Membres du jury
Monsieur le Professeur FURBER ALAIN | Président Monsieur le Docteur BIERE LOIC | Directeur Monsieur le Professeur PRUNIER FABRICE | Membre
Monsieur le Docteur MATEUS VICTOR | Membre
ECG abnormalities during an episode of acute myocarditis and its follow-
up beyond the diagnostic value .
Anomalies ECG pendant un épisode de myocardite aigüe et son suivi, au-delà de la valeur diagnostique.
PERAULT CAMILLE
Née le 29 Novembre 1990 à Roubaix (59)
Sous la direction de M. BIERE Loïc
2018-2019
THÈSE
pour le
DIPLÔME D’ÉTAT DE DOCTEUR EN MÉDECINE
Qualification en CARDIOLOGIE ET MALADIES VASCULAIRES
ENGAGEMENT DE NON PLAGIAT
Je, soussigné(e) Pérault Camille
déclare être pleinement conscient(e) que le plagiat de documents ou d’une partie d’un document publiée sur toutes formes de support, y compris l’internet, constitue une violation des droits d’auteur ainsi qu’une fraude caractérisée.
En conséquence, je m’engage à citer toutes les sources que j’ai utilisées pour écrire ce rapport ou mémoire.
signé par l'étudiant(e) le 11/08/2019.
LISTE DES ENSEIGNANTS DE LA FACULTÉ DE SANTÉ D’ANGERS
Doyen de la Faculté : Pr Nicolas Lerolle
Vice-Doyen de la Faculté et directeur du département de pharmacie : Pr Frédéric Lagarce
Directeur du département de médecine : Pr Cédric Annweiler PROFESSEURS DES UNIVERSITÉS
ABRAHAM Pierre Physiologie Médecine
ANNWEILER Cédric Gériatrie et biologie du
vieillissement Médecine
ASFAR Pierre Réanimation Médecine
AUBE Christophe Radiologie et imagerie médicale Médecine
AUGUSTO Jean-François Néphrologie Médecine
AZZOUZI Abdel Rahmène Urologie Médecine
BAUFRETON Christophe Chirurgie thoracique et
cardiovasculaire Médecine
BENOIT Jean-Pierre Pharmacotechnie Pharmacie
BEYDON Laurent Anesthésiologie-réanimation Médecine
BIGOT Pierre Urologie Médecine
BONNEAU Dominique Génétique Médecine
BOUCHARA Jean-Philippe Parasitologie et mycologie Médecine
BOUVARD Béatrice Rhumatologie Médecine
BOURSIER Jérôme Gastroentérologie ; hépatologie Médecine
BRIET Marie Pharmacologie Médecine
CAILLIEZ Eric Médecine générale Médecine
CALES Paul Gastroentérologe ; hépatologie Médecine CAMPONE Mario Cancérologie ; radiothérapie Médecine CAROLI-BOSC François-xavier Gastroentérologie ; hépatologie Médecine CHAPPARD Daniel Cytologie, embryologie et
cytogénétique Médecine
CONNAN Laurent Médecine générale Médecine
COUTANT Régis Pédiatrie Médecine
COUTURIER Olivier Biophysique et médecine nucléaire Médecine
CUSTAUD Marc-Antoine Physiologie Médecine
DE BRUX Jean-Louis
DE CASABIANCA Catherine Chirurgie thoracique et cardiovasculaire
Médecine Générale
Médecine Médecine DESCAMPS Philippe Gynécologie-obstétrique Médecine DINOMAIS Mickaël Médecine physique et de
réadaptation Médecine
DIQUET Bertrand Pharmacologie Médecine
DUBEE Vincent Maladies Infectieuses et Tropicales Médecine
DUCANCELLE Alexandra Bactériologie-virologie ; hygiène
hospitalière Médecine
DUVAL Olivier Chimie thérapeutique Pharmacie
DUVERGER Philippe Pédopsychiatrie Médecine
EVEILLARD Mathieu Bactériologie-virologie Pharmacie FANELLO Serge Épidémiologie ; économie de la
santé et prévention Médecine FAURE Sébastien Pharmacologie physiologie Pharmacie
FOURNIER Henri-Dominique Anatomie Médecine
FURBER Alain Cardiologie Médecine
GAGNADOUX Frédéric Pneumologie Médecine
GARNIER François Médecine générale Médecine
GASCOIN Géraldine Pédiatrie Médecine
GOHIER Bénédicte Psychiatrie d'adultes Médecine GUARDIOLA Philippe Hématologie ; transfusion Médecine
GUILET David Chimie analytique Pharmacie
HAMY Antoine Chirurgie générale Médecine
HUNAULT-BERGER Mathilde Hématologie ; transfusion Médecine IFRAH Norbert Hématologie ; transfusion Médecine
JEANNIN Pascale Immunologie Médecine
KEMPF Marie Bactériologie-virologie ; hygiène
hospitalière Médecine
LACCOURREYE Laurent Oto-rhino-laryngologie Médecine
LAGARCE Frédéric Biopharmacie Pharmacie
LARCHER Gérald Biochimie et biologie moléculaires Pharmacie LASOCKI Sigismond
LEGENDRE Guillaume Anesthésiologie-réanimation
Gynécologie-obstétrique Médecine Médecine
LEGRAND Erick Rhumatologie Médecine
LERMITE Emilie Chirurgie générale Médecine
LEROLLE Nicolas Réanimation Médecine
LUNEL-FABIANI Françoise Bactériologie-virologie ; hygiène
hospitalière Médecine
MARCHAIS Véronique Bactériologie-virologie Pharmacie
MARTIN Ludovic Dermato-vénéréologie Médecine
MENEI Philippe Neurochirurgie Médecine
MERCAT Alain Réanimation Médecine
MERCIER Philippe Anatomie Médecine
PAPON Nicolas Parasitologie et mycologie médicale Pharmacie
PASSIRANI Catherine Chimie générale Pharmacie
PELLIER Isabelle Pédiatrie Médecine
PETIT Audrey Médecine et Santé au Travail Médecine PICQUET Jean Chirurgie vasculaire ; médecine
vasculaire Médecine
PODEVIN Guillaume Chirurgie infantile Médecine
PROCACCIO Vincent Génétique Médecine
PRUNIER Delphine Biochimie et Biologie Moléculaire Médecine
PRUNIER Fabrice Cardiologie Médecine
RICHARD Isabelle Médecine physique et de
réadaptation Médecine
RICHOMME Pascal Pharmacognosie Pharmacie
RODIEN Patrice Endocrinologie, diabète et maladies
métaboliques Médecine
ROQUELAURE Yves Médecine et santé au travail Médecine ROUGE-MAILLART Clotilde Médecine légale et droit de la santé Médecine ROUSSEAU Audrey Anatomie et cytologie
pathologiques Médecine
ROUSSEAU Pascal Chirurgie plastique, reconstructrice
et esthétique Médecine
ROUSSELET Marie-Christine Anatomie et cytologie
