NSTEACS :

How to Stratify the Risk

and When to Refer

dr. Wenni Erwindia, SpJP

 ED  CCU  Cath Lab Risk Stratification for Chest Pain

Three levels of risk stratification are pertinent to the ED:

• Low, intermediate, or high risk that ischemic symptoms are a result of
CAD

• Low, intermediate, or high risk of short-term death or nonfatal MI

from ACS

• Dynamic, ongoing risk-oriented evaluation of low- or intermediate-

risk patients for “conversion” to high-risk status that is linked to
intensity of treatment
Risk Stratification Tools in the ED
• History and Physical
• Standard ECG and Non-standard ECG leads
· Cardiac Biomarkers
• Troponin I or T, CK-MB, myoglobin
· Predictive Indices / Schemes
· Non-Invasive Imaging Studies
· Echocardiogram
· Exercise testing
· Technetium-99m-sestamibi: stress and rest
 Initial Evaluation
Risk Stratification (1)
I IIa IIb III

Early risk stratification by symptoms, physical findings,

ECG, cardiac markers

12-lead ECG within 10 min for ongoing pain, or ASAP if pain

has resolved at presentation

Cardiac markers, Troponins and CK-MB, for initial

assessment

Monitoring, repeat ECG and cardiac markers in 6-12 hours, if

initial results normal
 Initial Evaluation
Risk Stratification (2)

I IIa IIb III

If <6 hours after symptom onset, add early
myoglobin or CK-MB to troponin

C-reactive protein, other markers of inflammation

Total CK, SGOT, HBDH, LDH

 Clinical Assessment (1)

· Rapid, focused evaluation

· Decisions based on this evaluation have substantial clinical
and economic consequences
· Are the symptoms a manifestation of ACS?
· If so, what is the prognosis?
· Identify signs of life-threatening instability
· Triage to most appropriate area
· Typically an ED or chest pain unit
 Clinical Assessment (2)

· Risk status determined in the ED by:

· Assessment of anginal symptoms
· Careful physical examination
· Electrocardiogram
· Cardiac biomarkers
· CAD risk factors
· Illicit drug use
· Initial risk stratification assignment drives pace of
subsequent evaluation and treatment
 Clinical Assessment (3)

· High-risk features apparent in the ED:

· Accelerated pattern of angina
· Ongoing rest pain > 20 min
· Signs of CHF
· Hemodynamic instability
· Arrhythmias - Atrial or ventricular
· Advanced age (> 75 years)
· Ischemic ECG changes
· Elevated cardiac markers
 Electrocardiogram

· Carries diagnostic and prognostic value

· Especially valuable if captured during pain
· ST-segment depression or transient ST-segment elevation are
primary ECG markers of UA/NSTEMI
· 75% of patients with + CK-MB do not develop Q waves
· Differentiation between UA and NSTEMI relies upon positive
biomarkers
· Inverted T-waves suggestive of ischemia, particularly with
good chest pain story
 Biomarkers: CK/CKMB

· Until recently the principal serum marker used in evaluation of

ACS despite known limitations:
· Low levels in healthy persons limits specificity
· MB band may be elevated in skeletal muscle damage
· Different MB isoforms exist in myocardium (MB2) and in
plasma (MB1), and differentiating assay is not widely
available
 Biomarkers: Troponins

· Very useful in diagnosis and prognosis of ACS

· Normally not detectable in blood of healthy persons;
· cTnI or cTnT can be positive with negative CK-MB = “minor
myocardial damage”
· Predictive of MI and death when elevated, independent of CK-
MB levels
· Elevated troponins validated as a predictor of enhanced
treatment benefit from aggressive therapies (LMW heparins, GP
IIb/IIIa inhibitors, early invasive strategy)
 Predictive Indices - Risk Scores in the ED

 Combine clinical history, physical exam findings, ECG

signs of ischemia, and cardiac marker results
• PURSUIT and TIMI Risk Scores
 Therapies such as LMW heparin and GP IIb/IIIa
inhibitors have greater benefit in patients with higher risk
scores
 Have not been tested prospectively in the ED
 Risk scores not specifically recommended by the
ACC/AHA Guidelines
 TIMI Risk Score* for NSTE-ACS
TIMI Risk All-Cause Mortality, New or Recurrent MI, or Severe
Score Recurrent Ischemia Requiring Urgent Revascularization
Through 14 d After Randomization, %
0–1 4.7
2 8.3
3 13.2
4 19.9
5 26.2
6–7 40.9

