tbuckley/cabot-search huggingface dataset:
ACTR-15. PHASE 1 TRIAL OF A KETOGENIC DIET IN PATIENTS RECEIVING STANDARD-OF-CARE TREATMENT FOR RECENTLY DIAGNOSED GLIOBLASTOMA
Authors: Gillian Gresham, Lauren Amaral, Laura Lockshon, Dana Levin, Jeremy Rudnick, Arlene Provisor, Stephen Shiao, Neil Bhowmick, Scott Irwin, Stephen Freedland, Jethro Hu
Journal: Neuro-Oncology (2019)

Abstract BACKGROUND There is abundant interest in the potential therapeutic and supportive role of a ketogenic diet (KD) in patients with glioblastoma (GBM). The KD is a high fat/low carbohydrate metabolic therapy that modulates several of the bioenergetic and biosynthetic pathways that are dysregulated in GBM. To date, studies of the KD in cancer patients have been limited in scope. This study will provide preliminary evidence on the safety and feasibility of a 16-week ketogenic diet in patients with GBM. METHODS This is an open-label single-arm feasibility trial being conducted at Cedars-Sinai Medical Center. We will recruit 20 recently diagnosed GBM patients who are receiving standard-of-care (SOC) treatment. Patients may enroll within 3 months of diagnosis, thus allowing patients who have already begun SOC chemoradiation the opportunity to participate. Excluded are patients with a KPS &lt; 70, BMI &lt; 22, or on high doses of steroids. Consenting patients will maintain a 16-week ketogenic diet (KD) supervised and monitored by study dietitians (RD). The primary outcome of safety will be assessed by monitoring weight, BMI, and adverse events. Secondary outcomes are: 1) Adherence to the KD, as assessed by BID blood glucose and ketone levels; 2) Time to progression and overall survival from date of KD initiation 3) Mean change in overall QOL, as measured using the QLQ30 and QLQ-BN20 questionnaires; and 4) Mean change in cognitive scores at 16 weeks from baseline. Exploratory outcomes include metabolic, inflammatory, and immune biomarkers; gut microbiota analysis; large oncosome analysis; and daily activity assessed with a wearable activity monitor. This novel trial incorporates multiple digital devices and mobile applications into the study design. Accrual is ongoing with 10 patients currently enrolled (NCT03451799).
Safe Use of Hydroxyurea in Sickle Cell Disease Patients Hospitalized for Painful Vaso-Occlusive Episodes: Results of the Randomized, Open-Label Helps Study
Authors: Nicola Conran, Kleber Yotsumoto Fertrin, Claudia de Alvarenga Maximo, Thais Oliveira, Clarisse Lobo, Fernando Ferreira Costa
Journal: Blood (2019)
COMP-08. COMPREHENSIVE RNA ANALYSIS OF CEREBROSPINAL FLUID FROM LEPTOMENINGEAL METASTASES
Authors: Dina Polyak, Yingmei Li, Boxiang Liu, Ian Connolly, Lina Khoeur, Bina Wasunga Kakusa, Eli Johnson, Stephanie Andersen, Wenying Pan, Seema Nagpal, Stephen B Montgomery, Melanie Hayden Gephart
Journal: Neuro-Oncology (2019)

Abstract Leptomeningeal metastases (LM), a diffuse form of brain metastases is rare and fatal progression of non-small cell lung cancer (NSCLC). In LM, metastatic cancer cells spread and resign on the brain meninges, the cerebrospinal fluid (CSF), cranial and spinal nerves. Rapid disease progression and scarce tissue availability hinder the progress of scientific study of LM and its treatment. To overcome the critical lack of tissue and to determine the genetic profile of NSCLC LM, we have developed methods to extract tumor-associated cell-free RNA from CSF, and isolated and sequenced circulating single cells from CSF. Herein, we used high throughput qPCR to target lung and brain-associated genes and identified NSCLC LM metastases-related RNA. Brain-specific gene signature (GFAP, NRGN, SNCB, ZBTB18) was detected in all CSF sample (control and metastases), whereas lung-specific genes (MUC1, SFTPB, SFTPD, SLC34A2) were detected in CSF of brain metastases patients. Normal, healthy CSF lacks cellular component, but CSF of patients with LM metastases inhabited with very low amount of circulating tumor cells. Single cells from CSF of 4 patients with NSCLC LM metastases were captured with microfluidic chip. Cells (n = 197) were clustered by significantly differential expressed genes demonstrating two distinct populations of white blood and tumor cells. These data identified specific cfRNA and single cell transcriptome profiles compared to normal cells or patients without NSCLC LM metastases, and highlighted metastases-associated carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) as highly expressed in patients with NSCLC LM metastases. CEACAM6 mRNA was detected in CSF of 86% of patients with NSCLC LM but not in the CSF of control patients. In vitro inhibition of CEACAM6 protein lead to decreased invasion in NSCLC cells which was rescued by overexpression of the protein. We have developed sensitive and robust techniques to leverage human CSF to study NSCLC LM.