pathologiques Médecine
ROY Pierre-Marie Thérapeutique Médecine
SAULNIER Patrick Biophysique et biostatistique Pharmacie
SERAPHIN Denis Chimie organique Pharmacie
SUBRA Jean-François Néphrologie Médecine
UGO Valérie Hématologie ; transfusion Médecine
URBAN Thierry Pneumologie Médecine
VAN BOGAERT Patrick Pédiatrie Médecine
VENIER-JULIENNE Marie-Claire Pharmacotechnie Pharmacie
VERNY Christophe Neurologie Médecine
WILLOTEAUX Serge Radiologie et imagerie médicale Médecine
MAÎTRES DE CONFÉRENCES
ANGOULVANT Cécile Médecine Générale Médecine
ANNAIX Véronique Biochimie et biologie moléculaires Pharmacie
BAGLIN Isabelle Chimie thérapeutique Pharmacie
BASTIAT Guillaume Biophysique et biostatistique Pharmacie
BEAUVILLAIN Céline Immunologie Médecine
BELIZNA Cristina Médecine interne Médecine
BELLANGER William Médecine générale Médecine
BELONCLE François Réanimation Médecine
BENOIT Jacqueline Pharmacologie Pharmacie
BIERE Loïc Cardiologie Médecine
BLANCHET Odile Hématologie ; transfusion Médecine
BOISARD Séverine Chimie analytique Pharmacie
CAPITAIN Olivier Cancérologie ; radiothérapie Médecine
CASSEREAU Julien Neurologie Médecine
CHEVAILLER Alain Immunologie Médecine
CHEVALIER Sylvie Biologie cellulaire Médecine
CLERE Nicolas Pharmacologie / physiologie Pharmacie
COLIN Estelle Génétique Médecine
DERBRE Séverine Pharmacognosie Pharmacie
DESHAYES Caroline Bactériologie virologie Pharmacie
FERRE Marc Biologie moléculaire Médecine
FLEURY Maxime Immunologie Pharmacie
FORTRAT Jacques-Olivier Physiologie Médecine
HAMEL Jean-François Biostatistiques, informatique médicale Médicale HELESBEUX Jean-Jacques Chimie organique Pharmacie
HINDRE François Biophysique Médecine
JOUSSET-THULLIER Nathalie Médecine légale et droit de la santé Médecine LACOEUILLE Franck Biophysique et médecine nucléaire Médecine
LANDREAU Anne Botanique/ Mycologie Pharmacie
LEBDAI Souhil Urologie Médecine
LEGEAY Samuel Pharmacocinétique Pharmacie
LE RAY-RICHOMME Anne-
Marie Pharmacognosie Pharmacie
LEPELTIER Elise Chimie générale Pharmacie
LETOURNEL Franck Biologie cellulaire Médecine
LIBOUBAN Hélène Histologie Médecine
MABILLEAU Guillaume Histologie, embryologie et
cytogénétique Médecine
MALLET Sabine Chimie Analytique Pharmacie
MAROT Agnès Parasitologie et mycologie médicale Pharmacie MAY-PANLOUP Pascale Biologie et médecine du développement
et de la reproduction Médecine
MESLIER Nicole Physiologie Médecine
MOUILLIE Jean-Marc Philosophie Médecine
NAIL BILLAUD Sandrine Immunologie Pharmacie
PAILHORIES Hélène Bactériologie-virologie Médecine
PAPON Xavier Anatomie Médecine
PASCO-PAPON Anne Radiologie et imagerie médicale Médecine
PECH Brigitte Pharmacotechnie Pharmacie
PENCHAUD Anne-Laurence Sociologie Médecine
PIHET Marc Parasitologie et mycologie Médecine
PY Thibaut Médecine Générale Médecine
RINEAU Emmanuel Anesthésiologie réanimation Médecine
RIOU Jérémie Biostatistiques Pharmacie
ROGER Emilie Pharmacotechnie Pharmacie
SAVARY Camille Pharmacologie-Toxicologie Pharmacie
SCHMITT Françoise Chirurgie infantile Médecine
SCHINKOWITZ Andréas Pharmacognosie Pharmacie
SPIESSER-ROBELET
Laurence Pharmacie Clinique et Education
Thérapeutique Pharmacie
TANGUY-SCHMIDT Aline TESSIER-CAZENEUVE Christine
Hématologie ; transfusion
Médecine Générale Médecine
Médecine
TRZEPIZUR Wojciech Pneumologie Médecine
AUTRES ENSEIGNANTS
AUTRET Erwan Anglais Médecine
BARBEROUSSE Michel Informatique Médecine
BRUNOIS-DEBU Isabelle Anglais Pharmacie
CHIKH Yamina Économie-Gestion Médecine
FISBACH Martine Anglais Médecine
O’SULLIVAN Kayleigh Anglais Médecine
PAST
CAVAILLON Pascal Pharmacie Industrielle Pharmacie
LAFFILHE Jean-Louis Officine Pharmacie
MOAL Frédéric Pharmacie clinique Pharmacie
ATER
FOUDI Nabil Physiologie Pharmacie
KILANI Jaafar Biotechnologie Pharmacie
WAKIM Jamal Biochimie et chimie biomoléculaire Médecine AHU
BRIS Céline Biochimie et biologie moléculaire Pharmacie
CHAPPE Marion Pharmacotechnie Pharmacie
LEBRETON Vincent Pharmacotechnie Pharmacie
CONTRACTUEL
VIAULT Guillaume Chimie organique Pharmacie
REME RC IEM ENTS
Je tenais en premier lieu à vous remercier Messieurs les membres du Jury d’avoir accepté de juger ce travail. Merci d’avoir partagé vos connaissances sur cette belle spécialité tout au long de mon internat.
C’est un honneur d’avoir pu évoluer à vos côtés.
Un grand remerciement au Docteur Bière d’avoir dirigé ce travail, merci pour ta patience et tes bons conseils.
Plus intimement, c’est à toi papa que je dédie l’ensemble de ce travail. A toi qui m’as transmis le goût du savoir, de la curiosité mais aussi de l’abnégation. A toi, mon supporteur de toujours ; toi qui m’as apporté tant d’amour et de bienveillance, qui m’a donné le meilleur et m’a préparé au pire. Ton absence reste insupportable mais l’envie de te rendre fier me permet de me surpasser et de vivre avec le chagrin.
Je n’ai pas de mots assez forts pour te dire combien je t’aime…Ta mimi chérie.
A mes frères, Tristan, Gaël et Méhieddine…La vie n’a pas toujours été un long fleuve tranquille mais chacun d’entre vous a su rebondir. Je suis si fière des hommes que vous êtes devenus. Vous êtes mon équilibre, ma fratrie et les épreuves que nous avons affrontées ensemble ont permis de souder des liens indéfectibles à mon sens. A mon galou, le petit dernier, quel homme brillant et intègre tu es devenu. Bravo pour ton parcours qui selon moi est exemplaire.
