1. The document discusses the management of elderly patients presenting with possible acute coronary syndrome (ACS). Biomarkers like high-sensitivity troponin have improved detection of myocardial infarction in this population, but interpretation can be challenging due to age-related changes. 2. Risk stratification tools like the HEART score and evaluation of troponin kinetics can help identify low-risk elderly patients for early discharge. A pathway integrating HEART score, high-sensitivity troponin levels, and clinical judgement may optimize care for these patients. 3. Guidelines recommend aspirin, a P2Y12 inhibitor like clopidogrel, and consideration of extended dual antiplatelet therapy based on risk assessment for secondary prevention

1. Nicolas PESCHANSKI
MD, PhD – CHI Eure-Seine Evreux
SCA non-ST+
Personne Âgée
@DocNikko

2. Sanofi©
Lilly©
Daiichi-Sankyo©
AstraZeneca©
Roche Diagnostics©
ThermoFisher©
Verathon© Heartscape™
Nihon-Koden©
Zoll©

3. Thygesen K. Eur Heart J 2007;28:2525-2538
Reichlin et al./ Keller et al. NEJM 2009
SCA ST+
10% SCA Non
ST+
10%
Angor
Instable
14%
Autres/non-
IDM
66%
Douleur Thoracique

4. Rapport de la DRESS 2003, 215:1-12
O. Lacroix. Thèse de Médecine, Strasbourg 2008DRESS 2003, 215:1-12
O. Lacroix. Thèse de Médecine, Strasbourg 2008
>70 ans = 12-21% passages
>75 ans = 65% hospitalisation
>80 ans = 38% recours/an
Population à risque !!!
Mêmes pathologies graves
Diminution réserves organiques
Comorbidités importantes
Urgences = Fragilité

5. Mattu A. Univ of Maryland School of Medicine, 2009
Epidémio(bobo)logie

6. SCA
Prévalence ⇗⇗
France -> 120000 IDM/an
N-STEMI > STEMI
Mortalité hospitalière = (3 vs 3%)
Mortalité 6 mois ≈ (5,3 vs 6,8%)
Mortalité long terme > N-STEMI
Puymirat E, et al. Circulation 2017

7. 1ère cause mortalité CV
85% décès IDM >65 ans
SCA
Gopta R. Emerg Med Clin N Am 2016;34:523-42
>75 ans + SCA omis
= 50% décès < 72 h
DRESS 2003, 215:1-12

9. Body R, et al. Resuscitation 2010
Anamnèse
Douleur identique LR+ 0,7
Douleur > 1h LR+ 1,4
Irradiation MSD LR+ 2,3
Sueurs LR+ 6,3
Douleur punctiforme LR- 1,0
Douleur thoracique

10. Cannon C, et al. Circulation. 2007;115:2549-69
Fanaroff AC, et al. JAMA 2015;314(18):1955-65

11. Kelly BS. Clin Geriatr Med 2007;23:327-49
Douleur
Absente/Atypique
Imprécise
≠ Irradiations
2nd plan

12. 3ème interrogatoire
= sémiologie sup. 20-75%
Kelly BS. Clin Geriatr Med 2007;23:327-49
65% = DT<7j
IDM « indolore » = 33% DT

13. Swap CJ. JAMA 2005;294:2623-9
DT+1 1+DT

14. Rich MW. Am J Geriatr Cardiol 2006;15:7–11

15. Smith SC. J Am Coll Cardiol. 1990;16:784-92Grave !!!

16. Kelly BS. Clin Geriatr Med, 2007;23:327-49

17. Swap CJ. JAMA. 2005;294:2623-9

19. Définition
Nouveau sous-décalage du segment ST horizontal ou
descendant au niveau du point J dans au moins deux
dérivations contiguës ou adjacentes et ≥ 0,5 mm
Thygesen K, et al. Circula4on 2012

20. Définition
Onde T inversée ≥ 1 mm dans au moins deux
dérivations contiguës où l’onde R est
proéminente ou R/S > 1
Thygesen K, et al. Circulation 2012

