AbstractBackground:Limited data exist on training of European paediatric and adult congenital cardiologists.Methods:A structured and approved questionnaire was circulated to national delegates of Association for European Paediatric and Congenital Cardiology in 33 European countries.Results:Delegates from 30 countries (91%) responded. Paediatric cardiology was not recognised as a distinct speciality by the respective ministry of Health in seven countries (23%). Twenty countries (67%) have formally accredited paediatric cardiology training programmes, seven (23%) have substantial informal (not accredited or certified) training, and three (10%) have very limited or no programme. Twenty-two countries have a curriculum. Twelve countries have a national training director. There was one paediatric cardiology centre per 2.66 million population (range 0.87–9.64 million), one cardiac surgical centre per 4.73 million population (range 1.63–10.72 million), and one training centre per 4.29 million population (range 1.63–10.72 million population). The median number of paediatric cardiology fellows per training programme was 4 (range 1–17), and duration of training was 3 years (range 2–5 years). An exit examination in paediatric cardiology was conducted in 16 countries (53%) and certification provided by 20 countries (67%). Paediatric cardiologist number is affected by gross domestic product (R2 = 0.41).Conclusion:Training varies markedly across European countries. Although formal fellowship programmes exist in many countries, several countries have informal training or no training. Only a minority of countries provide both exit examination and certification. Harmonisation of training and standardisation of exit examination and certification could reduce variation in training thereby promoting high-quality care by European congenital cardiologists.

Background: Limited data exist on training of European paediatric and adult congenital cardiologists. Methods: A structured and approved questionnaire was circulated to national delegates of Association for European Paediatric and Congenital Cardiology in 33 European countries. Results: Delegates from 30 countries (91%) responded. Paediatric cardiology was not recognised as a distinct speciality by the respective ministry of Health in seven countries (23%). Twenty countries (67%) have formally accredited paediatric cardiology training programmes, seven (23%) have substantial informal (not accredited or certified) training, and three (10%) have

OBJECTIVES:To report the numbers of consultant congenital cardiac surgeons and cardiologists who have joined and left UK practice over the last 10 years and explore the reasons for leaving. METHODS:Retrospective observational questionnaire study completed between 11 June 2019 and 1 July 2020 by UK level 1 congenital cardiac centres of 10-year consultant staff movement and reasons suggested for leaving UK practice. RESULTS:At survey completion there were 218 (202 whole time equivalent (WTE)) consultant cardiologists and surgeons working within level 1 centres made up of 39 (38 WTE) surgeons, 137 (128.5 WTE) paediatric cardiologists, 42 (35.5 WTE) adult congenital heart disease (ACHD) cardiologists. 161 (74%) consultants joined in the last 10 years of whom 103 (64%) were UK trained. There were 91 leavers giving a staff turnover rate 42% (surgeons 56%, paediatric cardiologists 42%, ACHD cardiologists 29%). Of those, leaving 43% moved to work abroad (surgeons 55%, paediatric cardiologists 40%, ACHD cardiologists 67%). Among the 65 reported reasons for leaving 16 were financial, 9 for work life balance, 6 to working conditions within the National Health Service (NHS) and 12 related to the profession in the UK including six specifically highlighting the national review process. CONCLUSIONS:There has been a high turnover rate of consultant staff within UK congenital cardiac services over the last 10 years with almost half of those leaving moving to work overseas. Financial reasons and pressures relating to working in the NHS or the specialty in the UK were commonly reported themes for leaving. This has major implications for future planning and staff retention within this specialised service.

Transcatheter therapy for partial anomalous pulmonary venous connection with dual drainage is unique and rarely reported. We report a 69-year-old female with recurrent brain abscess and partial anomalous connection of the left upper pulmonary vein with dual drainage to the vertical vein (VV) and left atrium (LA). Transcatheter occlusion of the VV was done using an 18-mm St. Jude Amplatzer Vascular Plug II, thus redirecting the left-sided pulmonary venous drainage to LA. Careful evaluation of partial anomalous pulmonary venous drainage with cross-sectional imaging is essential to allow the delineation of dual connections, enabling a less invasive transcatheter treatment approach.

