ESC 2020 guidelines for NSTEMI, what is new in 2020, early invasive startey in NSTEMI, Quality indicators,

1. ESC Guidelines for the management
of acute coronary syndromes in
patients presenting without
persistent ST-segment
elevation(2020)
(NSTEMI)
By: Dr. Himanshu Rana

2. 2020 ESC updates
• Acute Coronary Syndromes (ACS) in Patients
Presenting without Persistent ST-Segment
Elevation
• Adult Congenital Heart Disease
• Atrial Fibrillation
• Sports cardiology and exercise in patients with
CVD

3. Universal definition of MI
Detection of increase and/or decrease of cardiac biomarker,
preferably hs-cTn – T / I, with one value above the 99th
percentile of URL & at least one of the following:
1) Symptoms of myocardial ischaemia.
2) New ischaemic ECG changes.
3) Development of pathological Q waves on ECG.
4) Imaging evidence of loss of viable myocardium or new
RWMA in a pattern consistent with ischaemic etiology.
5) Intracoronary thrombus detected on angiography or
autopsy.

4. What is new?
Diagnosis
• ESC 0 h/1 h hs-cTn algorithm is recommended. (Class I,
Level B)
• As an alternative to ESC 0 h/1 h algorithm, 0 h/2 h
algorithm. (Class I, Level B)
• Additional testing after 3 h if the first two hs-cTn
inconclusive and the clinical condition is still suggestive of
ACS. (Class I, Level C)
• For diagnosis, not recommended to routinely measure
additional biomarkers such as CK, CK-MB, h-FABP, or co-
peptin, in addition to hs-cTn. (Classs III)

5. Risk stratification
• Measuring BNP or NT-proBNP plasma concentrations should be
considered to gain prognostic information. (Class IIa, Level B)
Antithrombotic treatment
• Routine pre-treatment with P2Y12 receptor inhibitor is not
recommended to patients with unkown coronary anatomy
and early invasive management is planned.
(Class III)
• In patients with NSTEMI who cannot undergo an early
invasive strategy, pre-treatment with a P2Y-12 receptor
inhibitor may be considered depending on bleeding risk.
(Class IIb)

6. Antithrombotic treatment
• De-escalation of P2Y inhibitor treatment (e.g. with a
switch from prasugrel/ticagrelor to clopidogrel) may
be considered as an alternative DAPT strategy,
especially for ACS patients deemed unsuitable for
potent platelet inhibition. (Class IIb)
• De-escalation may be done unguided based on
clinical judgment, or guided by platelet function
testing, or CYP2C19 genotyping depending on the
patient’s risk profile and availability of respective
assays.(Class IIb)

7. Antithrombotic treatment
• In patients with AF (CHA2DS2-VASc score ≥1 in men/ ≥2 in women),
DAT is recommended after a short period of TAT (up to 1 week), as
default strategy using NOAC at the recommended dose for stroke
prevention & single oral antiplatelet (preferably clopidogrel).
(Class-I)
• Discontinuation of antiplatelet in patients treated with OACs is
recommended after 12 months. (Class-I)
• In patients with moderate/high risk of stent thrombosis DAT with
an OAC and ticagrelor/prasugrel may be considered as an
alternative to TAT with an OAC, aspirin, and clopidogrel. (Class IIb)

8. Invasive treatment
An early invasive strategy within 24 h recommended in patients
with any high-risk criteria: (Class I)
– Diagnosis of NSTEMI.
– Dynamic or presumably new contiguous ST/T-segment changes
suggesting ongoing ischaemia.
– Transient ST-segment elevation.
– GRACE risk score >140.
• Selective invasive strategy after appropriate ischaemia testing
or detection of obstructive CAD by CCTA is recommended in
patients considered at low risk. (Class I)
• Delayed, as opposed to immediate, angiography should be
considered in haemodynamically stable patients without ST-
segment elevation successfully resuscitated after an out-of-
hospital cardiac arrest. (Class IIa)

9. Invasive treatment
• Complete revascularization should be considered in
NSTE-ACS patients without cardiogenic shock and
with multivessel CAD. (Class IIa)
• Complete revascularization during index PCI may be
considered in NSTE-ACS patients with multivessel
disease. (Class IIb)
• FFR-guided revascularization of non-culprit NSTEMI
lesions may be used during index PCI. (Class IIb)

