observed that receptor associated PP2A activity was reduced specifically in the endosomes with minimal changes of activity at the plasma membranes. Given that β-blockers confer beneficial effects, we tested whether β-blockers (propranolol or carvedilol) would prevent βARs phosphorylation under hypoxia or normoxia. Consistently, β-blocker treatment in normoxia results in increased β2AR phosphorylation. Remarkably β-blocker treatment in hypoxia results in loss of β2AR phosphorylation and reduction in GRK2 expression. These studies suggest agonist-independent hypoxia-driven β2AR dysfunction can be ameliorated by β-blockers and the underlying mechanisms driving this hypoxia mediated β2AR dysfunction will be discussed in the presentation. These unexpected findings have significant clinical implications given that hypoxia underlies stroke/myocardial infarction and understanding these mechanisms could provide novel insights into the benefits provided by β-blockers.
Abstract 200: Engineering Evolution: Tetraploidization of Human Cardiac Stem Cells to Enhance Functional Activity
Authors: Kathleen M Broughton, Dena Yaareb, Carolina Y Esquer, Giulio Pompilio, Mark A Sussman
Journal: Circulation Research (2018)

Introduction: Reparative and regenerative capacity is consistently observed in lower vertebrate species, but translational implementation has failed to yield comparable results in the clinical setting. Cardiac stem cells (CSC) isolated from rodent or swine heart possess capacity for tetraploidization resulting in 4n chromatin content associated with override of cell cycle arrest and senescence, but comparable tetraploid CSC are not present in human samples. Furthermore, diploid:tetraploid CSC ratio in rodent myocardium increases following infarction injury suggesting ploidy is a dynamic cellular condition influencing response to pathologic damage. Since polyploidization correlates with enhanced regenerative throughout evolution, ploidy differences raise provocative questions regarding translational applicability of experimental studies of myocardial regeneration. Hypothesis: Mononuclear chromatin duplication in human stem cells improves functional capabilities by inhibiting cellular senescence and increasing stress resistance. Methods and Results: Tetraploidy was artificially induced in human CSCs, ESCs and MSCs from multiple patient samples by transient exposure to demecolcine that blocks mitotic spindle formation and chromosome segregation. Mononuclear tetraploid content confirmed by karyotype analysis was consistently induced in hCSCs and hEPCs, unlike hMSCs which underwent apoptosis. Mononuclear tetraploid content in hCSCs and hEPCs was stable for continued multiple passages demonstrated by flow cytometry with proliferation rates equivalent to the parent diploid line. Stress induction through hydrogen peroxide demonstrate tetraploid hCSCs respond equivalent or better than parental lines measured through apoptosis and necrosis. Double strand DNA breaks in tetraploid hCSCs were reduced by half compared to the parental line, measured by gamma H2AX per total DNA. Conclusion: Tetraploid content induction in human CSCs and EPCs enhances functional activity by increased resistance to stress and inhibition of senescence without promoting oncogenic transformation. Ongoing studies focus upon potential of tetraploid hCSCs to exert enhanced capabilities for mediating myocardial repair and regeneration.
ASSOCIATION OF BODY FAT MASS WITH LEFT VENTRICULAR MYOCARDIAL SYSTOLIC LONGITUDINAL DYSFUNCTION IN TYPE 2 DIABETES MELLITUS
Authors: Yutaka Hatani, Hidekazu Tanaka, Yasuhide Mochizuki, Makiko Suto, Hiroki Takada, Fumitaka Soga, Kumiko Dokuni, Keiko Hatazawa, Eriko Hisamatsu, Kensuke Matsumoto, Ken-Ichi Hirata
Journal: Journal of the American College of Cardiology (2019)
CORONARY PLAQUE BURDEN IS ASSOCIATED WITH CHOLESTEROL EFFLUX CAPACITY PARTIALLY MEDIATED BY THE HEMATOPOIETIC SYSTEM IN PSORIASIS
Authors: Milena Aksentijevich, Heather Teague, Martin Playford, Amit Dey, Aarthi Reddy, Youssef Elnabawi, Aditya Goyal, Abhishek Chaturvedi, Harry Choi, Noor Khalil, Jenis Argueta-Amaya, Parag Shukla, Justin Rodante, Andrew Keel, Veit Sandfort, Marcus Chen, David Bluemke, Andrew Choi, Ramesh Mazhari, Joel Gelfand, Nehal Mehta
Journal: Journal of the American College of Cardiology (2019)
A RARE CASE OF INFILTRATIVE CARDIOMYOPATHY: ISOLATED EOSINOPHILIC CARDIOMYOPATHY
Authors: Pedro Santiago Rodriguez, Robert Rodriguez, Eduardo Hernandez Pons, Edgar Vazquez-Vargas, Gilberto Baez-Rios, David Bermudez-Nunez, Hector Martinez-Gonzalez, Francisco Perez, Milton Carrero
Journal: Journal of the American College of Cardiology (2019)
LONG-TERM USE OF ORAL BETA-BLOCKER IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION WHO UNDERWENT PRIMARY CORONARY INTERVENTION: A SYSTEMATIC REVIEW AND META-ANALYSIS
Authors: Wasawat Vutthikraivit, Pattara Rattanawong, Saranapoom Klomjit, Pakpoom Tantrachoti, Narut Prasitlumkum, Prapaipan Putthapiban, Mohamed Elmassry, Pablo Paz, Mohammad Ansari, Scott Shurmur
Journal: Journal of the American College of Cardiology (2019)