Quoiqu’il advienne, je serai là pour vous…
A Damien, mon chéri, merci pour ton soutien sans faille depuis toutes ces années. Merci d’être une épaule solide sur laquelle je peux m’appuyer. Merci pour ta patience et les longues nuits à m’attendre. J’aime ta vision réconfortante du monde qui me berce lorsque je suis tourmentée. A nous, maintenant d’écrire la suite de l’histoire…
A mes grands-parents. A mon Papi Claude, toi qui étais un homme si bon, si doux. Merci pour ta sagesse.
A Mamie Lette, toi qui as été une vraie mère pour moi. Merci d’avoir bercé et égayé mon enfance.
A mes oncles et tantes. A Tati Mireille, ma marraine ; merci d’avoir été là pour lui, pour moi … A mes cousins, cousines…Souvenirs d’enfances et de moments heureux ensemble.
A Auriane, ma meilleure amie. Merci d’avoir réchauffé mon enfance et mon adolescence ; tu as été la sœur que je n’ai pas eue. Loin des yeux, si près du cœur…
A ma belle-famille, merci pour votre soutien.
A mes cointernes, ma promotion, Flore, Floriane, Claire ; la « team girly » de la cardiologie. A ces moments difficiles mais aussi aux bons instants que nous avons partagés durant ces 4 ans. Je vous souhaite « bons vents les filles ». Que vos projets se réalisent…
Aux plus vieux, Céleste, Yohan, Jean et Gabriel ; mais aussi aux plus jeunes Camille, Ali, Thomas, Antoine, Lisette, Alban, Eloi…Que la solidarité entre cointernes perdure. Bonne continuation et accrochez-vous car ça en vaut la peine.
Aux cointernes de réanimation médicale avec qui j’ai passé un excellent semestre.
Sans oublier mes chtis coexternes Clovis, Sarah et Laureline avec qui j’ai débuté en médecine.
Et à tous les chefs, internes, auprès desquels j’ai eu plaisir à travailler.
A tous autant que vous êtes, je vous remercie…
Liste des abréviations
CMR T0 CMR FU CMR
Cardiovascular magnetic resonance imaging Baseline CMR
Follow-up CMR ECG
ECG 1 ECG 2 FU ECG
Electrocardiogram
First medical contact ECG Hospital discharge ECG Follow-up ECG
IQR Interquartile range
InvT T wave inversion
LGE Late gadolinium enhancement
LVEDVI Left ventricular end-diastolic volume index
LVEF Left ventricular ejection fraction
LVESVI Left ventricular end-systolic volume index
LVMI Left ventricular mass index
T2W T2-weighted
STE ST segment elevation
Plan
ABSTRACT
MATERIALS AND METHODS Study population
ECG procedure and criteria CMR protocol
CMR imaging analysis Statistical analysis RESULTS
Baseline clinical characteristics ECG characteristics
ECG abnormalities and CMR parameters
3.1. Baseline: CMR findings and correlation with STE and invT 3.2. Follow-up: CMR findings and correlation with STE and invT
Follow-up
4.1. Normal FU ECG and changes in CMR parameters 4.2. Outcomes
DISCUSSION
Relation between ECG abnormalities and LGE on CMR
Spatial correspondence between ECG findings and LGE areas on CMR Diagnostic value of ECG
ECG findings in monitoring acute viral myocarditis Strengths of the study
Study limitations CONCLUSION BIBLIOGRAPHIE LISTE DES FIGURES LISTE DES TABLEAUX TABLE DES MATIÈRES ANNEXES
1
ECG abnormalities during an episode of acute myocarditis and its follow-up, beyond the diagnostic
value.
Camille PERAULT
a,b, Floriane AUCLAIR
a,b, Yoann BOUILLAUD
a,b, Pascaud Adrien
a,b, Fabrice PRUNIER
a,b, Serge WILLOTEAUX
a,c, Alain FURBER
a,b,
Loïc BIERE
a,ba Department of Cardiology, University hospital of Angers, France
b UMR CNRS 6015 - INSERM U1083, Institut MitoVasc, University of Angers, Angers, France
c Department of Radiology, University Hospital of Angers, Angers, France
ABSTRACT
Introduction: There are few studies to describe the changes in ECG findings during myocarditis. Cardiac magnetic resonance (CMR) is on top of acute diagnosis and prognosis after myocarditis, providing new insights into myocardial healing and phenotypes.
The objective of this study was to correlate ECG findings with acute myocarditis CMR phenotype and changes over time and to assess whether ECG is a significant tool to identify healed myocarditis.
Methods: We performed a retrospective analysis of 103 patients who presented CMR-proven acute viral myocarditis between January 2008 and July 2018. Follow-up ECG and CMR were obtained in 62 patients.
Results: ST segment elevation (STE) (n= 64, 62%) and T wave inversion (invT) (n= 21, 20%) were the most frequent ECG abnormalities on admission. Mean age was 33±16 years. 56 patients (86%) were male, 39 (63%) presented with recent infectious syndrome and 57 (92%) had chest pain on hospital admission. InvT patients were older (p=0.022). There was no correlation between STE or invT location and LGE areas on CMR. InvT patients had a lower LVEF (p=0.029) and presented more transmural LGE (p=0.032). STE patients presented more frequent midwall LGE. On follow-up CMR, invT (n=10) was related to larger extent of LGE (p=0.002). There was no difference between patients with normal ECG and abnormal ECG about changes in LVEF (p=0.649), LGE extent (p=0.501), LVEDV index (p=0.362), LVESV index (p=0.771) and LVM index (p=0.503).
3 Conclusion: There was no significant difference in the regression of pre-existing CMR abnormalities between the normal and abnormal ECG group during follow-up. A normal ECG did not exclude the diagnosis, neither complete healing. STE and invT correlated with LGE pattern. Despite the absence of spatial correspondence between ECG and CMR findings, invT presence related with greater extent of LGE at follow-up. InvT might be considered as a surrogate marker for prognosis.
Keywords: ECG, CMR, acute viral myocarditis, ST segment elevation, T wave inversion.
INTRODUCTION
Myocarditis is an inflammatory pathology of the myocardium, commonly due to a viral or bacterial pathogen (1), and related with a dramatic 0.5% of hospital admissions for cardiovascular disease mainly in young, and usually male subjects (2). Often with a benign course, the temporary myocardial injury may lead to heart failure or fatal ventricular arrhythmia (3).
Along with symptoms, resting electrocardiogram (ECG) is one of the simple tools to guide us to the diagnosis of myocarditis (4). The most common anomalies are T wave inversion (invT) and the ST segment elevation (STE); followed by supraventricular or ventricular arrhythmias and atrioventricular or intraventricular conduction abnormalities (3). In recent years, cardiac magnetic resonance imaging (CMR) has become the first-intention non-invasive diagnostic tool in non-severe forms (5). It combines functional analysis with myocardial tissue characterisation, brought together under the “Lake Louise Criteria” (6), indicating myocardial edema by hyperintense or diffuse T2-weighted signal or myocardial enhancement after T1- weighted gadolinium injection, hyperemia by early enhancement, or late evidence of myocardial necrosis or fibrosis. At least one month after an episode of acute myocarditis, experts recommend to perform a follow-up CMR to assess myocardial healing and identify still ongoing myocardial inflammation – that is considered to increase the risk of progression towards dilated cardiomyopathy (7). Recent evidences pointed LGE presence and extent to mark prognosis after myocarditis (8), (9). While verifying the normalisation of CMR findings may be clinically relevant, CMR remains poorly available and expensive. Whether the use of a longitudinal assessment of ECG as a surrogate marker for cardiac healing after myocarditis
5 The objective of this study was to correlate ECG findings with acute myocarditis CMR phenotype and changes over time and to assess whether ECG is a significant tool to identify healed myocarditis.