10. 2015 2020Class I
Class IIa

11. 2015
2020Class I
Class IIa
Class IIb

12. New sections
• MINOCA
• SCAD
• QIs in NSTE-ACS treatment
New/revised concepts
• Rapid rule-in and rule-out algorithms
• Risk stratification for an early invasive approach
• Definition of high bleeding risk
• Definitions of very high and high ischaemic risk
• The gap in evidence and corresponding RCTs to
be performed

13. Diagnostic tools
Electrocardiogram
• Resting 12-lead ECG – first-line diagnostic tool
• To perform it within 10 min of the patient’s arrival & repeat
if recurrent symptoms/diagnostic uncertainty. (Class I, B/C)
• In patients with RBBB, ST-elevation is indicative of STEMI
while ST-segment depression in lead I, aVL, and V5-6 is
indicative of NSTEMI.
• Additional ECG leads (V3R, V4R, V7V9) are recommended if
ongoing ischaemia is suspected when standard leads are
inconclusive (Class Ic, Level C)
• In ECG with paced ventricular beats, the ECG is of no
diagnostic help.

14. Biomarkers: hs-cardiac troponin
Result in ~4% absolute and
~20% relative increases in
the detection of type 1 MI

15. Conditions other than MI a/w
troponin elevation
• Tachyarrhythmias
• Heart failure
• Hypertensive emergencies
• Critical illness (e.g. shock/sepsis/burns)
• Myocarditis
• Takotsubo syndrome
• Valvular heart disease (e.g. aortic
stenosis)
• Aortic dissection
• Pulmonary embolism, pulmonary
hypertension
• Renal dysfunction & associated cardiac
disease
• Acute neurological event (e.g. stroke or SAH)
• Cardiac contusion or cardiac procedures
(CABG, PCI, ablation, pacing, cardioversion, or
endomyocardial biopsy)
• Hypo- and hyperthyroidism
• Infiltrative diseases (e.g. amyloidosis,
haemochromatosis, sarcoidosis, scleroderma)
• Myocardial drug toxicity or poisoning (e.g.
doxorubicin, 5-FU, herceptin, snake venoms)
• Extreme endurance efforts
• Rhabdomyolysis

16. Clinical implications of hs-cTrop assays
Levels of hs-cTn should be interpreted as quantitative markers of
cardiomyocyte damage (i.e. the higher the level, the greater the like-lihood
of MI):
• Elevations >5-fold the URL have high (>90%) PPV for acute type 1 MI.
• Elevations up to 3-fold the URL have only limited (5060%) PPV for AMI &
may be associated with broad spectrum of conditions.
• It is common to detect circulating levels of cardiac troponin in healthy
individuals.
Rising and/or falling cardiac troponin levels differentiate acute (as in MI)
from chronic cardiomyocyte damage (the more pronounced the change,
the higher the likelihood of AMI).

17. Rapid ‘rule-in’ and ‘rule-out’ algorithms
RAPID – CPU
RAPID – TNT

19. Assay specific cut-off levels (in ng/l)

20. Imaging
• In patients with cardiac arrest/haemodynamic instability of
presumed cardiovascular origin, echocardiography is
recommended immediately following a 12-lead ECG. (Class I, C)
• In patients with no recurrence of chest pain, normal ECG,
Normal hs-cTn but still suspected ACS, a non-invasive stress test
(preferably with imaging) for inducible ischaemia or CCTA
before deciding on an invasive approach. (Class I, B)
• Echocardiography to evaluate regional and global LV function
and to rule in or rule out differential diagnoses. (Class I, C)
• CCTA as alternative to ICA to exclude ACS in low-to-intermediate
likelihood of CAD and normal/inconclusive cTn and/or ECG .
(Class I, A)

21. Monitoring
• Continuous rhythm monitoring till diagnosis of NSTEMI ruled in/out.
(Class I, C)
• It is recommended to admit NSTEMI patients to a monitored unit.
(Class I, C)
• Rhythm monitoring up to 24 h or to PCI (whichever comes first) is
recommended in NSTEMI patients at low risk for cardiac arrhythmias.
(Class I, C)
• Rhythm monitoring for >24 h is recommended in NSTEMI patients at
increased risk for cardiac arrhythmias. (Class I, C)
• In absence of signs/symptoms of ongoing ischaemia, rhythm
monitoring in UA may be considered inselected patients (e.g. suspicion
of coronary spasm or associated symptoms suggestive of arrhythmic
events). (Class II b, C)