21. Autres définitions
Sus-décalage de ST non persistant (transitoire), peu ample (< 1 mm)
ou dans une seule dérivation
Pseudo-normalisation sus-décalage de ST ou onde T inversée
Apparition progressive d’une onde Q de nécrose
Wang T, et al. Am Heart J 2009;157:716-23

22. Kosowsky. Emerg Med Clin N Am 2011;29:721-27
Normal
LR- 0,8
ST- LR+ 3,6
BBG LR+ 1,4
Modif. LR+ 3,4
Diagnostic ECG

23. Kelly BS. Clin Geriatr Med 2007;23:327-49
Personne Âgée
ECG≠∆ic

24. Kelly BS. Clin Geriatr Med 2007;23:327-49
Personne Âgée

25. Personne Âgée

26. Personne Âgée

27. Modifications ECG
Cinétique ECG
>>>
Cinétique Troponine
Eskola. J Electrocardiology 2011;44:e1–e64

28. Biomarqueurs
Troponine HS/US
Troponine 4ème g.
Brush JE, et al. JACC 2016

29. Algorithme décisionnel
Roffi M, et al. Eur Heart J 2016

30. Recommandations ESC
Hamm CW, et al. Eur Heart J 2012

31. Limites détection TnHS/US
NICE Guidelines. 2014

32. Limites détection TnHS/US

33. Hammarsten O, et al. Clin Chem 2012
Effets de l’âge

34. Amélioration ∆ique
Giannitis E, et al. Clin Chem 2010
ROCHE DIAGNOSTICS - 10 000 BIO N°81 - NOVEMBRE 2009
MÉDICALISATION
ous mettre en conformité
ommandations internatio-
éconisent une imprécision
rable de 10% à la valeur du
e d’une population de réfé-
oponine conventionnelle ne
e remplir ces exigences.
e-t-il pour
a troponine THs
’hui?
beaux:De multiples publi-
mmunications orales nous
p appris ces derniers mois,
mes techniquement prêts.
reste à explorer certains
plication cliniques et biolo-
mieux interpréter les résul-
en mesure d’informer nos
de façon exhaustive.
Meune:L a troponine THs
p tôt serait utilisée par les
mme une troponine conven-
nc de manière réductrice.
qu’elle est plus sensible
nostic de l’infarctus et de
ble et qu’un seul dosage
suffit(2)
. Mais nous avons
vail pour parvenir à un algo-
prétation clair et approfon-
stic de l’angor instable, qui
et de notre étude.
mode de prise en charge des patients:
nombre de dosages, interprétation, délai
dans lequel les patients seront mis sous
traitement ou renvoyés chez eux, etc.
Nous attendons des biologistes beaucoup
d’informations: qu’est-ce qui différencie
ce paramètre des autres troponines? L e
dosage est-il robuste en toutes circons-
tances? L e prélèvement est-il simple à réa-
liser et à acheminer? L a qualité du rendu
de résultats est-elle inchangée?, etc.
sation de ce nouveau paramètre: cela fait
partie de mon rôle de conseil.
(1) L aboratoire de biochimie interhospitalier
Cochin-Hôtel-Dieu, service du P r L . Cynober.
(2) Ce point a fait l’objet d’une publication
dans le New England Journal of Medicine.
Contact Roche Diagnostics:
nicolas.zeitoun@roche.com
Retard diagnostique
Seuil de détec=on TnT
RULE-IN
!