MATERIALS AND METHODS
Study population
We retrospectively screened 103 patients with acute myocarditis diagnosed by CMR in one single universitary hospital center between January 2008 and July 2018. Inclusion criteria were: (1) acute new-onset symptoms compatible with the diagnosis of myocarditis; (2) troponin release; (3) CMR diagnosis of myocarditis; and (4) absence of coronary artery disease. CMR diagnosis was based on modified Lake-Louise criteria (7) with the presence of LGE on post-contrast images in every patient, and T2-weighted (T2W) which was non mandatory as long as clinical presentation was timely related to CMR findings. Coronary artery disease was ruled out by coronary angiography in 44 (42%) patients, by CT-scan in 4 (4%) patients. The remaining 55 (53%) patients were considered as having a low pretest probability of coronary artery disease. ECGs were available in 103 patients at admission and at hospital discharge, then 87 at follow-up. Of those, 62 patients had follow-up CMR (Figure 1).
Clinical characteristics were collected from medical records. The study protocol was approved by local ethic committee and in respect with Helsinki conference.
ECG procedure and criteria
Standard 12-lead ECGs were analysed with a paper speed of 25 mm/s and amplification of 10 mm/mV (Figure 2). Electrocardiographic data were evaluated by two cardiologists (CP,
7 (32% for STE and 25% for invT), a third cardiologist reanalysed the tracing (LB). The first ECG (ECG 1) analysed was recorded at the fist medical contact either by mobile intensive care units, Emergency Department or cardiac intensive care unit, and obtained 1 [interquartile range (IQR) 0;4] days after symptoms onset. At hospital discharge, another 12-lead ECG (ECG 2) was recorded 5 [IQR 4;6] days after admission. At last, follow-up ECG (FU ECG) was selected as the timely closest to follow-up CMR (FU CMR) and recorded 102 [IQR 61;164] days after initial admission.
ECGs were evaluated according to the recommendations for the standardization and interpretation of the electrocardiogram published by AHA/ACCF/HRS (10), (11). QRS width and axis were measured. Conduction disturbances (bundle branch block, AV-block, sinus dysfunction), premature atrial or ventricular contraction so as atrial and ventricular arrythmia were collected. Sustained ventricular tachycardia lasted at least 30 seconds.
ECG findings’ definition were as follow:
Low voltage as QRS amplitude ≤10 mV in precordial leads and ≤5 mV in peripheral leads.
InvT was measured and confirmed if ≥0.1 mV deep in two or more leads except aVR. STE was measured and defined after the J point in 2 contiguous leads with the cut off points of ≥0.2 mV in leads V2–V3, and/or ≥0.1 mV in other leads. ST depression was considered if ≥0.1 mV. Q- wave was determined as >0.3 mV in depth and/or >40 ms in duration in at least 2 contiguous leads except aVR (8) . QT interval duration was measured and corrected according to the Bazett’s formula; QT was prolonged if > 450ms for men or 460ms for women.
The ECG findings were localized across the 12 leads in the following regions: septal (leads V1 and V2), anterior (leads V2 to V4), apical (V4), high lateral (aVL and DI), bottom lateral (V5-V6), and inferior (DII, DIII, aVF). Localization was considered as diffuse when affected ≥ 3 regions (except apical).
Normal ECG was defined as the absence of any of the above parameters.
CMR protocol
CMR was performed with a 1,5 or 3 Tesla imager (Avanto, Siemens, Erlangen, Germany) 9 [IQR 4; 17] days after symptoms onset and repeated 100 [IQR 91; 125] days thereafter.
Functional parameters were determined with cine imaging using a segmented steady-state free precession pulse sequence in multiple short-axis and four-chamber views covering the entire left ventricle. Typical in-plane resolution was 1.6×1.9 mm, with a section thickness of 7.0 mm (repetition time/echo time: 2.6 ms/1.3 ms; flip angle: 80°; matrix: 256×208;
temporal resolution: 35–45 ms). T2W inversion recovery prepared fast-spin echo sequence was performed on a stack of contiguous short axis views covering the entire LV in mid-diastole;
slice thickness/gap 7/0,8mm; TR (4000ms); TE 60-70 ms; FOV 264*385; matrix 176*320;
flip angle 180°. Late gadolinium enhancement (LGE) sequences were performed 9-12 min after gadolinium-based contrast agent administration (Dotarem®, Laboratoires Guerbet, Roissy- Charles de Gaulle, France) with acumulative dose of 0.2 mmol/kg of body weight, and a two- dimensional segmented inversion recovery gradient-echo pulse sequence. Typical in-plane resolution was 1.68×1.68 mm. Section thickness was 7.0 mm (TE: 4.66 ms; flip angle: 30°;
imaging was triggered to every other heartbeat; matrix: 256×208). The inversion time was individually adjusted to null normal myocardium.
CMR imaging analysis
9 The CMR images were transferred to a workstation for analysis and calculation (QMass MR 7.2, Medis, Leiden, The Netherlands). The images were interpreted on purpose for this study, by a single experienced cardiologist, blinded to clinical data. On all short-axis cine slices, the endocardial and epicardial borders were outlined manually on end-diastolic and end- systolic frames, excluding the trabeculae and papillary muscles. LV end-diastolic volume (LVEDV), end-systolic volume (LVESV), and mass were determined and indexed to body surface area (12). The presence of T2W or LGE hypersignal were reported. LGE pattern was classified as transmural, epicardial, endocardial, mid-wall and patchy (8). LGE localisation was reported on a 17 segments model. Segments were grouped into region: anterior (segments
#1, 7 and 13), lateral (#5, 6, 11, 12 and 16), inferior (#4, 10 and 15), septal (#2, 3, 8,9, and 14) and apical (#13,14 and 17). LGE extent was then measured and given in grams (8).
Statistical analysis
Continuous variables were related as mean±Standard Deviation (SD) or as median [interquartile range [IQR]]. Categorical variables were expressed as a number and percentage.
Between-group differences were assessed using the Pearson χ2 test for categorical data on no-matched sample and Cochran’s Q test for categorical data on matched sample. Baseline clinical presentation, biology and CMR findings were related with ECG on discharge (ECG 2).
ECG during follow-up (FU ECG) were related with CMR data during follow-up (FU CMR). All tests were performed with a type I error set at 0.05. Statistical analysis was performed using SPSS version 20.0 (IBM Inc., Chicago, IL).
RESULTS
Baseline clinical characteristics
62 patients, included in a follow-up analysis, were studied. Mean age was 33±16 years.
