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This Table Summarizes Changes to the HF Qxq As of 10/11/2019 Question
Updated HFS Instructions (QxQs) This table summarizes changes to the HF QxQ as of 10/11/2019 Question in HF QxQ Description of Changes in HF QXQ General Instructions, pg. 3 Clarification added to rules for history Q29.d.10., pg. 40 Clarification made on how to record pulmonary hypertention Q29.d.14., pg. 41 Clarification made on how to record diastolic dysfunction Q42., pg. 42 Clarification made on how to record troponin I Section VII: Medication, pg. 54 Clarificaiton made on how to record medications Appendix A, pg. 61 Updated list of medications Edoxaban (ACOAG, Generic) Lixiana (ACOAG, Trade) Prexxartan (ARB, Trade) INSTRUCTIONS FOR COMPLETING HEART FAILURE HOSPITAL RECORD ABSTRACTION FORM HFS Version C, 10/1/2015 HFA Version D, 10/1/2015 HF QxQ, 10/11/2019 Table of Contents Page General Instructions……………………………………………………………….. 2 Specific Items………………………………………………………………………. 3 Section l: Screening for Decompensation………………………………….. 5 Section ll: History of Heart Failure…………………………………………... 10 Section lll: Medical History ………………………………………………….. 13 Section lV: Physical Exam - Vital Signs…………………………………….. 24 Section V: Physical Exam - Findings……………………………………….. 26 Section Vl: Diagnostic Tests…………………………………………………. 31 Section Vll: Biochemical Analyses………………………………………….. 48 Section Vlll: Interventions…………………………………………………….. 51 Section lX: Medications………………………………………………………. 54 Section X: Complications Following Events………………………………… 59 Section Xl: Administrative……………………………………………………. 60 Appendix A: ARIC Heart Failure/Cardiac Drugs: ………………………………. 61 Alphabetical Sort Appendix B: Potential Scenarios of the Onset of Heart………………………. 73 Failure Event or Decompensation HF QxQ 10/11/2019 Page 1 of 73 General Instructions The HFAA form was initially used for all discharges selected for HF surveillance. It was replaced by the HFAB and HFSA forms and then updated June 2012 with HFAC and HFSB. -
Viruses and Myocarditis NORMAN R
Postgrad Med J: first published as 10.1136/pgmj.48.566.750 on 1 December 1972. Downloaded from Postgraduate Medical Journal (December 1972) 48, 750-753. Viruses and myocarditis NORMAN R. GRIST THE observations described here were made in the inoculated into newborn mice. Nevertheless, signi- course of the work ofthe Regional Virus Laboratory, cant differences have been observed between the Glasgow, which provides a widely-used diagnostic associations of different types of echovirus with service. Our investigations of cardiac cases have cardiac and Bornholm disease suggesting that some concentrated particularly on enteroviruses, the main (notably types 6 and 19) may occasionally mimic group of viruses associated with acute myocarditis. Coxsackie viruses by causing illnesses of this type Within this group the Coxsackie viruses have (Bell & Grist, 1970b). received particular attention, their well-known Some problems of virological interpretation are causal role in acute carditis and Bornholm disease illustrated by an adult male with acute pericarditis being possibly related to their characteristic proper- whose sera on the eighth and seventeenth days of ties of causing acute myositis in experimentally illness showed diagnostic rising antibody titres to infected newborn mice. Virological diagnoses were Coxsackie virus B types 1, 3, 4, and 6, high un- based on isolation of virus from faeces, and/or a changing titres to type B2, and a low rise (< 16 : 16) four-fold or greater rise in neutralizing antibody to type B5. These cross-reactions are fairly commonProtected by copyright. titres in paired sera (rarely a four-fold fall in titre and pose problems in specific interpretation; in this with acceptable time relationships) or an unusually particular case the infecting virus was demonstrated high antibody titre without significant fluctuation. -
Rheumatic Heart Disease in Children: from Clinical Assessment to Therapeutical Management