35. Evidence scientifique
10mg/mL (0,01g/mL)
Troponin T
HS-troponin T
35ng/L14ng/L
Sandoval Y, et al. Clin Chem 2017

37. Twerenbold R, et al. Eur Heart J 2012
Perte de spécificité

38. Valeur absolue TnTHS
Twerenbold R, et al. Eur Heart J 2012

39. Evidence clinique
Body R, et al. JACC 2011
Des patients suspects de douleur
thoracique d’origine coronarienne
Et
Qui ont une TnTHS > 0,14 ng/L
Ont un SCA

40. Mettre les patients dehors
!
RULE-OUT !

41. Algorithme décisionnel
Roffi M, et al. Eur Heart J 2016

42. Algorithme décisionnel
Roffi M, et al. Eur Heart J 2016

43. Cinétique TnTHS/
IUS
Evaluation dynamique
-> Plus de Rule-In
-> Plus de Rule-Out

44. SCORES
Score GRACEScore TIMI
Backus B, et al. Curr Cardiol Rev 2011;7(1):2-8

45. GRACE
Chez
le patient
âgé
Granger. Arch Intern Med 2003;163:2345-53
KO !

46. TIMI N-STEMI
Protocole de diagnostic accéléré
TIMI = 0
ASPECT (2011) = 9,8%
ADAPT (2012) = 20%
New Improved ADP (2012) = 12,3%

47. TIMI KO
Chez le patient
à bas risque

48. TIMI et GRACE
n’ont pas leur
place aux
urgences
Than. Emerg Med Australas 2014;26:34-44

49. HEART
Score

50. HEART Score
Six. Neth Heart J 2008;16:191-6
Score 2-3
≈20%

51. HEART Score 0-3
13 études > 17000 pts
Pts ≈40% à bas risque
1,6% ECV à 30–45 j
HEART
atherosclerotic disease:
uspicious 2
ely suspicious 1
uspicious 0
nt ST-deviation 2
cific repolarisation
nce / LBTB / PM
0
rs 2
< 65 years 1
rs 0
actors or history of
lerotic disease*
2
k factors 1
actors known 0
mal limit 2
< 3x normal limit 1
mal limit 0
Total
for chest pain patients
1
mia Cigarette smoking
Positive family history Fanaroff. JAMA. 2015;314(18):1955-65

52. HEART Taux ECV
Paper Pts HEART
Score ≤3
MACE in
HEART ≤3 (n)
MACE in
HEART ≤3 (%)
Six 2008 120 39 1 2.6%
Backus 2010 880 303 3 0.9%
Mahler 2011 1070 904 5 0.6%
Backus 2013 2388 870 15 1.7%
Mahler 2013 991 200 2 1%
Melki 2013 410 247 1 0.4%
Six 2013 2906 820 14 1.7%
Visser 2014 255 85 5 5.9%
Leite 2015 174 98 2 2%
Mahler 2015 141 66 0 0%
Sun 2016 8255 4039 72 1.8%
TOTAL 17,590 7,671 120 1.6%
Total Mahler 1132 266 2 0.8%