Persistence of the embryonic "fifth aortic arch" in postnatal life is a rare, enigmatic - and at times controversial - condition, with variable anatomical forms and physiological consequences. First described in humans over 40 years ago by Van Praagh, the condition was labelled the "great pretender" by Gerlis 25 years later, because of its apparent propensity to mimic anatomically similar structures. Despite many subsequent case reports citing the condition, the true developmental origin of these structures remains unresolved, and has been the subject of debate among embryologists for more than a century. A persistent fifth aortic arch has been defined as an extrapericardial structure, arising from the ascending aorta opposite or proximal to the brachiocephalic artery, and terminating in the dorsal aorta or pulmonary arteries via a persistently patent arterial duct. This description may therefore encompass various anatomical forms, such as a unilateral double-lumen aortic arch, an unrestrictive aortopulmonary shunt, or a critical vascular channel for either the systemic or pulmonary circulation. The physiological properties of these vessels, such as their response to prostaglandins, may also be unpredictable. In this article, we demonstrate a number of cases that fulfil the contemporary definition of "persistent fifth aortic arch" while acknowledging the embryological controversies associated with this term. We also outline the key diagnostic features, particularly with respect to the use of new cross-sectional imaging techniques.

Here, we report a four-day old neonate presenting with cardiovascular collapse secondary to a descending aorta to right atrial fistula. Echocardiography was suggestive of the diagnosis and confirmed with computed tomographic (CT) imaging. The fistula was successfully occluded via cardiac catheterization using an Amplatzer Vascular Plug II implanted from the right atrial aspect. This report includes the first CT imaging of this extremely rare congenital defect as well as detailing the first successful transcatheter occlusion of this particular lesion.

Aims: The pathophysiological entity of a persisting left-sided superior caval vein draining into the roof of the left atrium represents an extreme form of coronary sinus de-roofing. This is an uncommon, but well-documented condition associated with systemic desaturation due to a right-to-left shunt. Depending on the size of the coronary ostium, the defect may also present with right-sided volume loading. We describe two patients, both of whom presented with desaturation, and highlight the important anatomical features underscoring management. Methods and Results: Both patients were managed interventionally with previous assessment of the size of the coronary sinus ostium through cross-sectional imaging. This revealed a restrictive interatrial communication at the right atrial mouth of the coronary sinus in both patients, which permitted an interventional approach, as the residual left-to-right shunt subsequent to closure of the aberrant vessel would be negligible. At intervention, test occlusion of the left superior caval vein allowed assessment of decompressing vessels before successful occlusion using an Amplatzer Vascular Plug. Conclusions: Persistence of a left superior caval vein draining to the left atrium may be associated with an interatrial communication at the mouth of the unroofed coronary sinus. The ostium of the de-roofed coronary sinus can be atretic, restrictive, normally sized, or enlarged. Careful assessment of the size of this defect is required before treatment. In view of its importance, which has received little attention in the literature to date, we suggest an additional consideration to the classification of unroofed coronary sinus.

CHD is associated with poor growth, delayed motor and language skills development, and increased length of hospital stay; 28.2% of infants were stunted, with z-scores<-2. The severity of surgery score was not associated with an increased length of stay, suggesting that a low weight-for-age z-score at the time of surgery may impact on length of stay.

Introduction: Sildenafil (Revatio®) and tadalafil (Adcirca®) are specific inhibitors of the phosphodiesterase-5 enzyme and produce pulmonary vasodilation by inhibiting the breakdown of cyclic guanosine monophosphate (cGMP) in the walls of pulmonary arterioles.Areas covered: We focus on the efficacy and safety of sildenafil and tadalafil in the treatment of pulmonary hypertension (PH) in children through a PubMed literature search.Expert opinion: Although used since 1999 in the treatment of PH in children, it is only in the past few years that robust evidence for the use of sildenafil has emerged principally in the pivotal STARTS-1 study. The open-label extension of this study, STARTS-2, has revealed safety concerns substantiated by FDA post marketing surveillance leading to recommendations to use lower doses. More recently, tadalafil has been introduced allowing once daily dosing with apparently similar efficacy to sildenafil in children. Recently there have been suggestions that sildenafil and tadalafil may have a place in treating muscular dystrophy.