European Review for Medical and Pharmacological Sciences 2006; 10: 107-110 Rheumatic heart disease in children: from clinical assessment to therapeutical management G. DE ROSA, M. PARDEO, A. STABILE*, D. RIGANTE* Section of Pediatric Cardiology, *Department of Pediatric Sciences, Catholic University “Sacro Cuore” – Rome (Italy) Abstract. – Rheumatic heart disease is presence of valve disease or carditis can be still a relevant problem in children, adolescents easily recognized through echocardiographic and young adults. Molecular mimicry between examinations, but the combination of clinical streptococcal and human proteins has been pro- posed as the triggering factor leading to autoim- tools and echocardiography consents the munity and tissue damage in rheumatic heart most accurate assessment of heart involve- disease. Despite the widespread application of ment2. It is well known however that minimal Jones’ criteria, carditis is either underdiagnosed physiological mitral regurgitation can be or overdiagnosed. Endocarditis leading to mitral identified in normal people and might over- and/or aortic regurgitation influences morbidity diagnose the possibility of carditis. Only in and mortality of rheumatic heart disease, whilst myocarditis and pericarditis are less significant 30% patients serial electrocardiogram studies in determining adverse outcomes in the long- are helpful in the diagnosis of acute RF with term. Strategy available for disease control re- non-specific findings including prolonged PR mains mainly secondary prophylaxis with the interval, atrio-ventricular block, diffuse ST-T long-acting penicillin G-benzathine. changes with widening of the QRS-T angle and inversion of T waves. Carditis as an ini- Key Words: tial sign might be mild or even remain unrec- Rheumatic heart disease, Pediatrics. -
Treatment Options in Myocarditis and Inflammatory Cardiomyopathy
Main topic Herz 2018 · 43:423–430 B. Maisch1 ·P.Alter2 https://doi.org/10.1007/s00059-018-4719-x 1 Fachbereich Medizin, Philipps-Universität Marburg und Herz- und Gefäßzentrum (HGZ) Marburg, Published online: 15 June 2018 Marburg, Germany © The Author(s) 2018 2 Klinik für Innere Medizin-Pneumologie und Intensivmedizin, UKGM und Philipps-Universität Marburg, Marburg, Germany Treatment options in myocarditis and inflammatory cardiomyopathy Focus on i. v. immunoglobulins In 2012 we reviewed the treatment op- proBNP) and high-sensitivity (hs) tro- curtain of diabetic cardiomyopathy, viral tions in (peri)myocarditis and inflamma- ponin T or I as cardiac biomarkers of heart disease with or without inflamma- tory cardiomyopathy in a special issue of heart failure and necrosis, respectively. tion can be hidden. But which of the this journal devoted to heart failure and Of note, cardiac MRI is an important factors is then the major etiological de- cardiomyopathies [1]. Now, 5 years later, method for clarifying the presence of terminant? itistimelyandappropriatetotakestock inflammation or fibrosis in addition to This issue also holds true for alcoholic of old and new data on this topic. function and pericardial effusion, but it cardiomyopathy [8]. In these patients, al- cannot substitute endomyocardial biopsy cohol consumption of more than 40 g/day Evolution of diagnoses for establishing an etiologically based di- in men and more than 20g/day in women agnosis [1–5]. For the diagnosis of viral formorethan5yearsisthesomewhat In 2013, experts of the European Soci- vs. autoreactive (nonviral) myocarditis arbitrary diagnostic determinant for the ety of Cardiology (ESC) working group and for the diagnosis of eosinophilic or label of alcoholic cardiomyopathy. -
Childhood Acquired Heart Diseases in Jos, North Central Nigeria
ORIGINAL ARTICLE Childhood acquired heart diseases in Jos, north central Nigeria Fidelia Bode-Thomas, Olukemi O. Ige, Christopher Yilgwan Department of Paediatrics, University of Jos, Jos, Nigeria ABSTRACT Background: The patterns of childhood acquired heart diseases (AHD) vary in different parts of the world and may evolve over time. We aimed to compare the pattern of childhood AHD in our institution to the historical and contemporary patterns in other parts of the country, and to highlight possible regional differences and changes in trend. Materials and Methods: Pediatric echocardiography records spanning a period of 10 years were reviewed. Echocardiography records of children with echocardiographic or irrefutable clinical diagnoses of AHD were identified and relevant data extracted from their records. Results: One hundred and seventy five children were diagnosed with AHD during the period, including seven that had coexisting congenital heart disease (CHD). They were aged 4 weeks to 18 years (mean 9.84±4.5 years) and comprised 80 (45.7%) males and 95 (54.3%) females. Rheumatic heart disease (RHD) was the cause of the AHD in 101 (58.0%) children, followed by dilated cardiomyopathy (33 cases, 18.9%) which was the most frequent AHD in younger (under 5 years) children. Other AHD encountered were cor pulmonale in 16 (9.1%), pericardial disease in 15 (8.6%), infective endocarditis in 8 (4.6%) and aortic aneurysms in 2 (1.1%) children. Only one case each of endomyocardial fibrosis (EMF) and Kawasaki Disease were seen during the period. Conclusions: The majority of childhood acquired heart diseases in our environment are still of infectious aeitology, with RHD remaining the most frequent, particularly in older children. -