53. Troponine THS
H0-H3
2 études >1000 pts
≈25% pts à bas risque
0,8% ECV à J30

54. Comment s’en sortir
HEART
Score
TnTHS/IUS H0-H3
Hess. Circulation Cardiovasc Qual Outcom 2012;5:251-9

55. Mahler S, et al. Circ Cardiovasc Qual Outcomes. 2015;8:195-203
HEART Pathway

57. Recommandations ESC
erate increase could not be excluded. Extended DAPT, compared
with 12-month treatment, yielded a significant reduction in MI
[OR 0.53 (95% CI 0.42, 0.66), P , 0.001] and stent thrombosis
[OR 0.33 (95% CI 0.21, 0.51), P , 0.001] while more major bleeds
occurred [OR 1.62 (95% CI 1.26, 2.09), P , 0.001]. In addition, all-
cause death was significantly increased in the extended DAPT group
[OR 1.30 (95% CI 1.02, 1.66), P ¼ 0.03] while CV death did not dif-
fer among the groups.185
The Prevention of Cardiovascular Events in Patients with Prior
Heart Attack Using Ticagrelor Compared to Placebo on a Back-
ground of Aspirin-Thrombolysis in Myocardial Infarction 54
(PEGASUS-TIMI 54) trial randomized 21 162 patients who had had
an MI 1–3 years earlier to ticagrelor at a dose of 90 mg twice daily,
ticagrelor at a dose of 60 mg twice daily or placebo.186
At a median
follow-up of 33 months, the study demonstrated a reduced rate of
CV death, MI or stroke with ticagrelor [HR 0.85 (95% CI 0.75,
0.96), P ¼ 0.008 and HR 0.84 (95% CI 0.74, 0.95), P ¼ 0.004 for
90 mg and 60 mg of ticagrelor vs. placebo, respectively) and increased
rates of major bleeding events (2.60% with 90 mg, 2.30% with 60 mg
and 1.06% with placebo, P , 0.001).186
All-cause mortality did not
differ between the groups. Of importance, most patients began treat-
ment with ticagrelor after an interruption in DAPT and all had prior
MI (context of secondary prevention in high-risk patients), while
patients with a history of ischaemic stroke were excluded. In conclu-
sion, while a 1-year duration of DAPT in NSTE-ACS patients is re-
commended, based on individual patient ischaemic and bleeding
risk profiles, DAPT duration may be shortened (i.e. 3–6 months)
or extended (i.e. up to 30 months) in selected patients if required.
5.2.7 Glycoprotein IIb/IIIa inhibitors
Intravenous GPIIb/IIIa inhibitors block platelet aggregation by
inhibiting fibrinogen binding to a conformationally activated
form of the GPIIb/IIIa receptor on two adjacent platelets.128
A
meta-analysis of six RCTs involving 29 570 NSTE-ACS patients,
mainly medically managed, showed a 9% RRR in death or non-fatal
MI with GPIIb/IIIa inhibitors (10.7% vs. 11.5%, P ¼ 0.02) when
added to heparin.196
The greatest benefit was observed in patients
undergoing PCI while on these agents [10.5% vs. 13.6%; OR 0.74
(95% CI 0.57, 0.96), P ¼ 0.02]. The use of GPIIb/IIIa inhibitors
was associated with an increase in major bleeding complications
without a significant increase in intracranial haemorrhage. Many
of these trials predated the routine use of P2Y12 inhibitors. While
the relative efficacy of prasugrel and ticagrelor in the trials
5.2.9 Recommendations for platelet inhibition in
non-ST-elevation acute coronary syndromes
Recommendations for platelet inhibition in non-ST-
elevation acute coronary syndromes
Recommendations Classa
Levelb
Ref.c
Oral antiplatelet therapy
Aspirin is recommended for all
patients without contraindications at
an initial oral loading dosed
of 150–
300 mg (in aspirin-naive patients) and
a maintenance dose of 75–100 mg/
day long-term regardless of treatment
strategy.
I A
129–
132
A P2Y12 inhibitor is recommended, in
addition to aspirin, for 12 months
unless there are contraindications such
as excessive risk of bleeds.
I A
137,
148,
153
† Ticagrelor (180 mg loading dose,
90 mg twice daily) is recommended,
in the absence of contraindications,e