We present a neonate with an antenatal diagnosis of Scimitar syndrome and aortic arch hypoplasia. After delivery, computerised tomography scan additionally revealed an anomalous origin of the circumflex coronary artery from the main pulmonary artery. The management of this rare combination is discussed.

Chapter 21 Primary Pulmonary Arterial Hypertension in Children Alan G. Magee BSc, MRCP, MB, BCh (Hons), FRCP, Alan G. Magee BSc, MRCP, MB, BCh (Hons), FRCP Royal Brompton Hospital, London, UKSearch for more papers by this author Alan G. Magee BSc, MRCP, MB, BCh (Hons), FRCP, Alan G. Magee BSc, MRCP, MB, BCh (Hons), FRCP Royal Brompton Hospital, London, UKSearch for more papers by this author Book Editor(s):Piers E. F. Daubeney MA, DM, FRCP, FRCPCH, Piers E. F. Daubeney MA, DM, FRCP, FRCPCH Royal Brompton Hospital, London, UK National Heart and Lung Institute, Imperial College, London, UKSearch for more papers by this authorMichael L. Rigby MD, FRCP, FRCPCH, Michael L. Rigby MD, FRCP, FRCPCH Royal Brompton Hospital, London, UKSearch for more papers by this authorKoichiro Niwa MD, PhD, FACC, FAHA, Koichiro Niwa MD, PhD, FACC, FAHA Department of Cardiology, Cardiovascular Center, St Luke's International Hospital, Tokyo, JapanSearch for more papers by this authorMichael A. Gatzoulis MD, PhD, FACC, FESC, Michael A. Gatzoulis MD, PhD, FACC, FESC Royal Brompton Hospital, London, UK National Heart and Lung Institute, Imperial College, London, UKSearch for more papers by this author First published: 24 August 2012 https://doi.org/10.1002/9781444360981.ch21 AboutPDFPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShareShare a linkShare onEmailFacebookTwitterLinkedInRedditWechat Summary This chapter contains sections titled: Incidence and etiology Clinical features Investigations Management Prognosis Further reading Further reading Barst RJ, Rubin LJ, Long WA, et al. A comparison of continuous intravenous epoprostenol (prostacyclin) with conventional therapy for primary pulmonary hypertension. The primary pulmonary hypertension study group. N Engl J Med 1996; 334: 296–302. 10.1056/NEJM199602013340504 CASPubMedWeb of Science®Google Scholar Barst RJ, Ivy D, Dingemanse J, et al. Pharmacokinetics, safety and efficacy of bosentan in paediatric patients with pulmonary arterial hypertension. Clin Pharmacol Ther 2003; 73: 372–382. 10.1016/S0009-9236(03)00005-5 CASPubMedWeb of Science®Google Scholar D'Alonzo GE, Barst RJ, Ayers SM, et al. Survival in patients with primary pulmonary hypertension. Results from a national prospective registry. Ann Intern Med 1991; 115: 343–349. 10.7326/0003-4819-115-5-343 PubMedWeb of Science®Google Scholar Klepetko W, Mayer E, Sandoval J, et al. Interventional and surgical modalities of treatment for pulmonary arterial hypertension. J Am Coll Cardiol 2004; 43 (Suppl S): 73S–80S. 10.1016/j.jacc.2004.02.039 PubMedWeb of Science®Google Scholar Moledina S, Hislop AA, Foster H, Schulze-Neick I, Haworth SG. Childhood idiopathic pulmonary hypertension: a national cohort Study. Heart 2010; 96: 1401–1406. 10.1136/hrt.2009.182378 CASPubMedWeb of Science®Google Scholar Rich S, Kaufmann E, Levy PS. The effect of high doses of calcium-channel blockers on survival in primary pulmonary hypertension. N Engl J Med 1992; 327: 76–81. 10.1056/NEJM199207093270203 CASPubMedWeb of Science®Google Scholar The Task Force for the Diagnosis and Treatment of Pulmonary Hypertension of the European Society of Cardiology (ESC) and the European Respiratory Society (ERS). Guidelines for the diagnosis and treatment of pulmonary hypertension. European Heart Journal 2009; 30: 2493–2537. 10.1093/eurheartj/ehp297 PubMedWeb of Science®Google Scholar Thompson JR, Machado RD, Pauciulo MW, et al. Sporadic primary pulmonary hypertension is associated with germline mutations in BMPR2, a receptor member of the TGF-beta family. J Med Genet 2000; 37: 741–745. 10.1136/jmg.37.10.741 PubMedWeb of Science®Google Scholar Pediatric Heart Disease: A Practical Guide ReferencesRelatedInformation

