1. The document discusses Takotsubo syndrome, or stress-induced cardiomyopathy, which causes transient left ventricular dysfunction. 2. It was first reported in Japan in 1990 and predominantly affects post-menopausal women. A stressful trigger, either emotional or physical, often precedes the onset. 3. While the exact pathophysiology is unknown, it is thought to involve microvascular spasm and catecholamine cardiotoxicity leading to calcium overload. This causes transient apical and mid-ventricular akinesia or dyskinesia.

1. ETAT DE L’ART
‘ST+ Mimics’
Syndrome de takotsubo
…ou quand un poulpe vous brise le cœur
Nicolas PESCHANSKI MD, PhD @DocNikko
CHI Eure-Seine – CIRCE-NEV – INSERM U1096

2. Ce que l’on sait…

3. Japon, 1990…
Tremblement de terre à 80 km au sud-ouest de Tokyo

4. Registre (MACE)

5. 5 SCA-ST+ à coronaires saines
Contractilité ≈ Aspect atypique
FEVG abaissée
Population à risque !!!
Âge moyen >>> SCA
100% femmes
Sato H, et al. Kodama K, Haze K, Hon M, eds. Clinical Aspect of Myocardial Injury:
From Ischaemia to Heart Failure. Tokyo: Kagakuhyouronsya 1990:56-64.

6. Clinique/Biologie/ECG = SCA ST+
Dysfonction VG (transitoire) associée

7. Nouveau syndrome : le takotsubo !

8. tsubo
tako
Tako-Tsubo !

9. Un nouveau syndrome – le takotsubo !

10. Un nouveau syndrome – le takotsubo !

11. Définition(s)
Circulation Journal
Official Journal of the Japanese Circulation Society
http://www.j-circ.or.jp
Diagnosis of Takotsubo Cardiomyopathy
– Mayo Clinic Criteria –
Dawn C Scantlebury, MD; Abhiram Prasad, MD
Takotsubo cardiomyopathy, also known as left ventricular apical ballooning syndrome and stress-induced cardio-
myopathy, is typically characterized by transient systolic dysfunction of the apical and mid-segments of the left
ventricle, in the absence of obstructive coronary artery lesions. Patients may present with symptoms and signs of
acute coronary syndrome, and the provider is challenged to differentiate between these conditions. In this review,
we guide the reader through the diagnostic pathway, focusing on differential diagnoses and diagnostic criteria for
takotsubo cardiomyopathy. (Circ J 2014; 78: 2129– 2139)
Focus Issue on Takotsubo Cardiomyopathy

12. 2004-2008-20142130 SCANTLEBURY DC et al.
of severe chest pain and dyspnea lasting 2–3h. The chest painthe cardiomyopathy began to be recognized in the rest of the
Table 1. Mayo Clinic Criteria for ABS/TTC20
1. Transient hypokinesis, akinesis, or dyskinesis of the left ventricular mid-segments with or without apical involvement; the regional wall
motion abnormalities extend beyond a single epicardial vascular distribution; a stressful trigger is often, but not always present.*
2. Absence of obstructive coronary disease or angiographic evidence of acute plaque rupture.†
3. New electrocardiographic abnormalities (either ST-segment elevation and/or T-wave inversion) or modest elevation in cardiac troponin.
4. Absence of:
a. Pheochromocytoma
b. Myocarditis
ABS, apical ballooning syndrome; TTC, takotsubo cardiomyopathy; ACS, acute coronary syndrome.
*There are rare exceptions to these criteria such as those patients in whom the regional wall motion abnormality is limited to a single coronary
territory.
† It is possible that a patient with obstructive coronary atherosclerosis may also develop ABS. However, this is very rare in our experience and
in the published literature, perhaps because such cases are misdiagnosed as ACS.
In both of the above circumstances, the diagnosis of ABS should be made with caution and a clear stressful precipitating trigger must be
sought.

13. Définition(s)
European Journal of Heart Failure (2016) 18, 8–27 REVIEW
doi:10.1002/ejhf.424
Current state of knowledge on Takotsubo
syndrome: a position statement from the task
force on Takotsubo syndrome of the Heart
Failure Association of the European Society of
Cardiology
Alexander R. Lyon1,2,*, Eduardo Bossone3, Birke Schneider4, Udo Sechtem5,
Rodolfo Citro6, S.Richard Underwood1,2, Mary N. Sheppard7, Gemma A. Figtree8,9,
10 11 12 13

14. Ce que l’on croit savoir…

15. Spasme microcirculatoire
Wittstein IS, et al. N Engl J Med 2005;352:539-48.

16. Redistribution des récepteurs β
Cevik C, et al. Am Heart J 2008;156:e31.0002-8703.
Défaillance du VG prédominant à l’apex
(β2 isoformes Gs)
Réponse augmentée à la stimulation 𝜮 à la base
(β1 isoformes G1)