Therapeutic Targeting of CCR1 to Prevent Dissemination of Multiple Myeloma Plasma Cells
Authors: Mara N Zeissig, Duncan R Hewett, Krzysztof M Mrozik, Vasilios Panagopoulos, Monika Engelhardt, Luen Bik To, Peter J Croucher, Andrew CW Zannettino, Kate Vandyke
Journal: Blood (2019)
Surgical Anatomy of the Parotid Gland
Authors: J. McKenzie
Journal: BMJ (1948)

The presenilin containing γ-secretase complex is responsible for the regulated intramembraneous proteolysis of the amyloid precursor protein (APP), the Notch receptor, and a multitude of other substrates. γ-Secretase catalyzes the final step in the generation of Aβ<sub>40</sub> and Aβ<sub>42</sub> peptides from APP. Amyloid β-peptides (Aβ peptides) aggregate to form neurotoxic oligomers, senile plaques, and congophilic angiopathy, some of the cardinal pathologies associated with Alzheimer9s disease. Although inhibition of this protease acting on APP may result in potentially therapeutic reductions of neurotoxic Aβ peptides, nonselective inhibition of the enzyme may cause severe adverse events as a result of impaired Notch receptor processing. Here, we report the preclinical pharmacological profile of GSI-953 (begacestat), a novel thiophene sulfonamide γ-secretase inhibitor (GSI) that selectively inhibits cleavage of APP over Notch. This GSI inhibits Aβ production with low nanomolar potency in cellular and cell-free assays of γ-secretase function, and displaces a tritiated analog of GSI-953 from enriched γ-secretase enzyme complexes with similar potency. Cellular assays of Notch cleavage reveal that this compound is approximately 16-fold selective for the inhibition of APP cleavage. In the human APP-overexpressing Tg2576 transgenic mouse, treatment with this orally active compound results in a robust reduction in brain, plasma, and cerebral spinal fluid Aβ levels, and a reversal of contextual fear-conditioning deficits that are correlated with Aβ load. In healthy human volunteers, oral administration of a single dose of GSI-953 produces dose-dependent changes in plasma Aβ levels, confirming pharmacodynamic activity of GSI-953 in humans.
Dendritic Cells Drive Osteosarcomagenesis through Newly Identified Oncogene and Tumor Suppressor
Authors: Kevin B. Jones
Journal: Cancer Discovery (2019)

Abstract Summary: GRM4, a GWAS-suspected tumor suppressor, is tested in a mouse model of osteosarcomagenesis as well as the putative oncogene it suppresses, IL23. Both are expressed in and exert the bulk of their influence among tumor-infiltrating myeloid-derived antigen-presenting cells, rather than osteosarcoma cells. See related article by Kansara et al., p. 1511.