56 patients (86%) were male, 39 (63%) presented with recent infectious syndrome and 57 (92%) had chest pain on hospital admission. Patients had few cardiovascular risk factors. CRP was 40± 51 mg/L (n=58) (Table 1). Mean LVEF was 55±9%, LGE extent was 9±9 gr. LGE appeared as subepicardial in 56 (90%) cases, transmural in 11 (18%), and mid-ventricular in 15 (24%). Predominant distribution was inferior (n=46, 74%) and lateral (n=52, 84%) (Table III).
ECG characteristics
ECG findings are given in table II. Overall, normal ECG was found in 19 (18%) at admission, 28 (27%) at hospital discharge and in 59 (68%) patients at follow-up. STE (n=64, 62%) and invT (n=21, 20%) were the most frequent ECG abnormalities. 11 (11%) patients had both STE and invT on the hospital admission ECG. InvT maximal amplitude was 0.23±0.14 mV, and STE was 0.23±0.10 mV. Out of 64 STE patients, 40 (63%) presented with concave STE, and 15 (23%) convex STE. Atrio-ventricular block was found in 3 patients on admission (2 first degree AV block and 1 second degree AV block), and in 1 patient with first degree AV
11 During hospitalization, 15 patients presented non-sustained ventricular tachycardia; 3 patients presented supraventricular tachycardia and 2 patients had a sinus dysfunction. There was no sustained ventricular tachycardia recorded.
Table I showed baseline characteristics about STE and InvT patterns. InvT patients were significantly older with more dyslipidemia, presented less often chest pain and had less aspirin prescription. STE patients had a trend with a lower BMI. No difference was found about peak of troponin.
ECG abnormalities and CMR parameters
3.1. Baseline: CMR findings and correlation with STE and invT
Initial CMR (T0 CMR) was performed 9 [IQR 4; 17] days after symptom-onset. LVEF was 55±9%. LVM index (LVMI) were 59±12g/m². LVEDV index (LVEDI) and LVESV (LVESVI) index were respectively 94±18 ml/m² and 43±12 ml/m². T2-weighted hypersignal was present in 41 patients (66%).
STE patients (ECG 2) presented a trend for smaller LGE extent, corresponding with less sub-epicardial (80% vs 95%, p=0.058) and more mid-wall LGE pattern (45% vs 14%, p=0.008) compared with non-STE patients. InvT patients had lower LVEF (52±12% vs 57±7%, p=0.029), and more transmural LGE pattern (32% vs 10%, p= 0.032) compared with non- invT patients. LGE distribution was similar whatever the presence of STE or invT (Table III).
Spatial correspondence between LGE areas and ECG findings was 35% for STE and 29% for invT (Figure 3).
3.2. Follow-up: CMR findings and correlation with STE and invT
FU CMR was performed after 100 [IQR 91; 125] days. T2 weighted hypersignal persisted in 7 patients (11%). As T0 CMR, sub-epicardial LGE pattern was the most prevalent and affected 55 patients (89%) and LGE was more often depicted in inferior and lateral territories, respectively, 66% (n=41) and 77% (n=48). There was a significant decrease in LVEF (p<0.0001), LVEDVI (p=0.034), LVESVI (p<0.0001), LVMI(p<0.0001) and LGE extent (p<0.0001). It’s the same for T2-weighted hypersignal (p<0.0001).
Time between FU ECG and FU CMR was 51 [IQR 27; 86] days. InvT patients presented similar data with lower LVEF (55±7% vs 59±4%, p=0.009) and a trend towards predominant transmural LGE (20% vs 4%, p=0.057). InvT was associated with higher LVMI (60±11 g/m2 vs 52±9 g/m2, p=0.023) and greater LGE extent (11±11g vs 5±5g, p=0.002) (Table III).
Spatial correspondence between LGE areas and ECG findings was 3% for STE and 18% for invT (Figure 3).
Follow-up
4.1. Normal FU ECG and changes in CMR parameters
13 There was no relation between normal FU ECG and changes in LVEF and LGE extent or indexed left ventricular volumes and mass in follow-up (Table IV). Nevertheless, patients with normal FU ECG had higher LVEF (60±4% vs 56±7%, p=0.011), lower LVEDVI (88±14 ml/m2 vs 98±21 ml/m2, p=0.031), lower LVESVI (36±7 ml/m2 vs 43±14 ml/m2, p=0.004) and lower LGE extent (4±5 g vs 8±9 g, p=0.028) compared with abnormal FU ECG.
4.2. Outcomes
1 patient with an important LGE mass has died of rhythm disorders one year after symptoms onset. 2 patients recurred an episode of myocarditis. 1 patient (versus 9 patients on hospital time) kept reduced LVEF <50%.
DISCUSSION
In our study, we showed there was no correlation between STE or invT location and LGE areas on CMR. InvT patients had a lower LVEF and to present more transmural LGE. STE patients presented more frequent midwall LGE at baseline. On follow-up CMR, invT was related with larger extent of LGE. There was no relation between normal FU ECG and changes in LVEF and LGE extent or indexed left ventricular volumes and mass in follow-up. Nevertheless, patients with normal FU ECG had higher LVEF, lower indexed ventricular volumes and lower LGE extent compared with abnormal FU ECG.
Relation between ECG abnormalities and LGE on CMR
STE (n= 64, 62%) and invT (n= 21, 20%) were the most frequent ECG abnormalities on admission.
On the one hand, STE is expected in case of myocardial damage (notably transmural ischemia, or subepicardial injury) or pericardial inflammation. Others provided pathophysiological explanation (3), trying to assimilate STE in myocarditis to any coronary or vascular injuries. Nevertheless, the absence of direct relation of STE with neither LGE extent nor localization challenge these hypotheses. LGE extent was not different between STE pattern and non-STE pattern, while invT at follow-up showed larger extent of LGE.
On the other hand, T wave rely on both negative current of membrane repolarization combined with a repolarization vector that is opposite direction of depolarization. Their combination ends in a positive T wave that will be inverted in case of myocardial fibrosis (either due to ischemic or non-ischemic injury). invT appears to be related to inflammatory – that is
15 reported in the acute phase, LGE reflected mainly the increased distribution volume of contrast due to altered sarcolemnal permeability and tissue oedema whilst in the sub-acute phase LGE reflects predominantly permanent tissue damage (14).
Spatial correspondence between ECG findings and LGE areas on CMR
The locating value of ECG abnormalities remains controversial. In our study, LGE was overrepresented among inferior and lateral areas with an sub-epicardial distribution, as found in the literature (15),(16). Nevertheless, Ukena et al. described that repolarization abnormalities were neither associated with immunohistological signs of inflammation in patients with biopsy proven myocarditis (17). Di Bella et al. didn’t find relationship between ECG pattern and CMR location of myocarditis (15). We also showed here that there was no spatial correspondence between ECG and CMR findings, despite a 40 to 50% correlation of invT with LGE in the inferior and lateral wall (see figure 3), either at both acute and chronic stage of myocarditis. This suggest that ECG findings may be due to diffuse myocardial damage or pericardial inflammation.