*The TIMI risk score is determined by the sum of the presence of 7 variables at
admission; 1 point is given for each of the following variables: ≥65 y of age; ≥3 risk
factors for CAD; prior coronary stenosis ≥50%; ST deviation on ECG; ≥2 anginal
events in prior 24 h; use of aspirin in prior 7 d; and elevated cardiac biomarkers.
 GRACE Risk Model Nomogram

To convert serum creatinine level to micromoles per liter, multiply by 88.4.

 Immediate Management

I IIa IIb III

Classify as non-cardiac, chronic stable angina, possible ACS,
or definite ACS
Evaluate for immediate reperfusion therapy if definite ACS
and ST-segment  present

Pharmacological or exercise stress test, if possible ACS and

serial biomarkers and ECGs are normal

Admit pts with definite ACS, ongoing pain,  biomarkers,

new ST  or deep T-wave inversion, abnormal
hemodynamics, or (+) stress test
 Early Hospital Care

Ischemia-Guided Strategy
Versus
Early Invasive Strategies
Algorithm for Management of Patients With Definite or Likely NSTE-ACS
NSTE-ACS:
Definite or Likely

Ischemia-Guided Strategy Early Invasive Strategy

Initiate DAPT and Anticoagulant Therapy Initiate DAPT and Anticoagulant Therapy
1. ASA (Class I; LOE: A) 1. ASA (Class I; LOE: A)

2. P2Y12 inhibitor (in addition to ASA) (Class I; LOE: B) : 2. P2Y12 inhibitor (in addition to ASA) (Class I; LOE: B):
·Clopidogrel or ·Clopidogrel or
·Ticagrelor ·Ticagrelor

3. Anticoagulant: 3. Anticoagulant:
·UFH (Class I; LOE: B) or ·UFH (Class I; LOE: B) or
·Enoxaparin (Class I; LOE: A) or ·Enoxaparin (Class I; LOE: A) or
·Fondaparinux (Class I; LOE: B) ·Fondaparinux† (Class I; LOE: B) or
·Bivalirudin (Class I; LOE: B)
Can consider GPI in addition to ASA and P2Y12 inhibitor
in high-risk (e.g., troponin positive) pts
(Class IIb; LOE: B)
·Eptifibatide
·Tirofiban

Medical therapy
chosen based on cath
findings

Therapy Therapy
Effective Ineffective

PCI With Stenting CABG

Initiate/continue antiplatelet and anticoagulant Initiate/continue ASA therapy and
therapy discontinue P2Y12 and/or GPI therapy
1. ASA (Class I; LOE: B) 1. ASA (Class I; LOE: B)

2. P2Y12 Inhibitor (in addition to ASA) : 2. Discontinue clopidogrel/ticagrelor 5 d

·Clopidogrel (Class I; LOE: B) or
·Prasugrel (Class I; LOE: B) or
·Ticagrelor (Class I; LOE: B)
3. GPI (if not treated with bivalirudin at time of PCI)
·High-risk features, not adequately pretreated
with clopidogrel (Class I; LOE: A)
·High-risk features adequately pretreated with
clopidogrel (Class IIa; LOE: B)
4. Anticoagulant:
·Enoxaparin (Class I; LOE: A) or
·Bivalirudin (Class I; LOE: B) or
·Fondaparinux† as the sole anticoagulant (Class
III: Harm; LOE: B) or
·UFH (Class I; LOE: B)
before, and prasugrel at least 7 d before
elective CABG
3. Discontinue clopidogrel/ticagrelor up to
24 h before urgent CABG (Class I; LOE: B).
May perform urgent CABG <5 d after
clopidogrel/ticagrelor and <7 d after
prasugrel discontinued
4. Discontinue eptifibatide/tirofiban at
least 2-4 h before, and abciximab ≥12 h
before CABG (Class I; LOE: B)
Late Hospital/Posthospital Care
1. ASA indefinitely (Class I; LOE: A)
2. P2Y12 inhibitor (clopidogrel or
ticagrelor), in addition to ASA, up
to 12 mo if medically treated
(Class I; LOE: B)