Development of CD38 CAR Engineered Human Placental Hematopoietic Stem Cell Derived Natural Killer Cells (PNK-CAR38) As Allogeneic Cancer Immunotherapy
Authors: Srinivas Somanchi, Xuan Guo, Shuyang He, Rohit Mathur, Andrea Difiglia, Hemlata Rana, Weifang Ling, James Edinger, Gunnar F. Kaufmann, Jerome B. Zeldis, Henry Ji, Robert Hariri, Xiaokui Zhang
Journal: Blood (2019)
Outcomes of Total Body Irradiation- Versus Chemotherapy-Based Myeloablative Conditioning Regimen in Haploidentical Hematopoietic Cell Transplantation with Post-Transplant Cyclophosphamide for Acute Lymphoblastic Leukemia: ALWP of the EBMT Study
Authors: Bhagirathbhai Dholaria, Myriam Labopin, Emanuele Angelucci, Johanna Tischer, Mutlu Arat, Fabio Ciceri, Zafer Gülbas, Hakan Ozdogu, Simona Sica, Jose L. Diez-Martin, Yener Koc, Jane Apperley, Gerard Socie, Sebastian Giebel, Bipin N. Savani, Arnon Nagler, Mohamad Mohty
Journal: Blood (2019)
PATH-45. DIFFERENT TYPES OF HYPERMUTATOR PHENOTYPE OF GLIOBLASTOMA ACCORDING TO MUTATION PATTERNS OF MISMATCH REPAIR GENES
Authors: Kuniaki Saito, Saki Shimizu, Eriko Nozaki, Keiichi Kobayashi, Nobuyoshi Sasaki, Yuki Yamagishi, Yoshiaki Shiokawa, Motoo Nagane
Journal: Neuro-Oncology (2019)

Abstract BACKGROUND Although precision medicine has been widely applied to routine care, only few molecular targeted drugs have been developed for glioma. Immune checkpoint inhibitors hold a potential promise to improve outcome of malignant glioma especially with the hypermutator phenotype. Mismatch repair deficiency could induce hypermutation during temozolomide (TMZ) treatment, but the mechanism of mutation acquisition is not well understood. METHODS We present the results of target sequencing of 57 longitudinal specimens from 27 individuals with glioblastoma (GBM). We used Ion AmpliSeq Cancer Hotspot Panel v2 (CHP) and/or Ion AmpliSeq Comprehensive Cancer Panel (CCP) for target sequencing. RESULTS Acquired mutations with G:C &gt;A:T transition at non-CpG sites were found in 70% of recurrent MGMT methylated samples, whereas only 8% in MGMT unmethylated cases (p&lt; 0.001). Two cases of hypermutator phenotype were identified in MGMT methylated, IDH wild type recurrent GBMs after TMZ chemotherapy. One case gained mutations in mismatch repair genes of MLH1, MSH2, MSH6, and PMS1. Most of the acquired mutations were G:C &gt;A:T mutations typical to TMZ-induced hypermutation. The recurrent tumor was highly aggressive with overall survival after recurrence of 3.7 months. The other case gained mutations in mismatch repair genes of MLH1 and PMS1 only. Most of the acquired mutations were insertion mutations. The prognosis after recurrence was much longer. CONCLUSIONS We identified two types of hypermutator phenotype according to mutation pattern of mismatch repair genes. It has been suggested that MSH2-MSH6 complex deficient tumor cannot repair TMZ-induced mismatch mutation, thereby causing hypermutation. Conversely, MLH1-PMS1 complex deficient tumor with intact MSH2-MSH6 complex can repair mismatch mutation but is susceptible to insertion mutation. Taken together, MSH6 mutation plays a key role in TMZ-induced hypermutation, while MLH1 and PMS1 mutations might cause insertion-based hypermutation. Larger and prospective studies are warranted to clarify the mechanism, outcome, and effectiveness of checkpoint inhibitors.