22. Risk assessment and outcomes
Biomarkers
• To measure hs-cTn serially for prognostication.
(Class Ib, B)
• Measuring BNP or NT-proBNP should be
considered for prognosis. (Class IIa, B)
• Additional biomarkers like mr pro-ANP, hs CRP,
mr pro-adrenomedullin, GDF-15, copeptin, and
h-FABP not recommended for routine
risk/prognosis assessment. (Class III, B)

23. Score to risk stratify in NSTE-ACS
• GRACE risk score should be considered for
estimating prognosis. (Class IIa, Level B)
• The use of risk scores designed to evaluate the
benefits and risks of different DAPT durations
may be considered. (Class IIb, Level A)
• To estimate bleeding risk, the use of scores may
be considered in patients undergoing coronary
angiography. (Class IIb, Level B)

24. GRACE Risk Score
GRACE risk score 1.0
• www.outcomes-umassmed.org/risk_models_grace_orig.aspx
GRACE risk score 2.0
• www.outcomes-umassmed.org/grace/acs_risk2/index.html

26. Bleeding risk assessment
• Can Rapid risk stratification of Unstable angina patients Suppress
ADverse outcomes with Early (CRUSADE);
https://www.mdcalc.com/crusade-score-post-mibleeding-risk)
• Acute Catheterization and Urgent Intervention Triage strategY
(ACUITY) scores
• Alternative to these scores is Academic Research Consortium for
High Bleeding Risk (ARC-HBR).
• DAPT and the PREdicting bleeding Complications In patients
undergoing Stent implantation and subsEquent Dual Anti Platelet
Therapy (PRECISE-DAPT) scores

27. Academic Research Consortium for High
Bleeding Risk at the time of PCI
• High bleeding risk if at least one major or two minor
criteria are met

28. Recommendations for antithrombotic treatment
• Aspirin for all patients without contraindications initial oral LD
150 – 300 mg (or 75 – 250 mg i.v.), and MD of 75 – 100 mg o.d.
for long-term t/t. (I, A)
• P2Y12 receptor inhibitor with aspirin, and maintained over 12
months unless there are contraindicated or excessive bleeding
risk. (I, A)
• Options are:
– Prasugrel in P2Y receptor inhibitor-naı¨ve patients proceeding to PCI
(60 mg LD, 10 mg/d as standard dose, 5 mg/d for patients aged >_75
years or with a body weight <60 kg). (I, B)
– Ticagrelor irrespective of the planned treatment strategy (invasive or
conservative) (180 mg LD, 90 mg b.i.d.). (I, B)
– Clopidogrel (300600 mg LD, 75 mg daily dose), only if
prasugrel/ticagrelor not available/not tolerated/contraindicated.
(I, C)

29. • Prasugrel in preference to ticagrelor for NSTE-ACS who proceed to
PCI.(IIa, B)
• GP IIb/IIIa antagonists only for bail-out in evidence of no-reflow/
thrombotic complication.(IIa, C)
• Cangrelor may be considered in P2Y12 receptor inhibitor-nai¨ve
patients undergoing PCI. .(IIb, B)
• Pre-treatment with a P2Y12 receptor inhibitor may be considered in
patients with NSTE-ACS who are not planned to undergo an early
invasive strategy and do not have an HBR. .(IIa, C)
• GP IIb/IIIa antagonists contraindicated in patients with unknown
coronary anatomy.(III, A)
• Routine pre-treatment with P2Y12 receptor inhibitor not
recommended in patients with unknown coronary anatomy & an early
invasive management is planned.(III, A)

30. Peri-interventional anticoagulant t/t
• Parenteral anticoagulation for all patients, in addition to antiplatelet at diagnosis
&during revascularization according to both ischaemic and bleeding risks.(I, A)
• UFH (weight-adjusted i.v. bolus during PCI of 70100 IU/kg, or 5070 IU/kg in combination
with a GP IIb/IIIa inhibitor; ACT target of 250 – 350s, or 200 – 250s with GP IIb/IIIa
inhibitor) in patients undergoing PCI. (I, A)
• In cases of medical treatment or logistical constraints for transferring the patient to PCI
within the required time frame, fondaparinux is recommended and, single bolus UFH is
recommended at the time of PCI. (I, B)
• To select anticoagulation according to both ischaemic and bleeding risks, and according
to efficacy safety profile of chosen agent. (I, C)
• Enoxaparin (i.v.) in patients pre-treated with subcutaneous enoxaparin. (IIa, B)
• Discontinuation of parenteral anticoagulation immediately after invasive procedure(IIa,
C)
• Bivalirudin may be considered as alternative to UFH. (IIb, A)
• Crossover of UFH and LMWH is not recommended(III)

