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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 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

BIBLIOGRAPHIE

1. Le Congrès Conférence d’actualisation © 2017, Sfar, Paris /Myocardite /Pr Julien Amour /Département d’Anesthésie et de Réanimation, Hôpital Pitié-Salpêtrière.

https://sfar.org/wp-content/uploads/2017/10/Amour-Myocardite.pdf.

2. Kytö V, Sipilä J, Rautava P. The effects of gender and age on occurrence of clinically suspected myocarditis in adulthood. Heart. 2013 Nov;99(22):1681-4.

3. Punja M, Mark DG, McCoy JV, Javan R, Pines JM. Punja M, Mark DG, McCoy JV, Javan R, Pines JM. Electrocardiographic manifestations of cardiac infectious-inflammatory disorders.

Am J Emerg Med. 2010 Mar;28(3):364–77. Am J Emerg Med. mars 2010;28(3):364‑77.

4. Caforio ALP, Pankuweit S, Arbustini E, Basso C, Gimeno-Blanes J, Felix SB, et al. 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. Eur Heart J. 1 sept 2013;34(33):2636‑48.

5. Grün S, Schumm J, Greulich S, Wagner A, Schneider S, Bruder O, et al. Long-Term Follow-Up of Biopsy-Proven Viral Myocarditis: Predictors of Mortality and Incomplete Recovery. J Am Coll Cardiol. 1 mai 2012;59(18):1604‑15.

6. Ferreira VM, Schulz-Menger J, Holmvang G, Kramer CM, Carbone I, Sechtem U, et al.

Cardiovascular Magnetic Resonance in Nonischemic Myocardial Inflammation: Expert Recommendations. J Am Coll Cardiol. 10 déc 2018;72(24):3158‑76.

7. Friedrich MG, Sechtem U, Schulz-Menger J, Holmvang G, Alakija P, Cooper LT, et al.

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.

8. Gräni C, Eichhorn C, Bière L, Murthy VL, Agarwal V, Kaneko K, et al. Prognostic Value of Cardiac Magnetic Resonance Tissue Characterization in Risk Stratifying Patients With Suspected Myocarditis. J Am Coll Cardiol. 9 oct 2017;70(16):1964‑76.

9. Aquaro GD, Perfetti M, Camastra G, Monti L, Dellegrottaglie S, Moro C, et al. Cardiac MR With Late Gadolinium Enhancement in Acute Myocarditis With Preserved Systolic Function.

J Am Coll Cardiol. oct 2017;70(16):1977‑87.

10. Surawicz B, Childers R, Deal BJ, Gettes LS. AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram: Part III: Intraventricular Conduction Disturbances A Scientific Statement From the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society Endorsed by the International Society for Computerized Electrocardiology. J Am Coll Cardiol. 17 mars 2009;53(11):976‑81.

11. Rautaharju et al. JACC Vol. 53, No. 11, 2009 Standardization and Interpretation of the ECG, Part IV: the ST segment, T and U waves, and the QT interval: a scientific statement

from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. J Am Coll Cardiol 2009;53:982–91.

12. Clerfond G, Bière L, Mateus V, Grall S, Willoteaux S, Prunier F, et al. End-systolic wall stress predicts post-discharge heart failure after acute myocardial infarction. Arch Cardiovasc Dis. mai 2015;108(5):310‑20.

13. De Lazzari M, Zorzi A, Baritussio A, Siciliano M, Migliore F, Susana A, et al. Relationship between T-wave inversion and transmural myocardial edema as evidenced by cardiac magnetic resonance in patients with clinically suspected acute myocarditis: clinical and prognostic implications. J Electrocardiol. juill 2016;49(4):587‑95.

14. Ammirati E, Moroni F, Sormani P, Peritore A, Milazzo A, Quattrocchi G, et al. Quantitative changes in late gadolinium enhancement at cardiac magnetic resonance in the early phase of acute myocarditis. Int J Cardiol. mars 2017;231:216‑21.

15. Di Bella G, Florian A, Oreto L, Napolitano C, Todaro MC, Donato R, et al.

Electrocardiographic findings and myocardial damage in acute myocarditis detected by cardiac magnetic resonance. Clin Res Cardiol. août 2012;101(8):617‑24.

16. Deluigi CC, Ong P, Hill S, Wagner A, Kispert E, Klingel K, et al. ECG findings in comparison to cardiovascular MR imaging in viral myocarditis. Int J Cardiol. 30 avr 2013;165(1):100‑6.

17. Ukena C, Mahfoud F, Kindermann I, Kandolf R, Kindermann M, Böhm M. Prognostic electrocardiographic parameters in patients with suspected myocarditis. Eur J Heart Fail.

avr 2011;13(4):398‑405.

18. Chopra H, Arangalage D, Bouleti C, Zarka S, Fayard F, Chillon S, et al. Prognostic value of the infarct- and non-infarct like patterns and cardiovascular magnetic resonance parameters on long-term outcome of patients after acute myocarditis. Int J Cardiol. juin 2016;212:63‑9.

19. Florian A, Schäufele T, Ludwig A, Rösch S, Wenzelburger I, Yildiz H, et al. Diagnostic value of CMR in young patients with clinically suspected acute myocarditis is determined by cardiac enzymes. Clin Res Cardiol. févr 2015;104(2):154‑63.

20. Jhamnani S, Fuisz A, Lindsay J. The spectrum of electrocardiographic manifestations of acute myocarditis: An expanded understanding. J Electrocardiol. nov 2014;47(6):941‑7.

21. Anzini M1, Merlo M, Sabbadini G, Barbati G, Finocchiaro G, Pinamonti B, Salvi A, Perkan A, Di Lenarda A, Bussani R, Bartunek J, Sinagra G. Long-term evolution and prognostic stratification of biopsy-proven active myocarditis. Circulation. 2013; 128(22):2384-94.

22. Morgera T, Di Lenarda A, Dreas L, Pinamonti B, Humar F, Bussani R, et al.

Electrocardiography of myocarditis revisited: Clinical and prognostic significance of electrocardiographic changes. Am Heart J . 1 août 1992;124(2):455‑67.

21 23. Nakashima H, Katayama T, Ishizaki M, Takeno M, Honda Y, Yano K. Q Wave and

Non-Q Wave Myocarditis with Special Reference to Clinical Significance. Jpn Heart J.

1998;39(6):763‑74.

24. Mahrholdt H, Wagner A, Deluigi CC, Kispert E, Hager S, Meinhardt G, et al. Presentation, Patterns of Myocardial Damage, and Clinical Course of Viral Myocarditis. Circulation. 10 oct 2006;114(15):1581‑90.

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

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 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 Peak troponin T, µg/l (n=15)

CRP, mg/l (n=58)

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

tachycardia/ventricular fibrillation 7 (7) 0 (0) 0 (0)

PQ segment depression 17 (17) 4 (4) 0 (0)

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)

Delay T0 CMR-FU CMR, days 100 (91-125) Delay FU ECG-FU CMR, days 51 (27- 86)

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.

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