ATRIALSEPTALDEFECT EditedbyP.SyamasundarRao Atrial Septal Defect Edited by P. Syamasundar Rao Published by InTech Janeza Trdine 9, 51000 Rijeka, Croatia Copyright © 2012 InTech All chapters are Open Access distributed under the Creative Commons Attribution 3.0 license, which allows users to download, copy and build upon published articles even for commercial purposes, as long as the author and publisher are properly credited, which ensures maximum dissemination and a wider impact of our publications. After this work has been published by InTech, authors have the right to republish it, in whole or part, in any publication of which they are the author, and to make other personal use of the work. Any republication, referencing or personal use of the work must explicitly identify the original source. As for readers, this license allows users to download, copy and build upon published chapters even for commercial purposes, as long as the author and publisher are properly credited, which ensures maximum dissemination and a wider impact of our publications. Notice Statements and opinions expressed in the chapters are these of the individual contributors and not necessarily those of the editors or publisher. No responsibility is accepted for the accuracy of information contained in the published chapters. The publisher assumes no responsibility for any damage or injury to persons or property arising out of the use of any materials, instructions, methods or ideas contained in the book. Publishing Process Manager Ivona Lovric Technical Editor Teodora Smiljanic Cover Designer InTech Design Team First published April, 2012 Printed in Croatia A free online edition of this book is available at www.intechopen.com Additional hard copies can be obtained from orders@intechopen.com Atrial Septal Defect, Edited by P. Syamasundar Rao p. cm. ISBN 978-953-51-0531-2 Contents Preface IX Section 1 General Review of Atrial Septal Defects 1 Chapter 1 Atrial Septal Defect – A Review 3 P. Syamasundar Rao Chapter 2 Pregnancy Issues in Women with Atrial Septal Defect 21 Duraisamy Balaguru Section 2 Natural History 29 Chapter 3 Prevalence of Secundum Atrial Septal Defect and Associated Findings 31 Mark D. Reller Section 3 Creation of ASDs 37 Chapter 4 Computer-Aided Automatic Delivery System of High-Intensity Focused Ultrasound for Creation of an Atrial Septal Defect 39 Hiromasa Yamashita, Gontaro Kitazumi, Keri Kim and Toshio Chiba Section 4 Transcatheter Closure of ASD 55 Chapter 5 Historical Aspects of Transcatheter Occlusion of Atrial Septal Defects 57 Srilatha Alapati and P. Syamasundar Rao Chapter 6 Role of Transesophageal Echocardiography in Transcatheter Occlusion of Atrial Septal Defects 85 Gurur Biliciler-Denktas VI Contents Chapter 7 Role of Intracardiac Echocardiography (ICE) in Transcatheter Occlusion of Atrial Septal Defects 99 Ismael Gonzalez, Qi-Ling Cao and Ziyad M. Hijazi Section 5 ASD Closure in Adults and Elderly 119 Chapter 8 Why, When and How Should Atrial Septal Defects Be Closed in Adults 121 P. Syamasundar Rao Chapter 9 Atrial Septal Defect Closure in Geriatric Patients 139 Teiji Akagi Section 6 Patent Foramen Ovale 153 Chapter 10 Atrial Septal Defect/Patent Foramen Ovale and Migraine Headache 155 Mohammed Tawfiq Numan Chapter 11 Transcatheter Occlusion of Atrial Septal Defects for Prevention of Recurrence of Paradoxical Embolism 167 Nicoleta Daraban, Manuel Reyes and Richard W. Smalling Preface Defectsintheatrialseptumareonethemostcommontypesofcongenitalheartdefects (CHDs)inchildrenandsuchadefectisthemostcommonCHDinadults.Atrialseptal defects(ASDs)causeleftto right shunt beca use the left atrial pressure is higher than that inthe right atrium. Th iscausesvolume overloadingofthe right ventricle. While thisisgenerallywelltoleratedduringinfancyandchildhood,developmentofexercise intolerance and arrhythmias in later childhood, adolescence and adulthood, and the risk for development of pulmonary vascular obstructive disease in adulthood make thesedefectsimportant.Themajortypesofatrialdefectsareostiumsecundum,ostium primum,sinusvenosusandcoronarysinusASDsandpatentforamenovale(PFO). In the first chapter, I review the clinical features and management of ASDs. Patients with small defects are usually asymptomatic while moderate to large defects may presentwithsymptoms. Physicalfindingsincludehyperdynamicprecor dium,widely split and fixed second heart sound, ejectionsystolicmurmur at the left upper sternal border and a mid‐diastolic flow rumble at the left lower sternal border. In patients withostiumprimumASDs,anapicalholosystolicmurmurmayalsobeheard.Clinical diagnosis is not difficult and the diagnosis can be confirmed and quantified by echocardiographic studies. While surgical intervention was used in the past, transcatheter methods are currently used for closure of ostium secundum ASDs. Surgical correction is necessary for the ostium