Updated Analysis: Novel Machine-Learning-Based Sepsis Prediction Model for Patients Undergoing Hematopoietic Stem Cell Transplantation (Early Sepsis Prediction/Identification for Transplant Recipients: ESPRIT)
Authors: Zahra Eftekhari, Sally Mokhtari, Tushondra Thomas, Dongyun Yang, Liana Nikolaenko, Deron Johnson, Jana Dickter, Justine Abella Ross, Bernard Tegtmeier, Eileen P. Smith, Monzr M. Al Malki, Ricardo Spielberger, Anna B Pawlowska, Argelia Sandoval, John Zaia, Stephen J Forman, Janet Munu, Sanjeet Dadwal, Ryotaro Nakamura
Journal: Blood (2019)
Flowsom: An R-Based Evaluation Strategy for Flow Cytometry-Based Measurable Residual Disease (MRD) Diagnostics in Acute Myeloid Leukemia (AML)
Authors: Veit Bücklein, Alexandra Stein, Benjamin Tast, Thomas Koehnke, Karsten Spiekermann, Francis Lacombe, Marion Subklewe
Journal: Blood (2019)
Selective Targeting BET Family Bdii Bromodomain with Abbv-744 and BCL-2 with Venetoclax (ABT-199) Is Synergistic in Primary Acute Myeloid Leukemia Models
Authors: Tianyu Cai, Vinitha Mary Kuruvilla, Xiaoyu Lin, Tamar Uziel, Xin Lu, Lu Zhang, Xiaoli Huang, Qi Zhang, Antonio Cavazos, Lina Han, Yu Shen, Marina Y Konopleva
Journal: Blood (2019)
AZD4573 Is a Highly Selective CDK9 Inhibitor That Suppresses MCL-1 and Induces Apoptosis in Hematologic Cancer Cells
Authors: Justin Cidado, Scott Boiko, Theresa Proia, Douglas Ferguson, Steven W. Criscione, Maryann San Martin, Petar Pop-Damkov, Nancy Su, Valar Nila Roamio Franklin, Chandra Sekhar Reddy Chilamakuri, Clive S. D'Santos, Wenlin Shao, Jamal C. Saeh, Raphael Koch, David M. Weinstock, Michael Zinda, Stephen E. Fawell, Lisa Drew
Journal: Clinical Cancer Research (2019)

Cyclin-dependent kinase 9 (CDK9) is a transcriptional regulator and potential therapeutic target for many cancers. Multiple nonselective CDK9 inhibitors have progressed clinically but were limited by a narrow therapeutic window. This work describes a novel, potent, and highly selective CDK9 inhibitor, AZD4573.The antitumor activity of AZD4573 was determined across broad cancer cell line panels in vitro as well as cell line- and patient-derived xenograft models in vivo. Multiple approaches, including integrated transcriptomic and proteomic analyses, loss-of-function pathway interrogation, and pharmacologic comparisons, were employed to further understand the major mechanism driving AZD4573 activity and to establish an exposure/effect relationship.AZD4573 is a highly selective and potent CDK9 inhibitor. It demonstrated rapid induction of apoptosis and subsequent cell death broadly across hematologic cancer models in vitro, and MCL-1 depletion in a dose- and time-dependent manner was identified as a major mechanism through which AZD4573 induces cell death in tumor cells. This pharmacodynamic (PD) response was also observed in vivo, which led to regressions in both subcutaneous tumor xenografts and disseminated models at tolerated doses both as monotherapy or in combination with venetoclax. This understanding of the mechanism, exposure, and antitumor activity of AZD4573 facilitated development of a robust pharmacokinetic/PD/efficacy model used to inform the clinical trial design.Selective targeting of CDK9 enables the indirect inhibition of MCL-1, providing a therapeutic option for MCL-1-dependent diseases. Accordingly, AZD4573 is currently being evaluated in a phase I clinical trial for patients with hematologic malignancies (clinicaltrials.gov identifier: NCT03263637).See related commentary by Alcon et al., p. 761.