A 13-year-old boy was referred to cardiology for evaluation of intermittent exertional breathlessness. Previous respiratory investigations had revealed normal lung function and no evidence of asthma on exercise spirometry. There was no past medical history of note. Cardiorespiratory examination was unremarkable except for a soft ejection systolic murmur at the lower left sternal border. ECG showed sinus rhythm and normal P-wave morphology and QRS axis, with a T-wave inversion in leads III and aVF. Chest radiograph demonstrated normal cardiothoracic ratio, but the heart was noted to be globular in shape (Figure 1). Transthoracic echocardiography revealed the presence of a large, thin-walled aneurysmal structure in continuity with the free wall of the right atrium, discrete from the caval veins (Figure 2). There was mild tricuspid regurgitation, with a Doppler velocity of 2.1 m/s. Both ventricles were of normal size and function. To further characterize this cardiac abnormality, the patient was referred for cardiac magnetic resonance (CMR) imaging. Cine imaging using a balanced steady-state free precession sequence showed a noncontractile, smooth-walled, right atrial appendage aneurysm (RAAA) extending anterior to the body of the right atrium (Figure 3A and 3B and Movie I of the online-only Data Supplement). The aneurysm had a broad-based pyramidal shape and was partially separated from the main atrial chamber by a membrane (total indexed right atrial volume 118 mL/m at end-ventricular systole). There was mild distortion of the right ventricular (RV) inlet, but no significant compression. No intracavity thrombus was identified. The pulmonary arteries were unobstructed and of normal caliber. There was a small pericardial effusion. The patient subsequently underwent exercise tolerance testing, managing 12 minutes and 15 seconds on the standard Bruce protocol and achieving a workload of 13.8 metabolic equivalents. The test was stopped because of dyspnea, with no ST-segment changes detected. A 1-week cardiac rhythm monitor revealed no evidence of arrhythmia. On review in the outpatient clinic, the patient had symptomatically improved. He was therefore commenced on aspirin for thromboembolic prophylaxis and managed conservatively with annual imaging surveillance.

Complex atrial septal anatomy can continue to present a challenge for transcatheter closure. We present the successful use of overlapping GORE® HELEX atrial septal defect occluders in an adult patient with five distinct fenestrations in an aneurismal septum and how 3D echo can aid device positioning. © 2011 Wiley Periodicals, Inc.

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Total anomalous pulmonary venous connection to the inferior vena cava is a rare form of total anomalous pulmonary venous connection infrequently described in the literature. We report two cases where the pulmonary venous connection was to the supradiaphragmatic portion of the inferior vena cava. In both patients, preoperative echocardiography findings were misleading, which suggested a cardiac type of total anomalous pulmonary venous connection.