3. P2Y12 inhibitor (clopidogrel,

prasugrel, or ticagrelor), in
addition to ASA, at least 12 mo if
treated with coronary stenting
(Class I; LOE: B)
 NSTE-ACS:
Definite or Likely

Ischemia-Guided Strategy Early Invasive Strategy

Initiate DAPT and Anticoagulant Therapy Initiate DAPT and Anticoagulant Therapy
1. ASA (Class I; LOE: A) 1. ASA (Class I; LOE: A)

2. P2Y12 inhibitor (in addition to ASA) (Class I; LOE: B) : 2. P2Y12 inhibitor (in addition to ASA) (Class I; LOE: B):
·Clopidogrel or ·Clopidogrel or
·Ticagrelor ·Ticagrelor

3. Anticoagulant: 3. Anticoagulant:
·UFH (Class I; LOE: B) or ·UFH (Class I; LOE: B) or
·Enoxaparin (Class I; LOE: A) or ·Enoxaparin (Class I; LOE: A) or
·Fondaparinux (Class I; LOE: B) ·Fondaparinux† (Class I; LOE: B) or
·Bivalirudin (Class I; LOE: B)
Can consider GPI in addition to ASA and P 2Y12 inhibitor
in high-risk (e.g., troponin positive) pts
(Class IIb; LOE: B)
·Eptifibatide
·Tirofiban

Medical therapy
chosen based on cath
findings

Therapy Therapy
Effective Ineffective

PCI With Stenting CABG

Initiate/continue antiplatelet and anticoagulant Initiate/continue ASA therapy and
therapy discontinue P2Y12 and/or GPI therapy
1. ASA (Class I; LOE: B) 1. ASA (Class I; LOE: B)

2. P2Y12 Inhibitor (in addition to ASA) : 2. Discontinue clopidogrel/ticagrelor 5 d

·Clopidogrel (Class I; LOE: B) or
·Prasugrel (Class I; LOE: B) or
·Ticagrelor (Class I; LOE: B)
3. GPI (if not treated with bivalirudin at time of PCI )
·High-risk features, not adequately pretreated
with clopidogrel (Class I; LOE: A)
·High-risk features adequately pretreated with
clopidogrel (Class IIa; LOE: B)
4. Anticoagulant:
·Enoxaparin (Class I; LOE: A) or
·Bivalirudin (Class I; LOE: B) or
·Fondaparinux† as the sole anticoagulant (Class
III: Harm; LOE: B) or
·UFH (Class I; LOE: B)
before, and prasugrel at least 7 d before
elective CABG
3. Discontinue clopidogrel/ticagrelor up to
24 h before urgent CABG (Class I; LOE: B).
May perform urgent CABG <5 d after
clopidogrel/ticagrelor and <7 d after
prasugrel discontinued
4. Discontinue eptifibatide/tirofiban at
least 2-4 h before, and abciximab ≥12 h
before CABG (Class I; LOE: B)
Late Hospital/Posthospital Care
1. ASA indefinitely (Class I; LOE: A)
2. P2Y12 inhibitor (clopidogrel or
ticagrelor), in addition to ASA, up
to 12 mo if medically treated
(Class I; LOE: B)

3. P2Y12 inhibitor (clopidogrel,

prasugrel, or ticagrelor), in
addition to ASA, at least 12 mo if
treated with coronary stenting
(Class I; LOE: B)

†
In patients who have been treated with fondaparinux (as upfront therapy) who are undergoing PCI, an
additional anticoagulant with anti-IIa activity should be administered at the time of PCI because of the
risk of catheter thrombosis.
The “Key” to Risk Stratification

 Link ongoing evaluation of risk to changes

in intensity of therapy
 Develop risk stratification schemes that
reflect capabilities of ED and
needs/preferences of cardiologists
 Develop treatment pathways that provide for
independent response of emergency
physicians to recognition of higher risk
levels
 The “Rallying Cry” for CRUSADE . . .

A seamless transition of optimal care—diagnostic and

therapeutic—from the ED to the Cardiology Service . . .

. . . starts with a successful risk stratification strategy