Diagnostic value of ECG
The diagnostic value of ECG in myocarditis is limited. Aside from a low specificity, either ST-segment elevation or T-wave inversion were present as the most sensitive ECG criterions in 50% of patients, even during the first weeks of the disease (7). 18% of patients had a normal admission ECG and 68% in follow-up. We found similar results in the study of Chopra
et al. with 25% of hospital time ECG with normal repolarization (18). Florian et al. reported 19% of normal ECG (19) and Di Bella et al. reported 1/3 of normal ECG in patients with a recent acute myocarditis detected by CMR (15). Normal ECG is not the exact reflection of the damage caused within the myocardium. Nevertheless, it remains an interesting diagnostic tool.
Consequently, a normal ECG does not exclude the diagnosis in patients with appropriate symptoms (20).
ECG Findings in monitoring acute viral myocarditis
Monitoring acute myocarditis requires symptoms relief, drug management and prognostic assessment against long-term adverse outcomes, mainly driven by ventricular arrythmia with sudden cardiac death and cardiac remodeling with heart failure. Yet the expected course of acute viral myocarditis is usually benign (21) but the body of proof in this field is scarce. To our knowledge, no studies assessed the value of normal ECG in the follow- up. We showed that a normal ECG did not mean complete healing. Indeed, during the follow- up, while changes in LVEF, LV volumes and myocardial mass improved favourably, there was a decrease but persistence in LGE extent. Change in CMR parameters did not correlate with ECG finding, including FU-ECG. Nevertheless, patients with normal ECG had significantly higher LVEF, lower myocardial volumes, and lower LGE mass.
Some studies have shown the prognostic impact of CMR damage and the prognostic value of ECG abnormalities. QRS abnormalities (duration, Q wave) appear to be related to the prognostic of myocarditis with lower LVEF (17), (22), (23). Contrary to Chopra et al. who suggested STE – as an infarct-like pattern of myocarditis – to be associated with MACE occurrence (18). Our STE patients presented a trend for smaller LGE extent and higher LVEF
17 while invT pattern related with lower LVEF and greater LGE extent. Gräni et al. showed LGE extent (per 10% increase) corresponded to a 79% increase in risk of MACE (8). LGE is prognostic. In follow-up, InvT may be bad prognostic because they are correlated with LGE extent; it could be a surrogate marker for prognosis in myocarditis.
Strengths of the study
Both ECG and CMR were specifically analysed on purpose of this study, blinded to clinical data. Concerning ECG and CMR analysis, we had a very good correlation with the current literature; but none of the studies performed these data on longitudinal follow-up.
Study limitations
In the first place, this is a retrospective study on a small population with the biases that implies. Follow-up ECG were not specifically obtained the same day as follow-up CMR. A large prospective study should be required to best determine the prognosis of the ECG in acute myocarditis follow-up to end up with cardiovascular outcomes. There is no clear definition for cardiac healing after myocarditis (21).
Secondly, our results are set on a population of myocarditis with preserved LVEF and conclusions apply to these patients only.
Thirdly, we have no data about viral aetiology, whereas specific LGE patterns have been described and may interfere with our results (24).
CONCLUSION
STE and invT were the most frequent ECG abnormalities in patients with CMR-proven myocarditis. A normal ECG did not exclude the diagnosis, neither complete healing. While STE and invT correlated with LGE pattern, there was no spatial correspondence between STE or invT and LGE areas on CMR, but invT presence related with greater extent of LGE at follow- up. Further studies are needed to determine whether invT may be considered as a surrogate marker for prognosis in myocarditis.
19
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Friedrich MG, Sechtem U, Schulz-Menger J, Holmvang G, Alakija P, Cooper LT, et al., International Consensus Group on Cardiovascular Magnetic Resonance in Myocarditis.
Cardiovascular magnetic resonance in myocarditis: A JACC White Paper. J Am Coll Cardiol.
2009 Apr 28;53(17):1475–87. J Am Coll Cardiol. avr 2009;53(17):1475‑87.
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LISTE DES FIGURES
Figure 1: Flow chart ... I Figure 2: 12 leads ECG abnormalities obtained in admission. ... II Figure 3: Spatial correspondence between ECG findings and LGE areas on CMR………. III
23
LISTE DES TABLEAUX
Table I: Patients included in a follow-up analysis: Baseline characteristics related to STE and invT on hospital discharge ECG (ECG 2) ... IV Table II: ECG findings during follow-up ... V Table III: Relation between baseline and follow-up ECG findings and CMR parameters ... VI Table IV: Follow-up: Changes in CMR parameters according to FU ECG findings. ... VII
TABLE DES MATIÈRES
ABSTRACT ... 2
MATERIALS AND METHODS ... 6
Study population ... 6
ECG procedure and criteria... 6
CMR protocol ... 8
CMR imaging analysis ... 8
Statistical analysis ... 9
RESULTS ... 10
Baseline clinical characteristics ...10
ECG characteristics ...10
ECG abnormalities and CMR parameters ...11
3.1. Baseline: CMR findings and correlation with STE and invT ...11
3.2. Follow-up: CMR findings and correlation with STE and invT ...12
Follow-up ...12
4.1. Normal FU ECG and changes in CMR parameters ...12
4.2. Outcomes ...13
DISCUSSION ... 14
Relation between ECG abnormalities and LGE on CMR ...14
Spatial correspondence between ECG findings and LGE areas on CMR ...15
Diagnostic value of ECG ...15
ECG findings in monitoring acute viral myocarditis ...16
Strengths of the study ...17
Study limitations ...17
CONCLUSION ... 18
BIBLIOGRAPHIE... 19
LISTE DES FIGURES ... 22
LISTE DES TABLEAUX ... 23
TABLE DES MATIERES ... 24 ANNEXES ... I Figure 1: Flow chart ... I Figure 2: Baseline: 12 leads ECG findings. ... II Figure 3: Spatial correspondence between ECG findings and LGE areas on CMR. ... III Table I: Patients included in a follow-up analysis: Baseline characteristics related to STE and invT on hospital discharge ECG (ECG 2) ... IV Table II: ECG findings during follow-up ... V Table III: Relation between baseline and follow-up ECG findings and CMR parameters ... VI
I
ANNEXES
Figure 1: Flow chart
103 patients screened with acute myocarditis confirmed by clinical data
and CMR
62 patients with follow-up CMR
25 patients did not have a follow- up CMR
103 patients with admission and discharge ECG
87 patients with follow-up ECG
Figure 2: Baseline: 12 leads ECG findings.
a) Concave and diffuse STE , b) Convex and infero-latero-apical STE/anterior mirror reflection, c) infero-lateral invT and septal STE.
a)
b)
c)
III
Figure 3: Spatial correspondence between ECG findings and LGE areas on CMR.
A) STE:
Spatial correspondence between LGE areas and STE was 35% on baseline and 3%on follow-up.
Baseline Follow-up
B) InvT:
Spatial correspondence between LGE areas and invT was 29% on baseline and 18% on follow-up.Baseline Follow-up
Table I: Patients included in a follow-up analysis: Baseline characteristics related to STE and invT on hospital
discharge ECG (ECG 2)
He following numbers were available for the laboratory testing: troponin I n=46 (12 missing), troponin T n=15 (47 missing), C reactive protein n=58 (4 missing).