17. Cardiotoxicité catécholergique
Akashi YJ, et al. Circulation 2008;118:2754-62.
Pelliccia F, et al. Circulation. 2017;135:2426-41.
Surcharge en Ca++ médiée par libération de Rx libres
Stimulation des canaux calciques AMP-dépendants

18. Physiopathologie (on progresse…)
Pelliccia F, et al. Circulation. 2017;135:2426-41.
Pelliccia et al
Figure 4. Autonomic nervous system (ANS) activation and cardiovascular system.
ANS activation is mediated by release of norepinephrine (NE) and epinephrine (Epi) and occurs via the following m
(1) Release of norepinephrine by cardiac sympathetic nerve terminals (resulting in tachycardia and an increased force
(2) release of epinephrine into the circulation by the adrenal medulla, modulating both myocardium and peripheral

19. La physiopathologie

20. Physiopathologie (pour les nuls en poulpe)

21. Physiopathologie (pour les nuls en poulpe)
VG normal VG Takotsubo

22. Physiopathologie (pour tout le monde)
VG normal VG Takotsubo
Akashi JY, et al. Nat. Rev. Cardiol. 2015;12:387-97.

23. Très forte prédominance féminine
Âge moyen post-ménopausique
Facteur de stress physique ou émotionnel
Ce que l’on doit savoir…

25. Takotsubo ≠ rare & féminin !
Incidence/Prévalence
Âge 65-72 ans
Femmes 82-100 %
1,7 -2,3 % SCA
5-7 % SCA chez les femmes
Variation saisonnière/circadienne
Incidence x 2 à 4 l’été
Diurne/matinal
Wedekind H, et al. Herz. 2006;31(4):339-46.
Citro R, et al. JACC. 2009;54(2):180-81.
Templin C, et al. N Engl J Med. 2015;373:929-38.
the first reported case of takotsubo syndrome. Diastole (A) and systo
lar wall motion abnormality two weeks after the event (C and D). Co

26. Triggers
Tristesse
Schlossbauer SA, et al. Praxis. 2016;105:1185-92.

27. Évènements
négatifs
Schlossbauer SA, et al. Praxis. 2016;105:1185-92.

28. Colère
Schlossbauer SA, et al. Praxis. 2016;105:1185-92.

29. Catastrophes
naturelles
Schlossbauer SA, et al. Praxis. 2016;105:1185-92.

30. Peurs
Schlossbauer SA, et al. Praxis. 2016;105:1185-92.

31. Le facteur émotionnel pas toujours négatif !
Schlossbauer SA, et al. Praxis. 2016;105:1185–1192.

32. Happy Heart Syndrome
Ghadri JR, et al. Eur Heart J. 2016;37(37):2823-9.

33. Agressions
physiques
fréquentes !

34. AVC
TC
Épilepsie
PRESS
Schlossbauer SA, et al. Praxis. 2016;105:1185-92.

35. Phéochromocytome
CNA
Urosepsis
Schlossbauer SA, et al. Praxis. 2016;105:1185-92.

36. Pancréatite
HD
Crohn
Hernies, occlusions
Péritonite
Schlossbauer SA, et al. Praxis. 2016;105:1185-92.

37. EA BPCO
AAG
IRB
EP
Laryngospasme
Schlossbauer SA, et al. Praxis. 2016;105:1185-92.

38. Schlossbauer SA, et al. Praxis. 2016;105:1185-92.
Hémorragie
Accouchement

39. Anesthésie
Catecholamines
Dialyse
Schlossbauer SA, et al. Praxis. 2016;105:1185-92.

40. Chirurgie
Cancers
Chimiothérapie
Fractures, plaies, …
Schlossbauer SA, et al. Praxis. 2016;105:1185-92.

41. Défaillance cardiaque transitoire
Absence de lésion coronaire
Ce que l’on croit savoir…

42. Constatations angiographiques < 2010
Bybee K.A. et al. Circulation. 2008;18(4):397-409.
Dyskinésie/akinésie des zones apicale +/- moyenne du VG
Hyperkinésie de la base du VG
Résolution généralement en 1-2 à 3-4 semaines
Absence de spasme macro-circulatoire ou d’occlusion coronaire

43. Lyon AR, et al. Nat Clin Pract Cardiovasc Med. 2008;5:22-9.
Prasad A, et al. Am Heart J. 2008;155(3):408-17.

44. Nef HM, et al. Heart 2007;93:1309-15.

45. Prasad A, et al. Am Heart J. 2008;155(3):408-17.
Sharkey SW, et al. Circulation. 2005;111;472-9.

46. Templin C, et al. N Engl J Med. 2015;373:929-38.

47. Templin C, et al. N Engl J Med. 2015;373:929-38.

48. coronary intervention; STEMI, ST-segment elevation myocardial infarction; TNT, troponin T.
Lüscher TF, Templin C. Eur Heart J. 2016;37:2816-20.