Infections and the Cardiovascular System New Perspectives Emerging Infectious Diseases of the 21St Century
Infections and the Cardiovascular System New Perspectives Emerging Infectious Diseases of the 21st Century Series Editor: I. W. Fong Professor of Medicine, University of Toronto Head of Infectious Diseases, St. Michael’s Hospital INFECTIONS AND THE CARDIOVASCULAR SYSTEM: New Perspectives Edited by I. W. Fong Infections and the Cardiovascular System New Perspectives Edited by I. W. Fong Professor of Medicine, University of Toronto Head of Infectious Diseases, St. Michael's Hospital Toronto, Ontario, Canada KLUWER ACADEMIC PUBLISHERS NEW YORK, BOSTON, DORDRECHT, LONDON, MOSCOW eBook ISBN: 0-306-47926-5 Print ISBN: 0-306-47404-2 ©2004 Kluwer Academic Publishers New York, Boston, Dordrecht, London, Moscow Print ©2003 Kluwer Academic/Plenum Publishers New York All rights reserved No part of this eBook may be reproduced or transmitted in any form or by any means, electronic, mechanical, recording, or otherwise, without written consent from the Publisher Created in the United States of America Visit Kluwer Online at: http://kluweronline.com and Kluwer's eBookstore at: http://ebooks.kluweronline.com Preface Infectious agents have been recognized to involve the heart and vascular system for well over a century. Traditional concepts and teachings of their involvement in the pathogenesis of disease have been by a few established mechanisms. Bacterial and occasionally fungal microorganisms were known to invade and multiply on the endocardium of valves, vascular prostheses or shunts and aneurysm. Similarly viral, bacterial, mycobacterial, fungal, and parasitic pathogens could cause disease by invasion of the pericardium and muscles of the heart. Pathogenesis of some diseases of the endocardium, myocardium, and pericardium could involve indirect mechanisms with molecular mimicry inducing injury through an autoimmune process, such as in rheumatic heart disease and post viral cardiomyopathy. -
Currentstateofknowledgeonaetiol
European Heart Journal (2013) 34, 2636–2648 ESC REPORT doi:10.1093/eurheartj/eht210 Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases Downloaded from Alida L. P. Caforio1†*, Sabine Pankuweit2†, Eloisa Arbustini3, Cristina Basso4, Juan Gimeno-Blanes5,StephanB.Felix6,MichaelFu7,TiinaHelio¨ 8, Stephane Heymans9, http://eurheartj.oxfordjournals.org/ Roland Jahns10,KarinKlingel11, Ales Linhart12, Bernhard Maisch2, William McKenna13, Jens Mogensen14, Yigal M. Pinto15,ArsenRistic16, Heinz-Peter Schultheiss17, Hubert Seggewiss18, Luigi Tavazzi19,GaetanoThiene4,AliYilmaz20, Philippe Charron21,andPerryM.Elliott13 1Division of Cardiology, Department of Cardiological Thoracic and Vascular Sciences, University of Padua, Padova, Italy; 2Universita¨tsklinikum Gießen und Marburg GmbH, Standort Marburg, Klinik fu¨r Kardiologie, Marburg, Germany; 3Academic Hospital IRCCS Foundation Policlinico, San Matteo, Pavia, Italy; 4Cardiovascular Pathology, Department of Cardiological Thoracic and Vascular Sciences, University of Padua, Padova, Italy; 5Servicio de Cardiologia, Hospital U. Virgen de Arrixaca Ctra. Murcia-Cartagena s/n, El Palmar, Spain; 6Medizinische Klinik B, University of Greifswald, Greifswald, Germany; 7Department of Medicine, Heart Failure Unit, Sahlgrenska Hospital, University of Go¨teborg, Go¨teborg, Sweden; 8Division of Cardiology, Helsinki University Central Hospital, Heart & Lung Centre, -
CARDIOLOGY Section Editors: Dr