31. Risk criteria for extended treatment
with a second antithrombotic agent

33. Recommendations for maintenance
treatment in patients with NSTE-ACS
• Patients treated with coronary stent implantation, DAPT with a P2Y12 receptor
inhibitor with aspirin for 12 months unless contraindicated such as excessive
risk of bleeding. (I, A)
• Prolonged antithrombotic duration with second antithrombotic agent to aspirin
for long-term secondary prevention to be considered in patients with high risk
of ischaemic events & without increased risk of major/life-threatening
bleeding. (IIa, A)
• Adding a second antithrombotic agent to aspirin for extended long-term
secondary prevention may be considered in patients with moderately increased
risk of ischaemic events & without increased risk of major or life-threatening
bleeding. (IIb, A)
• In ACS patients with no prior Stroke/TIA at high ischaemic risk and low
bleeding risk and receiving aspirin and clopidogrel, low-dose rivaroxaban (2.5
mg b.i.d. for approximately 1 year) may be considered after discontinuation of
parenteral anticoagulation. (IIb, B)

34. Shortening antithrombotic treatment duration
• After PCI with high risk of bleeding (e.g. PRECISE-DAPT >_25 or ARC-HBR
criteria met), discontinuation of P2Y12 receptor inhibitor therapy after 3
months should be considered. (IIa, A)
• After PCI in patients with DAPT, stopping aspirin after 3 – 6 months should be
considered, depending on balance between ischaemic and bleeding risk. (IIb, A)
• Patients unsuitable for potent platelet inhibition unguided/guided de-
escalation of P2Y12 receptor inhibitor (e.g. from prasugrel/ticagrelor to
clopidogrel) may be considered an alternative strategy based on clinical
judgment or by platelet function testing or CYP2C19 genotyping, depending on
patient’s risk profile and availability of respective assays(IIb, A)

35. Recommendations for anti-ischaemic
drugs in acute phase of NSTEMI
• S/l or i.v. nitrates & early initiation of beta-blocker in
patients with ongoing ischaemic symptoms and without
contraindications. (I, C)
• To continue chronic β-blocker therapy unless in overt HF. (I,
C)
• i.v. nitrates in patients with uncontrolled HTN or signs of HF.
(I, C)
• In patients with suspected/confirmed vasospastic angina,
CCB’s and nitrates to be considered and β-blocker avoided.
(IIa, B)

36. Recommendations for combining
antiplatelet agents and anticoagulants

37. Recommendations for combining
antiplatelet agents and anticoagulants

39. Recommendations for bleeding
management and blood transfusion

40. (I, C) (I, A) (I, A)

41. Very high risk
• Haemodynamic instability or CS.
• Recurrent or refractory chest pain despite medical treatment.
• Life-threatening arrhythmias.
• Mechanical complications of MI.
• Heart failure clearly related to NSTE-ACS.
• Presence of ST-segment depression >1 mm in >_6 leads additional to
ST-segment elevation in aVR and/or V1
High risk
• Diagnosis of NSTEMI
• Dynamic or presumably new contiguous ST/T-segment changes
suggesting ongoing ischaemia.
• Transient ST-segment elevation.
• GRACE risk score >140

42. Technical aspects

43. MINOCA
1. AMI (modified from the ‘Fourth Universal Definition of MI)
2. Non-obstructive coronary arteries on angiography:
– Defined as the absence of obstructive disease on angiography (i.e. no
coronary artery stenosis ≥50%) in any major epicardial vessel
– This includes patients with:
• Normal coronary arteries (no angiographic stenosis)
• Mild luminal irregularities (angiographic stenosis <30% stenoses)
• Moderate coronary atherosclerotic lesions (stenoses >30% but
<50%efinition of Myocardial Infarction’ criteria)
3. No specific alternate diagnosis for the clinical presentation:
– Alternate diagnoses include, but are not limited to, non-ischaemic
causes such as sepsis, pulmonary embolism, and myocarditis

45. Recomendation

46. NSTEMI with HF/Shock

47. Lifestyle management

48. Pharmacological long term treatment

50. Management strategy