HomeCirculationVol. 116, No. 6Myocarditis and Sudden Cardiac Death in the Young Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessReview ArticlePDF/EPUBMyocarditis and Sudden Cardiac Death in the YoungExtensive Fibrosis Suggested by Cardiovascular Magnetic Resonance In Vivo and Confirmed Post Mortem Sonya V. Babu-Narayan, Karen P. McCarthy, Siew Yen Ho, Alan G. Magee, Philip J. Kilner and Mary N. Sheppard Sonya V. Babu-NarayanSonya V. Babu-Narayan From the Royal Brompton Hospital and the National Heart and Lung Institute, Imperial College, London, United Kingdom. Search for more papers by this author , Karen P. McCarthyKaren P. McCarthy From the Royal Brompton Hospital and the National Heart and Lung Institute, Imperial College, London, United Kingdom. Search for more papers by this author , Siew Yen HoSiew Yen Ho From the Royal Brompton Hospital and the National Heart and Lung Institute, Imperial College, London, United Kingdom. Search for more papers by this author , Alan G. MageeAlan G. Magee From the Royal Brompton Hospital and the National Heart and Lung Institute, Imperial College, London, United Kingdom. Search for more papers by this author , Philip J. KilnerPhilip J. Kilner From the Royal Brompton Hospital and the National Heart and Lung Institute, Imperial College, London, United Kingdom. Search for more papers by this author and Mary N. SheppardMary N. Sheppard From the Royal Brompton Hospital and the National Heart and Lung Institute, Imperial College, London, United Kingdom. Search for more papers by this author Originally published7 Aug 2007https://doi.org/10.1161/CIRCULATIONAHA.107.693085Circulation. 2007;116:e122–e125A 15-year-old male presented clinically with myocarditis. At follow-up, a 12-lead ECG (Figure 1A) and chest x-ray were performed (Figure 1B). Echocardiography was reported to show at least mildly impaired left ventricular function, and cardiovascular magnetic resonance (CMR) demonstrated a severely dilated impaired left ventricle (end-diastolic volume index, 160 mL/m2; ejection fraction, 42%), normal proximal coronary arteries, and a pattern of late gadolinium enhancement (LGE) which indicated extensive myocardial scarring as a result of myocarditis (Figure 2). The patient remained asymptomatic. Unfortunately, he died suddenly 2 years later. The post mortem distribution of scarring was concordant with the in vivo CMR LGE findings. Download figureDownload PowerPointFigure 1. A, 12 lead ECG demonstrates sinus arrhythmia with a single junctional beat and normal axis. Peaked T waves of uncertain significance are noted. B, Chest x-ray showed a cardiothoracic ratio of 0.47.Download figureDownload PowerPointFigure 2. The 12-panel figure shows echocardiographic images in the left column (from top to bottom) in parasternal long-axis, basal short-axis, mid short-axis, and apical short-axis orientations. Cine CMR images in corresponding planes are shown in the middle column with late gadolinium imaging in the right column. Of note, the cine CMR images clearly show thinning of the lateral wall with dyskinetic wall motion toward the apex, a region of the heart well documented by CMR, even in adults. Pathological changes that affect the apex of the heart can be more difficult to image with echocardiography. Finally, in the right column, images after contrast provided more information. Normal myocardium appears black, and scarred myocardium appears white. Full-thickness scarring was associated with thinning and wall motion abnormality, but small patches of scarring, particularly of the papillary muscle, could not have been suspected from the echocardiographic or CMR cine images alone.CMR inversion recovery images acquired late after application of paramagnetic contrast agents provide a sensitive tool for detection of myocardial fibrosis, which is distinguished by bright late-enhancement regions where the contrast lingers in the extracellular spaces of scarred myocardium. In our patient, full-thickness late enhancement of the lateral wall was seen (Figure 3, A, B, C, and D(i)) with a corresponding wall motion abnormality. Anterolateral papillary muscle scarring (Figure 3, B(i) and D(i), dotted arrows) was noted. If seen in isolation, these findings would be compatible with ischemic heart disease etiology, but additional patchy foci of enhancement in the septum and regions of patchy LGE with sparing of the subendocardium were also demonstrated suggesting nonischemic cardiomyopathy (Figures 3, C(i) and D(i), and 4A(i), dashed arrows). Fibrosis after ischemic infarction includes the subendocardial