2 CARDIOLOGY Section Editors: Dr. Mustafa Toma and Dr. Jason Andrade Aortic Dissection DIFFERENTIAL DIAGNOSIS PATHOPHYSIOLOGY (CONT’D) CARDIAC DEBAKEY—I ¼ ascending and at least aortic arch, MYOCARDIAL—myocardial infarction, angina II ¼ ascending only, III ¼ originates in descending VALVULAR—aortic stenosis, aortic regurgitation and extends proximally or distally PERICARDIAL—pericarditis RISK FACTORS VASCULAR—aortic dissection COMMON—hypertension, age, male RESPIRATORY VASCULITIS—Takayasu arteritis, giant cell arteritis, PARENCHYMAL—pneumonia, cancer rheumatoid arthritis, syphilitic aortitis PLEURAL—pneumothorax, pneumomediasti- COLLAGEN DISORDERS—Marfan syndrome, Ehlers– num, pleural effusion, pleuritis Danlos syndrome, cystic medial necrosis VASCULAR—pulmonary embolism, pulmonary VALVULAR—bicuspid aortic valve, aortic coarcta- hypertension tion, Turner syndrome, aortic valve replacement GI—esophagitis, esophageal cancer, GERD, peptic OTHERS—cocaine, trauma ulcer disease, Boerhaave’s, cholecystitis, pancreatitis CLINICAL FEATURES OTHERS—musculoskeletal, shingles, anxiety RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT HAVE AN ACUTE THORACIC PATHOPHYSIOLOGY AORTIC DISSECTION? ANATOMY—layers of aorta include intima, media, LR+ LRÀ and adventitia. Majority of tears found in ascending History aorta right lateral wall where the greatest shear force Hypertension 1.6 0.5 upon the artery wall is produced Sudden chest pain 1.6 0.3 AORTIC TEAR AND EXTENSION—aortic tear may Tearing or ripping pain 1.2–10.8 0.4–0.99 produce -
Novel Ph1n1 Viral Cardiomyopathy Requiring Veno-Venous Extracorporeal Membrane Oxygenation
Novel pH1N1 viral cardiomyopathy requiring veno-venous extracorporeal membrane oxygenation Sujata Subramanian, MD; Jonna D. Clark, MD; Howard E. Jeffries, MD, MBA; D. Michael McMullan, MD Objective: To report a case of pH1N1 viral infection presenting Measurements and Main Results: Discovery of severe dilated as heart failure requiring mechanical extracorporeal life support. cardiomyopathy and respiratory failure. Design: Case report. Conclusions: Patients with pH1N1 may present in profound Setting: Pediatric intensive care unit at a regional children’s hospital. heart failure in addition to respiratory failure. Extracorporeal Patient: Obese 14-yr-old boy who presented with pH1N1-related membrane oxygenation may play an important role in manag- cardiomyopathy and respiratory failure that required extracorporeal ing these complex patients. (Pediatr Crit Care Med 2011; 12: membrane oxygenation. 000–000) Interventions: Extracorporeal membrane oxygenation, echo- KEY WORDS: pH1N1; swine flu; cardiomyopathy; extracorporeal cardiography, high-frequency oscillating ventilation. membrane oxygenation; obesity; children ince the first North American presenting in acute heart failure due to phy. These findings prompted transtho- cases of novel pH1N1 influenza novel viral myocarditis. racic echocardiography, which revealed A were described in April 2009 severe dilated cardiomyopathy with an es- (1), the Centers for Disease Case Summary timated 15% to 20% left ventricular ejec- SControl estimates that, as of December tion fraction. Laboratory studies were 2009, there have been between 39–80 The Institutional Review Board of Se- significant for elevated serum creatinine million cases in the United States. The attle Children’s Hospital approved this (1.3 mg/dL), B-type natriuretic peptide clinical spectrum of novel pH1N1 infec- project and provided exemption to the (1031 pg/mL; normal, Ͻ100 pg/mL), and tion ranges from mild upper respiratory requirement of informed consent. -
Consensus Statement on Endomyocardial Biopsy
Cardiovascular Pathology 21 (2012) 245–274 Original Article 2011 Consensus statement on endomyocardial biopsy from the Association for European Cardiovascular Pathology and the Society for Cardiovascular Pathology ⁎ ⁎ Ornella Leone a, , John P. Veinot b, , Annalisa Angelini c, Ulrik T. Baandrup d, Cristina Basso c, Gerald Berry e, Patrick Bruneval f, Margaret Burke g, Jagdish Butany h, Fiorella Calabrese c, Giulia d'Amati i, William D. Edwards j, John T. Fallon k, Michael C. Fishbein l, Patrick J. Gallagher m, Marc K. Halushka n, Bruce McManus o, Angela Pucci p, E. René Rodriguez q, Jeffrey E. Saffitz r, Mary N. Sheppard g, Charles Steenbergen n, James R. Stone r, Carmela Tan q, Gaetano Thiene c, Allard C. van der Wal s, Gayle L. Winters r aBologna, Italy bOttawa, Ontario, Canada cPadua, Italy dHjoerring, Denmark eStanford, CA, USA fParis, France gLondon, UK hToronto, Ontario, Canada iRome, Italy jRochester, MN, USA kNew York, NY, USA lLos Angeles, CA, USA mSouthampton, UK nBaltimore, MD, USA oVancouver, BC, Canada