for all patients at moderate-to-high
risk of ischaemic events (e.g. elevated
cardiac troponins), regardless of
initial treatment strategy and
including those pretreated with
clopidogrel (which should be
discontinued when ticagrelor is
started).
I B 153
† Prasugrel (60 mg loading dose,
10 mg daily dose) is recommended
in patients who are proceeding to
PCI if no contraindication.e
I B
148,
164
† Clopidogrel (300–600 mg loading
dose, 75 mg daily dose) is
recommended for patients who
cannot receive ticagrelor or
prasugrel or who require oral
anticoagulation.
I B 137
P2Y12 inhibitor administration for a
shorter duration of 3–6 months after
DES implantation may be considered in
patients deemed at high bleeding risk.
IIb A
187–
189,
192
Roffi M, et al. Eur Heart J 2016
ticagrelor 180 mg loading dose followed by 90 mg twice a day.153
Patients undergoing PCI were allowed to receive an additional
blinded 300 mg loading dose of clopidogrel (total loading dose
600 mg) or its placebo. Treatment was continued for up to 12
months, with a median duration of drug exposure of 9 months.153
In the NSTE-ACS subgroup (n ¼ 11 080), the primary composite ef-
ficacy endpoint (death from CV causes, MI or stroke) was signifi-
cantly reduced with ticagrelor compared with clopidogrel [10.0%
5.2.2.4 Cangrelor
Cangrelor is an i.v. adenosine triphosphate (ATP) analogue that binds
reversibly and with high affinity to the platelet P2Y12 receptor and has
a short plasma half-life (,10 min) (Table 8). It produces a highly ef-
fective inhibition of ADP-induced platelet aggregation immediately
after i.v. bolus administration and allows for restoration of platelet
function within 1–2 h of infusion discontinuation in NSTE-ACS pa-
tients.157
Cangrelor (30 mg/kg bolus and 4 mg/kg/min infusion) in-
Table 8 P2Y12 inhibitors
Clopidogrel
Chemical class Thienopyridine
Administration Oral
Dose
300–600mg orally
then 75 mg a day
Dosing in CKD
• Stage 3
(eGFR 30–59 mL/min/1.73m2
)
No dose adjustment
• Stage 4
(eGFR 15–29 mL/min/1.73m2
)
No dose adjustment
• Stage 5
(eGFR <15 mL/min/1.73m2
)
Use only for selected indications
(e.g.stent thrombosis prevention)
Binding reversibility Irreversible
Activation
Prodrug,with variable
liver metabolism
Onset of loading dose effecta
2–6 hoursb
Duration of effect 3–10 days
Withdrawal before surgery 5 daysc
Plasma half-life of active P2Y12 inhibitord
30–60 min
Inhibition of adenosine reuptake No
Prasugrel Ticagrelor Cangrelor
Thienopyridine Cyclopentyl-triazolopyrimidine StabilizedATP analogue
Oral Oral Intravenous
60 mg orally then
10 mg a day
180 mg orally then
90 mg twice a day
30 µg/kg bolus and
4 µg/kg/min infusion
No dose adjustment No dose adjustment No dose adjustment
No dose adjustment No dose adjustment No dose adjustment
Not recommended Not recommended No dose adjustment
Irreversible Reversible Reversible
Prodrug,with predictable
liver metabolism
Active drug,with additional
active metabolite
Active drug
30 minb
30 minb
2 min
7–10 days 3–5 days 1–2 hours
7 daysc
5 daysc
1 hour
30–60 mine
6–12 hours 5–10 min
No Yes Yes (‘inactive’ metabolite only)
ADP ¼ adenosine diphosphate; ATP ¼ adenosine triphosphate; CKD ¼ chronic kidney disease; eGFR ¼ estimated glomerular filtration rate.
a
50% inhibition of ADP-induced platelet aggregation.
b
Onset of effect may be delayed if intestinal absorption is delayed (e.g. by opiate).
c
Shortening may be considered if indicated by platelet function tests and low bleeding risk.
d
Affecting the response to platelet transfusion.
e
The distribution phase half-life is reported since it most likely reflects duration of clinically-relevant plasma levels, while the corresponding elimination phase half-life is
approximately 7 hours.
ESC Guidelines284