Data are presented as the mean value±SD, number (%) of subjects or median (interquartile range).
P values are given to compare STE or invT patients with non-STE and non-invT patients, respectively.
CRP: C-reactive protein, ACE: angiotensin-converting enzyme, ARB: angiotensin receptor blockers, VT:
ventricular tachycardia, VF: ventricular fibrillation, NA: not available.
All patients (n=62)
STE (n=20)
invT (n=22) Value p Value p
Age, years 33±16 31±16 0.132 40±18 0.022
Male gender 56 (90) 20 (100) 0.075 19 (86) 0.434
Hypertension 5 (8) 0 (0) 0.108 3 (14) 0.232
Dyslipidemia 5 (8) 1 (5) 0.541 5 (23) 0.002
Diabetes mellitus 0 (0) 0 (0) NA 0 (0) NA
Active or previous smoker 24 (39) 10 (50) 0.208 9 (41) 0.792
Previous coronary artery disease 0 (0) 0 (0) NA 0 (0) NA
Weight, kg 76±14 73±12 0.188 78±16 0.584
Heigh, cm 175±7 176±8 0.322 174±7 0.406
Body mass index, kg/m² 25±4 23±4 0.071 26±5 0.343
Symptoms to admission time, days 1 (0-3.75) 2 (0-7) 0.481 1 (0-3) 0.429 Recent infectious syndrome 39 (63) 15 (75) 0.174 13 (59) 0.645 Length of hospital stay, days 5 (4-6) 5 (4-6) 0.336 6 (4-7) 0.054 Clinical presentation
Chest pain Dyspnea Palpitation Heart failure Syncopal episode Cardiogenic shock
VT/VF
57 (92) 2 (3) 4 (6) 3 (5) 5 (8) 4 (6) 5 (8)
19 (95) 2 (10) 1 (5) 2 (10) 1 (5) 2 (10) 0 (0)
0.541 0.037 0.748 0.191 0.541 0.433 0.108
18 (82) 1 (5) 1 (5) 1 (5) 3 (14) 2 (9) 3 (14)
0.030 0.663 0.650 0.936 0.232 0.530 0.232 Medication
Aspirin 34 (55) 14 (70) 0.098 7 (32) 0.007
ACE inhibitors/ARB 26 (42) 7 (35) 0.445 12 (55) 0.136
Beta-blockers 46 (74) 12 (60) 0.078 19 (86) 0.104
Diuretics 0 (0) 0 (0) NA 0 (0) NA
Laboratory data
Peak troponin I, µg/l (n=46) Peak troponin T, µg/l (n=15)
CRP, mg/l (n=58)
9 (3.1-0.5) 1.4 (0.8-1.9) 40±51
14 (7.3-26.7) 1.5 (0.5-3) 38±52
0.974 0.481 0.872
8,6 (3.9-15.6) 1.2 (0.9-1.4) 37±46
0.463 0.247 0.809
V
Table II: ECG findings during follow-up
BBB, bundle branch block.
Data are presented as the mean value±SD or number (%) of subjects.
Data were available for 1 patient about STE and invT characteristics.
ECG characteristics ECG 1
(n=103) ECG 2
(n=103) FU ECG
(n=87)
Timing Admission Hospital
discharge 4.4±3 months
Normal ECG 19 (18) 28 (27) 59 (68)
Sinus rhythm 97 (94) 103 (100) 87 (100)
Premature atrial contraction 3 (3) 0 (0) 0 (0)
Supraventricular tachycardia 3 (3) 0 (0) 0 (0)
Premature ventricular contraction 4 (4) 0 (0) 0 (0)
Atrio-ventricular block 3 (3) 2 (2) 1 (1)
Sinus dysfonction 0 (0) 0 (0) 0 (0)
Non-sustained ventricular
tachycardia 1 (1) 0 (0) 0 (0)
Sustained ventricular
tachycardia/ventricular fibrillation 7 (7) 0 (0) 0 (0)
PQ segment depression 17 (17) 4 (4) 0 (0)
Q wave 12 (12) 9 (9) 7 (8)
Poor R wave progression 13 (13) 11 (11) 8 (10)
InvT 21 (20) 34 (33) 14 (16)
invT, # of derivations, no. 4±2 5±2 4±2
invT max amplitude (mV) 0.23±0.14 0.24±0.19 0.2±0.1
STE 64 (62) 38 (37) 6 (7)
Concave STE 40 (63) 25 (66) 4 (67)
Convex STE 15 (23) 10 (26) 1 (17)
Concave and convex STE 9 (14) 2 (5) 1 (17)
STE, # of derivations, no. 6±2 5±2 5±2
STE max amplitude (mV) 0.23±0.10 0.21±0.08 0.25±0.10
STE and InvT 11 (11) 6 (6) 1 (1)
ST-segment depression 7 (7) 2 (1) 1 (1)
Left BBB 0 (0) 1 (1) 0 (0)
Right BBB 4 (4) 2 (2) 2 (2)
Undifferentiated BBB 0 (0) 1 (1) 1 (1)
Prolonged QTC interval 5 (5) 1 (1) 1 (1)
Low QRS voltage 3 (3) 6 (6) 1(1)
QRS axis, degree 53±34 51±40 51±38
Table III: Relation between baseline and follow-up ECG findings and CMR parameters
Data are presented as the mean value±SD or number (%) of subjects or median (interquartile range).