pPisa, Italy qCleveland, OH, USA rBoston, MA, USA sAmsterdam, The Netherlands Received 3 August 2011; received in revised form 28 September 2011; accepted 7 October 2011 Abstract The Association for European Cardiovascular Pathology and the Society for Cardiovascular Pathology have produced this position paper concerning the current role of endomyocardial biopsy (EMB) for the diagnosis of cardiac diseases and its contribution to patient management, focusing on pathological issues, with these aims: • Determining appropriate EMB use in the context of current diagnostic strategies for cardiac diseases and providing recommendations for its rational utilization ⁎ Corresponding authors. O. Leone is to be contacted at U.O. -
Heart Failure and Mouse Models
Disease Models & Mechanisms 3, 138-143 (2010) doi:10.1242/dmm.005017 CLINICAL PUZZLE © 2010. Published by The Company of Biologists Ltd Heart failure and mouse models Ross Breckenridge1,* Heart failure is a common, complex condition with a poor prognosis and increasing couraged in heart failure for many years on the basis of studies showing increased mor- incidence. The syndrome of heart failure comprises changes in electrophysiology, tality when given to acutely unwell patients contraction and energy metabolism. This complexity, and the interaction of the (Braunwald and Chidsey, 1965). Subse- clinical syndrome with very frequently concurrent medical conditions such as quently, blockers have been found to be diabetes, means that animal modelling of heart failure is difficult. The current animal beneficial when used in relatively low doses models of heart failure in common use do not address several important clinical in stable heart failure patients (CIBIS, 1999). problems. There have been major recent advances in the understanding of cardiac An increasingly commonly recognised biology in the healthy and failing myocardium, but these are, as yet, unmatched variant of heart failure is ‘diastolic’ or ‘sys- tolic function preserved’ heart failure, char- by advances in therapeutics. Arguably, the development of new animal models acterised by resistance to ventricular filling of heart failure, or at least adaptation of existing models, will be necessary to fully rather than defective contraction (Dodek et translate scientific advances in this area into new drugs. This review outlines the al., 1972; Zile et al., 2004). As the com- DMM mouse models of heart failure in common usage today, and discusses how monest causes of diastolic heart failure are adaptations in these models may allow easier translation of animal experimentation ischaemia, obesity, hypertension, diabetes into the clinical arena. -
Cardiology 2
Ch02.qxd 7/5/04 3:06 PM Page 13 Cardiology 2 FETAL CARDIOVASCULAR PHYSIOLOGY The ‘basic science’ nature of this topic – as well as the potential pathological implications in paediatric cardiology – makes it a likely viva question. Oxygenated blood from the placenta returns to the fetus via the umbilical vein (of which there is only one). Fifty per cent traverses the liver and the remaining 50% bypasses the liver via the ductus venosus into the inferior vena cava. In the right atrium blood arriving from the upper body from the superior vena cava (low oxygen saturation) preferentially crosses the tricus- pid valve into the right ventricle and then via the ductus flows into the descending aorta and back to the placenta via the umbilical arteries (two) to reoxygenate. The relatively oxygenated blood from the inferior vena cava, however, preferentially crosses the foramen ovale into the left atrium and left ventricle to be distributed to the upper body (including the brain and coro- nary circulation). Because of this pattern of flow in the right atrium we have highly oxygenated blood reaching the brain and deoxygenated blood reach- ing the placenta. High pulmonary arteriolar pressure ensures that most blood traverses the pulmonary artery via the ductus. Changes at birth 1. Occlusion of the umbilical cord removes the low-resistance capillary bed from the circulation. 2. Breathing results in a marked decrease in pulmonary vascular resistance. 3. In consequence, there is increased pulmonary blood flow returning to the left atrium causing the foramen ovale to close. 4. Well-oxygenated blood from the lungs and the loss of endogenous prostaglandins from the placenta result in closure of the ductus arteriosus.