58. Recommandations ESC
Roffi M, et al. Eur Heart J 2016
mmended to administer
atients in whom coronary
ot known.
III B 164
s antiplatelet therapy
ibitors during PCI should
d for bailout situations or
complications.
IIa C
ay be considered in P2Y12
ve patients undergoing PCI.
IIb A
158–
161
mmended to administer
bitors in patients in whom
tomy is not known.
III A
198,
199
P2Y12 inhibition
or administration
o aspirin beyond 1 year
idered after careful
of the ischaemic and
s of the patient.
IIb A
184,
186
commendations
mp inhibitor in
with DAPT is
ed in patients at higher
risk of gastrointestinal
istory of gastrointestinal
Table 10 Dosing of glycoprotein IIb/IIIa inhibitors in
patients with normal and impaired renal function
Drug Recommendations
Normal renal
function or stage
1–2 CKD
(eGFR
≥60 mL/
min/1.73m2
)
Stage 3 CKD
(eGFR
30–59 mL/
min/1.73m2
)
Stage 4 CKD
(eGFR
15–29 mL/
min/1.73m2
)
Stage 5 CKD
(eGFR
<15 mL/
min/1.73m2
)
Bolus
180 µg/kg i.v.,
infusion
2 µg/kg/min
No adjustment
of bolus,reduce
infusion rate to
1 µg/kg/min if
eGFR
<50 mL/min/1.73m2
Not
recommended
Not
recommended
Bolus 25 µg/kg
or 10 µg/kg i.v,
infusion
0.15 µg/kg/min
No dose
adjustment
No adjustment
of bolus,reduce
infusion to
0.05 µg/kg/min
Not
recommended
Bolus
0.25 mg/kg i.v.,
infusion
0.125 µg/kg/min
(max.10 µg/min)
or for dose adjustment in the case of renal failure.
Careful evaluation of haemorrhagic risk is needed.
CKD ¼ chronic kidney disease; eGFR ¼ estimated glomerular filtration rate; i.v. ¼
intravenous; kg ¼ kilograms bodyweight.
Recommendations for the use of drugs listed in this table may vary depending on
the exact labeling of each drug in the country where it is used.
287
It is not recommended to administer
prasugrel in patients in whom coronary
anatomy is not known.
III B 164
Intravenous antiplatelet therapy
GPIIb/IIIa inhibitors during PCI should
be considered for bailout situations or
thrombotic complications.
IIa C
Cangrelor may be considered in P2Y12
inhibitor–naive patients undergoing PCI.
IIb A
158–
161
It is not recommended to administer
GPIIb/IIIa inhibitors in patients in whom
coronary anatomy is not known.
III A
198,
199
Long-term P2Y12 inhibition
P2Y12 inhibitor administration
in addition to aspirin beyond 1 year
may be considered after careful
assessment of the ischaemic and
bleeding risks of the patient.
IIb A
184,
186
General recommendations
A proton pump inhibitor in
combination with DAPT is
Table 10 Dosing of glycoprotein IIb/IIIa inhibitors in
patients with normal and impaired renal function
Drug Recommendations
Normal renal
function or stage
1–2 CKD
(eGFR
≥60 mL/
min/1.73m2
)
Stage 3 CKD
(eGFR
30–59 mL/
min/1.73m2
)
Stage 4 CKD
(eGFR
15–29 mL/
min/1.73m2
)
Stage 5 CKD
(eGFR
<15 mL/
min/1.73m2
)
Bolus
180 µg/kg i.v.,
infusion
2 µg/kg/min
No adjustment
of bolus,reduce
infusion rate to
1 µg/kg/min if
eGFR
<50 mL/min/1.73m2
Not
recommended
Not
recommended
Bolus 25 µg/kg
or 10 µg/kg i.v,
infusion
0.15 µg/kg/min
No dose
adjustment
No adjustment
of bolus,reduce
infusion to
0.05 µg/kg/min
Not
recommended
Bolus
0.25 mg/kg i.v.,
infusion
0.125 µg/kg/min
(max.10 µg/min)
or for dose adjustment in the case of renal failure.
Careful evaluation of haemorrhagic risk is needed.
CKD ¼ chronic kidney disease; eGFR ¼ estimated glomerular filtration rate; i.v. ¼
intravenous; kg ¼ kilograms bodyweight.
SC Guidelines 287