layer of the myocardium. The patchy foci, epicardial LGE regions, and lateral wall distribution favored a CMR diagnosis of previously established myocarditis. Download figureDownload PowerPointFigure 3. LGE CMR images in [A(i), B(i), C(i), D(i)] shown with comparable heart specimen images beneath [A(ii), B(ii), C(ii), D(ii)] with corresponding areas of pathology indicated with arrows. The pale areas seen in the heart specimens are areas of fibrosis.Download figureDownload PowerPointFigure 4. LGE CMR image [A(i)) with corresponding histology inset (A(ii)] and further histology corresponding to lateral, patchy, epicardial LGE (B). The samples are stained with Picro Sirius red, which highlights collagen as a deep red/purple stain, in contrast to muscle, which appears relatively yellow.Patchy fibrotic change was confirmed post mortem, consistent with myocarditis as clinically suspected (Figures 3 and 4). The coronary arteries were normal. In view of the extensive myocardial structural abnormality with no other abnormal findings and the patient’s sudden death, the likely cause of death was concluded to be cardiac. The in vivo CMR findings correlated with the pathological appearances of the heart post mortem, as shown when comparing Figure 3, A, B, C, D (i) showing regions of LGE with Figure 3, A, B, C, D (ii), showing corresponding pathological sections. Figure 4, A(i) shows areas of LGE with corresponding histology Figure 4, A(ii), B.In Europe, viral infections represent the most important cause of myocarditis, though in chronic myocarditis viremia is often absent. Even when inflammatory changes of the myocardium are asymptomatic, as in most cases, myocardial fibrosis and dilated cardiomyopathy can occur, which results in heart failure. If at autopsy the subendocardial layer of the myocardium is not involved in the fibrosis, ischemic infarction is unlikely and can be excluded as a differential diagnosis of sudden death in the young in the vast majority of affected patients.Although there were macroscopic abnormalities in our case, these are not always found at autopsy after sudden death as a result of myocarditis. Extensive histological screening is required to reveal isolated areas of myocardial fibrosis that may be related to myocarditis. In patients with acute or chronic myocarditis, arrhythmia may be the only clinical symptom in the natural course of the disease. Factors responsible for the increased incidence of cardiac arrhythmias include structural changes, ventricular hemodynamics, and vascular changes. The potentially malignant tachyarrhythmias and bradyarrhythmias caused by myocarditis are of particular concern. Acutely, inflammatory processes in the cardiac myocytes and interstitium can lead directly to fluctuations in membrane potential, hence arrythmogenesis. Later, fibrosis and scarring of the myocardium with secondary hypertrophy and atrophy of the myocytes can provide a substrate for arrhythmia as it causes slow conduction and favors the development of ectopic pacemakers, late potentials, and re-entry as a result of inhomogeneous stimulus conduction.Myocarditis accounts for up to 20% of sudden cardiac deaths in young adults. In this case, CMR imaging with LGE provided in vivo tissue characterization as well as functional assessment, which allowed the etiology of the cardiomyopathy to be determined during life. Availability of the images directed the autopsy to enable the location of small areas of change within the myocardium. The extent of LGE on CMR is likely to reflect the burden of arrhythmogenic risk.The online-only Data Supplement, consisting of movies, can be found at http://circ.ahajournals.org/cgi/content/full/116/6/e122/DC1.Sources of FundingDr Babu-Narayan was supported by the British Heart Foundation.DisclosuresNone.FootnotesCorrespondence to Sonya V. Babu-Narayan, BSc, MRCP, Cardiovascular Magnetic Resonance Unit, Royal Brompton Hospital, Sydney St, London SW3 6NP, London, UK. Email [email protected] eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetailsCited By Kim J, Han K and Suh Y (2021) Prevalence of abnormal cardiovascular magnetic resonance findings in recovered patients from COVID-19: a systematic review and meta-analysis, Journal of Cardiovascular Magnetic Resonance, 10.1186/s12968-021-00792-7, 23:1, Online publication date: 1-Dec-2021. Weickmann J, Gebauer R and Paech C (2020) Junctional ectopic tachycardia in neonatal enterovirus myocarditis, Clinical Case Reports, 10.1002/ccr3.2796, 8:6, (987-990), Online publication date: 1-Jun-2020. Getman S, Romanov K and Butov A (2019) POSSIBILITIES OF MAGNETIC RESONANCE IMAGING FORDIAGNOSTIC ETIOLOGIC FACTORS IN THE OCCURRENCE OF ARRHYTHMIASOF THE MILITARYS, Marine Medicine, 10.22328/2413-5747-2019-5-3-17-23, 5:3, (17-23) Gannon M, Schaub E, Grines C and Saba S (2019) State of the art: Evaluation and prognostication of myocarditis using cardiac MRI, Journal of Magnetic Resonance Imaging, 10.1002/jmri.26611, 49:7, (e122-e131), Online publication date: 1-Jun-2019. Sramko M, Hoogendoorn J, Glashan C and Zeppenfeld K (2018) Advancement in cardiac imaging for treatment of ventricular arrhythmias in structural heart disease, EP Europace, 10.1093/europace/euy150, 21:3, (383-403), Online publication date: 1-Mar-2019. Jeserich M, Merkely B, Schlosser P, Kimmel S, Pavlik G and Biermann J (2018) Early diastolic septal movement in patients with myocarditis, Clinical Radiology, 10.1016/j.crad.2017.09.008, 73:2, (219.e9-219.e15), Online publication date: 1-Feb-2018. Tse G, Yeo J, Chan Y, Lai E and Yan B (2016) What Is the Arrhythmic Substrate in Viral Myocarditis? Insights from Clinical and Animal Studies, Frontiers in Physiology, 10.3389/fphys.2016.00308, 7 Mavrogeni S, Markousis-Mavrogenis G and Kolovou G (2015) How to approach the great mimic? Improving techniques for the diagnosis of myocarditis, Expert Review of Cardiovascular Therapy, 10.1586/14779072.2016.1110486, 14:1, (105-115), Online publication date: 2-Jan-2016. Jeserich M, Merkely B, Olschewski M, Kimmel S, Pavlik G and Bode C (2015) Patients with exercise-associated ventricular ectopy present evidence of myocarditis, Journal of Cardiovascular Magnetic Resonance, 10.1186/s12968-015-0204-3, 17:1, Online publication date: 1-Dec-2015. Jeserich M, Olschewski M, Kimmel S, Bode C and Geibel A (2014) Acute results and long-term follow-up of patients with accompanying myocarditis after viral respiratory or gastrointestinal tract infection, International Journal of Cardiology, 10.1016/j.ijcard.2014.04.196, 174:3, (853-855), Online publication date: 1-Jul-2014. Schelbert E, Fonarow G, Bonow R, Butler J and Gheorghiade M (2014) Therapeutic Targets in Heart Failure, Journal of the American College of Cardiology, 10.1016/j.jacc.2014.01.068, 63:21, (2188-2198), Online publication date: 1-Jun-2014. Burt J, Zimmerman S, Kamel I, Halushka M and Bluemke D (2014) Myocardial T1 Mapping: Techniques and Potential Applications, RadioGraphics, 10.1148/rg.342125121, 34:2, (377-395), Online publication date: 1-Mar-2014. Mavrogeni S, Dimitroulas T and Kitas G (2012) Multimodality imaging and the emerging role of cardiac magnetic resonance in autoimmune myocarditis, Autoimmunity Reviews, 10.1016/j.autrev.2012.05.005, 12:2, (305-312), Online publication date: 1-Dec-2012. Klingel K and Kandolf R (2008) Virale Myokarditis im KindesalterViral myocarditis in childhood, Rechtsmedizin, 10.1007/s00194-008-0543-6, 18:5, (349-358), Online publication date: 1-Oct-2008. WHYTE G (2008) Clinical Significance of Cardiac Damage and Changes in Function after Exercise, Medicine & Science in Sports & Exercise, 10.1249/MSS.0b013e318172cefd, 40:8, (1416-1423), Online publication date: 1-Aug-2008. August 7, 2007Vol 116, Issue 6 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCULATIONAHA.107.693085PMID: 17679621 Originally publishedAugust 7, 2007 PDF download Advertisement SubjectsArrhythmiasCardiomyopathyComputerized Tomography (CT)Imaging

A15-YEAR-OLD BOY ADMITTED WITH CHEST PAIN, and raised levels of Troponin I but normal viral titres, was treated acutely for presumed myocarditis. Several months later, cardiovascular magnetic resonance (Fig. 1) demonstrated a dilated and impaired left ventricle, with an ejection fraction of 42%, and normal proximal coronary arteries. Late gadolinium enhancement, indicative of myocardial damage, suggested ventricular scarring, but T2weighted Short Ti Inversion Recovery images, which give evidence of oedema in acute myocarditis, were normal. Full thickness scarring of the lateral wall, with corresponding abnormalities of wall motion shown on cine-magnetic resonance images, was seen on four chamber (Fig. 1a), coronal left ventricular outflow tract (Fig. 1b), and short-axis (Fig. 1c) views. Scarring of the anterolateral papillary muscle was also demonstrated (solid arrows, Figs 1b,c), and was presumed to cause the mild mitral regurgitation that was evident. Patchy focuses were additionally noted in the septum (dotted arrows – Figs 1a,c,d,e), while in certain regions there was sparing of the sub-endocardium Heartache in adolescence – non-invasive tissue characterization with cardiovascular magnetic resonance