Marrow Ring Sideroblasts Are Highly Predictive for TP53 Mutation in MDS with Excess Blasts
Authors: David M Swoboda, Jung-Hoon Lee, Onyee Chan, Rami S. Komrokji, Najla Al Ali, Eric Padron, Alan F. List, Mohammad O Hussaini, Jinming Song, David A Sallman
Journal: Blood (2019)
Immunomodulation with Azacytidine and Donor Lymphocyte Infusion Following Sequential Conditioning Allogenic Stem Cell Transplantation Improves Outcome of Unfavorable AML
Authors: Magalie Joris, Delphine Lebon, Amandine Charbonnier, Pierre Morel, Berengere Gruson, Alexis Caulier, Caroline Delette, Marie-Noëlle Lacassagne, Nicolas Guillaume, Loïc Garçon, Jean-Pierre Marolleau
Journal: Blood (2019)
INNV-15. CLINICAL DATA THAT MATTERS: A DISTILLATION OF NEURO-ONCOLOGY CLINICAL TRIAL INCLUSION CRITERIA USING MACHINE LEARNING
Authors: James Snyder, Michael Wells, Laila Poisson, Steven Kalkanis, Houtan Noushmehr, Adam Robin
Journal: Neuro-Oncology (2019)

Abstract INTRODUCTION Neuro-oncologic conditions have dismal outcomes, ineffective treatments, poor access to clinical trials, and variability in care. Clinical trials do not capture a patient’s complete journey and are restricted to select populations. ‘Real-world-evidence’ (RWE) attempts to inform point of care decisions through routine collection of data with a clinical-trial-like rigor. RWE complements existing knowledge through broad patient participation, collection throughout disease course, and creation of large multidimensional datasets “knowledge network of disease” 1,2. RWE implementation is hindered by unstructured data, uncertainty of relevant features, and semantic heterogeneity. Clinical attributes were selected from trial inclusion criteria and prioritized for structuring in clinic notes for abstraction. METHOD We queried Clinicaltrials.gov from 1/1/2018-12/31/2018, refined to North America, recruiting, interventional, and adult. Meningioma, pituitary, glioblastoma, astrocytoma, oligodendroglioma, and ependymoma were chosen based on incidence3. Lymphoma and nerve sheath tumors were omitted. “Brain tumor” and “glioma” were added. ‘K-nearest-neighbor’ tokenization parsed inclusion criteria4. Document term matrix (n-gram) converted text to vectors5. A generative probabilistic model using ‘Latent Dirichlet Allocation’ plotted words into 10 clusters6. Hierarchal clustering was used to compare histology with terms. RESULTS 401 trials parsed into 3676 statements and 4008 keywords. 10 clusters of terms were similarly distributed amongst histologies, suggesting generalizability across tumor types. Cluster revealed 8 categories: 1) Time: enrollment; 2) Performance status: KPS; 3) Testing: mutations, upper limit of normal, routine hematologic laboratory assays; 4) Imaging: extent of surgery; 5) Pregnancy/childbearing; 6) Tumor grade; 7) Treatment history: recurrence, chemotherapy, radiation, time; 8) Informed consent CONCLUSIONS Dissecting the compendium of clinical trials using machine learning can identify general parameters for trial enrollment to guide RWE clinical collection. Using practical definitions of the most germane trial data, specific information can be sought after and defined to improve research quality, maximize research yields and improve patient care whilst minimizing wasted research and clinical endeavors.
Coaltered <i>Ras/B-raf</i> and <i>TP53</i> Is Associated with Extremes of Survivorship and Distinct Patterns of Metastasis in Patients with Metastatic Colorectal Cancer
Authors: Jashodeep Datta, J. Joshua Smith, Walid K. Chatila, John C. McAuliffe, Cyriac Kandoth, Efsevia Vakiani, Timothy L. Frankel, Karuna Ganesh, Isaac Wasserman, Marla Lipsyc-Sharf, Jose Guillem, Garrett M. Nash, Philip B. Paty, Martin R. Weiser, Leonard B. Saltz, Michael F. Berger, William R. Jarnagin, Vinod Balachandran, T. Peter Kingham, Nancy E. Kemeny, Andrea Cercek, Julio Garcia-Aguilar, Barry S. Taylor, Agnes Viale, Rona Yaeger, David B. Solit, Nikolaus Schultz, Michael I. D'Angelica
Journal: Clinical Cancer Research (2019)