59. Recommandations ESC
early and/or delayed intervention in NSTE-ACS patients.304,328,329
analysis of high-risk patients (i.e. one-third of patients with a GRACE
EMS = emergency medical services; PCI = percutaneous coronary intervention.
Symptoms Onset
First medical contact NSTE-ACS diagnosis
PCI center
Very high
Immediate
Invasive
(<2 hr)
Early
invasive
(<24 hr)
Invasive
(<72 hr)
Non-invasive
testing if
appropriate
High
Intermediate
Immediate transfer to PCI center
Same-day transfer
Transfer
Transfer
optional
Riskstratification
Therapeutic
strategy
Low
EMS or Non–PCI center
Very high
High
Intermediate
Low
Figure 6 Selection of non-ST-elevation acute coronary syndrome (NSTE-ACS) treatment strategy and timing according to initial risk
stratification.
ESC Guidelines296
Roffi M, et al. Eur Heart J 2016

60. Recommandations ESC
< 2H
acute coronary syndromes
Recommendations for invasive coronary angiography
and revascularization in non-ST-elevation acute
coronary syndromes
Recommendations Classa
Levelb
Ref.c
An immediate invasive strategy
(<2 h) is recommended in patients with
at least one of the following
very-high-risk criteria:
– haemodynamic instability or
cardiogenic shock
– recurrent or ongoing chest
pain refractory to medical
treatment
– life-threatening arrhythmias or
cardiac arrest
– mechanical complications of MI
– acute heart failure with refractory
angina or ST deviation
– recurrent dynamic ST- or T-wave
changes, particularly with
intermittent ST-elevation.
I C
An early invasive strategy (<24 h)
is recommended in patients with at
least one of the following high-risk
criteria:
– rise or fall in cardiac troponin
compatible with MI
– dynamic ST- or T-wave changes
(symptomatic or silent)
– GRACE score .140.
I A
303,
326,
327
B
C
D
G
e
a
S
T
T
a
C
b
c
R
Roffi M, et al. Eur Heart J 2016
< 24H

61. Recommandations ESC
Roffi M, et al. Eur Heart J 2016
within the Heart Team if delayed CABG of
an option.
patients with cardiogenic shock
develop in up to 3% of NSTE-ACS patients
d has become the most frequent cause of
his setting.382 – 384
One or more partial or
ns may result in severe heart failure, espe-
ing LV dysfunction, reduced cardiac output
l organ perfusion. More than two-thirds of
el CAD. Cardiogenic shock may also be re-
mplications of NSTEMI, including mitral re-
pillary muscle dysfunction or rupture and
e wall rupture. In patients with cardiogenic
ary angiography is indicated and PCI is the
evascularization modality. If the coronary
or PCI, patients should undergo emergent
ra-aortic balloon counterpulsation in MI
enic shock has been challenged.385
Extra-
xygenation and/or implantable LV assist
ed in selected patients.
An invasive strategy (<72 h) is
recommended in patients with at least
one of the following intermediate-risk
criteria:
– diabetes mellitus
– renal insufficiency (eGFR
,60 mL/min/1.73 m2
)
– LVEF ,40% or congestive heart
failure
– early post-infarction angina
– recent PCI
– prior CABG
– GRACE risk score .109 and
,140,
or recurrent symptoms or known
ischaemia on non-invasive testing.
I A
322,
324
In patients with none of the above
mentioned risk criteria and no
recurrent symptoms, non-invasive
testing for ischaemia (preferably
with imaging) is recommended
before deciding on an invasive
evaluation.
I A
113,
114
In centres experienced with radial
ESC Guidelines
?

63. non-ST+
Fréquent…
TRÈS grave

65. Signes
Atypiques…
…mais
TRÈS fréquents

66. S’appuyer sur
l’ …
…même si cela peut être compliqué

67. Troponine HS

68. Même filière
Mêmes traitements

69. Ecoutez le patient, il est en train de
vous donner le diagnostic.
Sir William Osler
Ne jamais laisser notre savoir prendre
le dessus sur ce qui demeure le plus
important, notre ignorance.
Henry David Thoreau

70. @DocNikko
Nicolas PESCHANSKI
#FrOAMed