49. Table 1 International Takotsubo Diagnostic Criteria (InterTAK Diagnostic Criteria)
1. Patients show transienta
left ventricular dysfunction (hypokinesia, akinesia, or dyskinesia) presenting as apical ballooning or midventricular, basal,
or focal wall motion abnormalities. Right ventricular involvement can be present. Besides these regional wall motion patterns, transitions be-
tween all types can exist. The regional wall motion abnormality usually extends beyond a single epicardial vascular distribution; however, rare
cases can exist where the regional wall motion abnormality is present in the subtended myocardial territory of a single coronary artery (focal
TTS).b
2. An emotional, physical, or combined trigger can precede the takotsubo syndrome event, but this is not obligatory.
3. Neurologic disorders (e.g. subarachnoid haemorrhage, stroke/transient ischaemic attack, or seizures) as well as pheochromocytoma may serve as
triggers for takotsubo syndrome.
4. New ECG abnormalities are present (ST-segment elevation, ST-segment depression, T-wave inversion, and QTc prolongation); however, rare
cases exist without any ECG changes.
5. Levels of cardiac biomarkers (troponin and creatine kinase) are moderately elevated in most cases; significant elevation of brain natriuretic peptide
is common.
6. Significant coronary artery disease is not a contradiction in takotsubo syndrome.
7. Patients have no evidence of infectious myocarditis.b
8. Postmenopausal women are predominantly affected.
a
Wall motion abnormalities may remain for a prolonged period of time or documentation of recovery may not be possible. For example, death before evidence of recovery is
captured.
b
Cardiac magnetic resonance imaging is recommended to exclude infectious myocarditis and diagnosis confirmation of takotsubo syndrome.
4 J.-R. Ghadri et al.
Définition 2018
Ghadri JR, et al. Eur Heart J. 2018;39(22):2032-2046.

50. Récupération ad-integrum
Ce que l’on croyait savoir…

51. Eitel I, et al. JAMA. 2011;306(3):277-86.
IRM
InterTAK

52. C’est grave !
Mortalité
1 à 2 % (0-8%)
Récidive 10%
(1,8%/an/pt)
Akashi YJ, et al. Circulation 2008;118:2754-62.
Elesber A, et al. JACC 2007;50(5):448-52.
Patel SM, et al. J Card Fail. 2013;19:306-10.

53. C’est pour nous !
Si c’est grave…

54. Douleur thoracique 75%
Dyspnée 20%
Malaise 5%
Syncope 2%
Pilgrim TM, et al. Int Journal Card 2008;124:283-92.
Présentation clinique

55. Complications immédiates
OAPc 15-20%
Choc cardiogénique 1-10%
IM aiguë 5%
Péricardite <2%
Rupture septale,VG,VD <1%
Thrombus IV (embole systémique)
Mort subite 0,2-2% Buchholz S, et al. Postgrad Med J. 2007;83(978):261-4.
Prasad A, et al. Am Heart J. 2008;155(3):408-17.

56. Impossible à différencier d’un SCA !
Et l’ECG alors…
Vraiment…?

57. Madias C, et al. Heart Rhythm. 2011;8(4):555-61.
H0 H12
H12… et 1’

58. Dib C, et al. Am Heart J. 2009;157:933-8.
Toshiaki E, et al. JACC. 2010;55(22):2514-17.

59. Kosuge M, et al. JACC. 2010;55:2514-6.

61. Mugnai G, et al. J Electrocardiol. 2015;48:79-85.

62. Stimulation Σ + +
Catécholamines circulantes
BNP 2-3 x > MI (soit 7 à 30 x norme)
Et la bio …?

63. Wittstein IS, et al. N Engl J Med 2005;352:539-48.
Catécholamines circulantes

64. Nadir MA, et al. Am J Cardiol. 2011;107(5):662-7.
Biomarqueurs cardiaques
Peptides natriurétiques

65. Prasad A, et al. Am Heart J. 2008;155(3):408-17.
Biomarqueurs cardiaques
Peptides natriurétiques
Troponine

66. Biomarqueurs cardiaques
Troponine
Burgdorf C, et al. Peptides. 2012;34:389-94.

67. Spécial dédicace…

69. Mansencal N, et al. Arch Cardiovasc Dis. 2010;103:447-53.

70. Nef HM, et al. Heart 2007;93:1309-15.

71. Traitement(s)…?
Isogai T, et al. Heart 2016;102:1029-35.

72. ST+ Mimics

73. ST+ Mimics
Grave

74. ST+ Mimics
Grave
Défaillance
cardiaque aiguë

75. ST+ Mimics
Grave
Défaillance
cardiaque aiguë
Urgence