primum, sinus venosus and coronary sinusdefects.PFOispresentinnearlyonethirdofnormalpopulationandislik elyto beanormalvariantandsuchisolatedPFOsdonotneedintervention. Whenassociated with other CHDs, the PFO facilitates intra‐cardiac shunt to allow appropriate egress and/or mixing of blood flow. Hypoxemia in post‐surgical residual defects including Fontan fenestrations, right ventricular infarction and platypnea‐orthodexia syndrome maybesecondarytorighttoleftshuntacrossPFOandthesedefectsmayneedclosure. PFO, presumed to be the seat of paradoxical embolism resulting in stroke/transient ischemic attacks is the subject active investigation. Similarly the role of PFO in Caisson’s disease and migraine is not well‐establi shed. There is varying degrees of evidenceforbenefitoftranscatheterocclusionofthesePFOs. In the second chapter, Dr. Balaguru from the University of Texas Medical School, Houston, Texas discusses issues related to ASD in pregnant women. There are remarkable changes in cardiovascular physiology during pregnancy; the cardiac X Preface output increases, related to increased stroke volume and heart rate. The systemic vascular resistance decreases; however, concurrent increase in cardiac output keeps blood pressure stable. The blood volume increases (by 1.5 times) by raise in plasma volume; however, this is out of proportion to the increase in red cell mass with consequent relative anemia. These changes are tolerated well because the changes occu r gradually. During the third trimester, enlarging uterus compresses the inferior vena cava (IVC) in supine posture leading to decrease in cardiac output and predisposestodeepveinthrombosis.InpregnantwomenwithASD,thereisagreater increase in rig ht atrial and right ventricular size (compared to pregnant women with no heart defect) and a higher incidence of supraventricular tachycardia. The probability of paradoxical embolism via the ASD is high given the predisposition to deep vein thrombosis and hypercoagulable state.If the diagnosis is known prior to pregnancy and the ASD is larg e and associated with moderate or severe right heart enlargement and is a potential candidate for supraventricular tachycardia and thromboembolic events during pregnancy, labor or postpartum, the ASD should be closed prior to planned‐pregnancy. Transcatheter or surgical closure could be performedbasedonthesizeoftheASDandadequacyofseptalrims.WhentheASD is diagnosed during pregnancy but, the patient is asymptomatic without functional compromise (NYHA Class I and II) and has no heart failure, atrial arrhythmia, pulmonary hypertension or history of stroke, the these women are likely to do well throughout pregnancy and do not require transcatheter or su rgical closure. On the contrary, in the presence ofany of these issues, transcatheteror surgicalclosuremay be performed. If transcatheter is opted, second trimester (13‐28 weeks) is preferred instead of first trimester to avoid irradiation to the fetus. Local anesthesia with conscious sedation, intracardiac echocardiography to aid balloon sizing and device deployment and use of long venous sheath; the latter two to avoid or reduces radiation, may be appropriate. If the ASD is unsuitable for transcatheter closure, surgicalclosureofASDmaybeperformedinthesecond trimesterwith thefollowing precautions: infusion of high‐concentration of gl ucose (to provide energy for fetus), fetal monitoring, maintenance of high‐flow, high mean arterial pressure (60 mmHg) and high hematocrit (> 25%) and hyper oxygenation. The author concludes that the need for closure of ASD during pregnancy is rare and if possible avoided. When closure is indicated transcatheter or surgical closure may be performed, taking appropriateprecautions. InthethirdchapterRellerfromOregonHealth&ScienceUniversity,Portland,Oregon reviews data on the prevalence, associated cardiac and non‐cardiac findings and naturalhistoryofsecundumASDs,definedassizegreaterthan4mm.Theprevalence ofsecu ndumASDisestimated to be10.3per10,000births, prevalence comparable to thatofperi‐membranousventricular septaldefects.Theincreaseinthe prevalenceof secundumASDwasattributedtoevaluationbycolorflowDoppler‐echocardiography. Theassociationof secundumASDwithperi‐membranous VSDandvalvar pulmonary stenosisiswellrecognized.The cau se(s)ofsecundumASDremain largely unknown. Genetic syndromes associated with secundum ASD include Trisomy 21, 13 and 18; . ATRIAL SEPTAL DEFECT Edited by P. Syamasundar Rao Atrial Septal Defect Edited by P. Syamasundar Rao Published by InTech Janeza Trdine. Septal Defect, Edited by P. Syamasundar Rao p. cm. ISBN 978-953-51-0531-2 Contents Preface IX Section 1 General Review of Atrial Septal Defects 1 Chapter 1 Atrial Septal. Occlusion of Atrial Septal Defects 57 Srilatha Alapati and P. Syamasundar Rao Chapter 6 Role of Transesophageal Echocardiography in Transcatheter Occlusion of Atrial Septal Defects 85 Gurur