Abstract Purpose: We aimed to investigate genomic correlates underlying extremes of survivorship in metastatic colorectal cancer and their applicability in informing survival in distinct subsets of patients with metastatic colorectal cancer. Experimental Design: We examined differences in oncogenic somatic alterations between metastatic colorectal cancer cohorts demonstrating extremes of survivorship following complete metastasectomy: ≤2-year (n = 17) and ≥10-year (n = 18) survivors. Relevant genomic findings, and their association with overall survival (OS), were validated in two independent datasets of 935 stage IV and 443 resected stage I–IV patients. Results: In the extremes-of-survivorship cohort, significant co-occurrence of KRAS hotspot mutations and TP53 alterations was observed in ≤2-year survivors (P &amp;lt; 0.001). When validating these findings in the independent cohort of 935 stage IV patients, incorporation of the cumulative effect of any oncogenic Ras/B-raf (i.e., either KRAS, NRAS, or BRAF) and TP53 alteration generated three prognostic clusters: (i) TP53-altered alone (median OS, 132 months); (ii) Ras/B-raf–altered alone (65 months) or Ras/B-raf- and TP53 pan-wild-type (60 months); and (iii) coaltered Ras/B-raf–TP53 (40 months; P &amp;lt; 0.0001). Coaltered Ras/B-raf–TP53 was independently associated with mortality (HR, 2.47; 95% confidence interval, 1.91–3.21; P &amp;lt; 0.001). This molecular profile predicted survival in the second independent cohort of 443 resected stage I–IV patients. Coaltered Ras/B-raf–TP53 was associated with worse OS in patients with liver (n = 490) and lung (n = 172) but not peritoneal surface (n = 149) metastases. Moreover, coaltered Ras/B-raf–TP53 tumors were significantly more likely to involve extrahepatic metastatic sites with limited salvage options. Conclusions: Genomic analysis of extremes of survivorship following colorectal cancer metastasectomy identifies a prognostic role for coaltered Ras/B-raf–TP53 and its association with distinct patterns of colorectal cancer metastasis.
Spontaneous Breathing Trials and Successful Extubation
Authors: Jan O. Friedrich, Karen E. A. Burns
Journal: JAMA (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 HomeNew OnlineCurrent IssueFor Authors 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
SCIDOT-33. ULTRASOUND-FACILITATED DRUG DELIVERY DEVICE FOR LOCAL DRUG INFUSION AGAINST BRAIN TUMORS
Authors: Ryuta Saito, Wenting Jia, Aya Sato, Kenji Inoue, Saori Okuno, Yuji Ohashi, Kei Kamada, Akira Yoshikawa, Teiji Tominaga
Journal: Neuro-Oncology (2019)

Abstract OBJECT Local drug delivery into brain tumor faces a major problem: limitations of distribution. Recently, we have been working to develop a novel treatment strategy delivering chemotherapeutic agents directly into the tumor. Previously, we developed an ultrasound facilitated drug delivery (UFD) system in order to achieve extensive drug distribution (J Neurosurg 124, 2016). Subsequently, we fabricated a second-generation device by analyzing optimal ultrasound generating condition. Here, we tested the intraparenchymal and intratumoral drug distribution using the device. METHODS Resonance frequency of the device was determined by measuring the strength of sound field using hydrophone in water. Using the UFD system, applying resonance frequency, evans blue dye was infused into the striatum of Fisher344 rats. Immediately after the infusion, brains were harvested, quickly frozen, and sectioned to evaluate the distributions of the dye. Similar study was then performed in 9L brain tumor model. RESULTS The second-generation device successfully distributed the dye to the volume 1.5~2 times larger than simple CED with using half the driving voltage than first-generation device. Moreover, the distribution instability, which was a major problem with the first-generation device, was resolved achieving smaller standard deviation. Using multiple resonance frequencies of the device, we found the difference in drug distribution; suggesting the existence of optimal frequencies for brain interstitial drug delivery. This drug delivery strategy also worked in brain tumor model increasing the coverage inside the brain tumor. CONCLUSIONS The second generation UFD device successfully and stably achieved enlarged distribution in the brain parenchyma and in the brain tumor.
Abstract 11203: Posttraumatic Stress Disorder After Suspected Acute Coronary Syndrome is Associated With Lower Adherence to Cardiovascular Medication
Authors: Ian M Kronish, Talea Cornelius, Joseph E Schwartz, Ari Shechter, Keith Diaz, Emily K Romero, Donald Edmondson
Journal: Circulation (2019)

Introduction: Patients experiencing a suspected acute coronary syndrome (ACS) can develop PTSD. ACS patients with PTSD have double the risk for recurrent CVD events and mortality. CVD medications c...