He following numbers were available for Heart rate: n=57 patients (5 missing)
ECG characteristics
CMR parameters Total STE No STE p invT No invT p
T0 CMR ECG 2 (Hospital discharge)
Generic data n=62 n=20 n=42 n=22 n=40
Delay symptoms onset to T0 CMR,
days 9 (4-17)
Heart rate, bpm 69±12 72±14 68±11 0.233 68±13 69±12 0.808
LVESVI, ml/m² 43±15 40±9 45 ±17 0.262 48±20 41±10 0.073
LVEDVI, ml/m² 94±18 92±17 95±19 0.542 95±18 94±18 0.698
LVEF, % 55±9 57±7 54±10 0.216 52±12 57±7 0.029
LV mass index, g/m² 59±12 60±13 59±12 0.628 62±14 58±11 0.248 Pericardial effusion 19 (31) 6 (30) 15 (36) 0.6 6 (27) 13 (33) 0.150 T2W*, % 41 (66) 14 (70) 27 (64) 0.657 14 (64) 27 (68) 0.758 LGE parameters
LGE extent, g 9±9 7±5 10±7 0.156 12±10 8±7 0.121
LGE pattern (%)
Transmural 11 (18) 1 (5) 10 (24) 0.070 7 (32) 4 (10) 0.032
Sub-epicardial 56 (90) 16 (80) 40 (95) 0.058 20 (91) 36 (90) 0.908
Endocardial 0 (0) 0 (0) 0 (0) NA 0 (0) 0 (0) NA
Mid-wall 15 (24) 9 (45) 6 (14) 0.008 6 (27) 9 (23) 0.675
Patchy 1 (2) 0 (0) 1 (2) 0.487 1 (5) 0 (0) 0.174
FU CMR FU ECG (Follow-up)
Generic data n=62 n=5 n=57 n=10 n=52
Delay T0 CMR-FU CMR, days 100 (91-125) Delay FU ECG-FU CMR, days 51 (27- 86)
Heart rate, bpm 69±13 72±15 69±13 0.639 61±13 71±12 0.031
LVESVi, ml/m² 38±10 39±9 38±10 0.750 43±18 37±8 0.074
LVEDVi, ml/m² 91±17 98±19 90±17 0.385 94±27 90±15 0.531
LVEF, % 58±5 60±4 58±5 0.526 55±7 59±4 0.009
LVMi, g/m² 54±9 56±8 53±10 0.470 60±11 52±9 0.023
Pericardial effusion 3 (5) 1 (2) 2 (4) 0.099 0 (0) 3 (6) 0.436 T2W*, % 7 (11) 1(20) 6(11) 0.582 3 (30) 4 (8) 0.06 LGE parameters
LGE extent, g 6±6 5±5 6±7 0.862 11±11 5±5 0.002
LGE pattern, %
Transmural 4 (6) 1 (20) 3 (5) 0.198 2 (20) 2 (4) 0.057
Sub-epicardial 55 (89) 4 (80) 51 (89) 0.521 9 (90) 46 (88) 0.888
Endocardial 0 (0) 0 (0) 0 (0) NA 0 (0) 0 (0) NA
Mid-wall 15 (24) 2 (40) 13 (23) 0.389 4 (40) 11 (21) 0.203
Patchy 3 (5) 0 (0) 3 (5) 0.599 0 (0) 3 (6) 0.436
VII
Table IV: Follow-up: Changes in CMR parameters according to FU ECG findings.
Data are presented as the mean value±SD.
Changes in CMR parameters
(%) Total
n=62 Normal FU ECG
n=42 Abnormal FU ECG
n=20 p
LVESVI, % -9±18 -8±20 -9±12 0.771
LVEDVI, % -3±13 -2±14 -5±10 0.362
LVEF, % 9±21 8±16 11±29 0.649
LGE extent, % -38±34 -41±29 -34±40 0.501
LVMI, % -8±8 -9±7 -8±9 0.503
IX
PERAULT Camille
Anomalies ECG pendant un épisode de myocardite aigüe et son suivi, au-delà de la valeur diagnostique.
Mots-clés : ECG, IRM cardiaque, myocardite aigüe virale, sus décalage ST, onde T négative.
ECG abnormalities during an episode of acute myocarditis and its follow-up beyond the diagnostic value.
Keywords: ECG, CMR, acute viral myocarditis, ST segment elevation, T wave inversion.
RÉSUMÉ
Introduction : Peu d’études ont décrit les modifications ECG dans la myocardite. L’IRM cardiaque est actuellement le meilleur outil diagnostique et prognostique dans la myocardite.
L’objectif est de corréler les résultats ECG et IRM cardiaques, leurs variations et d’évaluer si l’ECG est un outil fiable pour identifier la guérison myocardique.
Méthode : Nous avons réalisé une étude rétrospective entre Janvier 2008 et Juillet 2018 sur 103 patients présentant une myocardite aiguë virale confirmée par l’IRM cardiaque. Le suivi ECG et IRM cardiaque était obtenu chez 62 patients.
Résultats : Le sus décalage du segment ST (sus ST) (n= 64, 62%) et l’onde T négative (n= 21, 20%) étaient les anomalies ECG prédominantes. La population comportait 56 hommes âgés en moyenne de 33 ans présentant pour 92% une douleur thoracique à l’admission et pour 63% un syndrome infectieux récent. La population avec onde T négative était plus âgée (p=0.022). Il n’y avait pas de corrélation entre le sus ST ou l’onde T négative et la localisation du rehaussement tardif en IRM. Les patients avec ondes T négatives avaient une FEVG plus basse (p=0.029) et présentaient plus de rehaussement tardif transmural (p=0.032). Les patients avec sus ST avaient davantage de rehaussement tardif medio-ventriculaire. Dans le suivi, les patients avec onde T négatives (n=10) avaient un rehaussement tardif plus étendu (p=0.002). En comparant les patients avec un ECG normal ou anormal dans le suivi, il n’y avait pas de différence concernant les variations de FEVG (p=0.649), de rehaussement tardif (p=0.501), de volumes et masses ventriculaires indexés (respectivement, (DTSVG : p=0.771), (DTDVG : p=0.362), (masse VG : p=0.503)).
Conclusion : On ne retrouvait aucune différence d’évolution des paramètres IRM entre les patients avec ECG normal ou anormal dans le suivi. Un ECG normal ne permettait pas d’exclure le diagnostic à l’admission ni d’affirmer la guérison dans le suivi. Le sus ST et l’onde T négative étaient corrélés au phénotype myocardique mais ne localisaient pas les dommages myocardiques. Néanmoins, dans le suivi, les ondes T négatives témoignaient d’un rehaussement tardif plus conséquent. Les ondes T négatives pourraient être un marqueur de substitution dans le pronostic des myocardites.
AB ST RACT
Introduction: There are few studies to describe the changes in ECG findings during myocarditis. Cardiac magnetic resonance (CMR) is on top of acute diagnosis and prognosis after myocarditis, providing new insights into myocardial healing and phenotypes.
The objective of this study was to correlate ECG findings with acute myocarditis CMR phenotype and changes over time and to assess whether ECG is a significant tool to identify healed myocarditis.
Methods: We performed a retrospective analysis of 103 patients who presented CMR-proven acute viral myocarditis between January 2008 and July 2018. Follow-up ECG and CMR were obtained in 62 patients.
Results: ST segment elevation (STE) (n= 64, 62%) and T wave inversion (invT) (n= 21, 20%) were the most frequent ECG abnormalities on admission. Mean age was 33±16 years. 56 patients (86%) were male. 39 (63%) presented with recent infectious syndrome. 57 (92%) had chest pain on hospital admission. InvT patients were older (p=0.022). There was no correlation between STE or invT location and LGE areas on CMR. InvT patients had a lower LVEF (p=0.029) and presented more transmural LGE (p=0.032). STE patients presented more frequent midwall LGE. On follow-up CMR, invT (n=10) was related to larger extent of LGE (p=0.002). There was no difference between patients with normal ECG and abnormal ECG about changes in LVEF (p=0.649), LGE extent (p=0.501), LVEDV index (p=0.362), LVESV index (p=0.771) and LVM index (p=0.503).
Conclusion: There was no significant difference in the regression of pre-existing CMR abnormalities between the normal and abnormal ECG group during follow-up. A normal ECG did not exclude the diagnosis, neither complete healing. STE and invT correlated with LGE pattern. Despite the absence of spatial correspondence between ECG and CMR findings, invT presence related with greater extent of LGE at follow-up. InvT might be considered as a surrogate marker for prognosis in myocarditis.
