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Risk Stratification, Electrocardiogram,

and Biomarker in ACS


Isman Firdaus
Management Strategy

Step 1. initial evaluation

Step 2. Diagnosis validation, risk assessment and


rhythm monitoring

Step 3. invasive strategy

Step 4. revascularization modalities

Step 5. hospital discharge


and post-discharge management

Roffi M et al. European Heart Journal 2015. doi:10.1093/eurheartj/ehv320 4


Benefit of Risk Stratification
Risk stratification should be performed to identify high-risk individuals rapidly and reduce the delay
to an early invasive approach vs. low-risk individuals who benefit from a conservative approach.

• Triage of patients to the appropriate location for


delivery of medical care

• Aids consideration of risks/benefits when choosing among


therapeutic options

• Encourages optimal usage of therapy and resources

5
Hamm CW, et al. Eur Heart J. 2011;32:2999-3054.
Components of Risk
Assessment for ACS
An overall estimate of patient risk is made from clinical findings as well as consideration of
patient history and comorbidities.

Initial ECG
Universal
Elevation of clinical
biomarkers markers of
risk

Risk-scoring
Presence of
tools:
symptoms
GRACE and
at rest
TIMI

6
Hamm CW, et al. Eur Heart J. 2011;32:2999-3054.
Risk Stratification is important in NSTEACS
Management
Hamm CW, et al. Eur Heart J. 2011;32:2999-3054.
Tools for Estimation of
Early Risk at Presentation
The TIMI and GRACE risk models help guide rapid treatment decisions when
patients present with symptoms of ACS.1

GRACE Risk Score1 TIMI Risk Score2


8 variables; requires a computer application Range 0-7, +1 for each of 7 variables, score is
to calculate calculated by adding the variables:
• Older age • Age ≥65 years
• Killip class • >3 CAD risk factors
• Systolic blood pressure • Known CAD (stenosis ≥50%)
• ST-segment deviation • ASA in past 7 days
• Cardiac arrest during presentation • ≥2 severe angina episodes in last
• Serum creatinine level 24 hours
• Positive initial cardiac markers • ST changes ≥0.5 mm
• Heart rate • Cardiac markers

The TIMI Risk Score is considered simpler but less


accurate than the GRACE Risk Score3

ASA=aspirin therapy 9
1. Anderson JL, et al. J Am Coll Cardiol. 2007;50:e1-e157. 2. www.timi.org 3. Hamm CW, et al. Eur Heart J. 2011;32:2999-3054.
Risk Scores and Clinical Outcomes
High GRACE risk scores are associated with increased risk of death,
both in-hospital and after discharge.

GRACE Risk In-Hospital


Risk Category
Score Death, %

Low ≤108 <1


Intermediate 109-140 1-3
High >140 >3

Post Discharge to
GRACE Risk
Risk Category 6-Month Death,
Score
%
Low ≤88 <3
Intermediate 89-118 3-8
High >118 >8

10
Hamm CW, et al. Eur Heart J. 2011;32:2999-3054.
GRACE REGISTRY
STEMI

NSTEMI
Higher mortality 6
months after discharge in
UA
NSTEMI vs STEMI

NSTEMI

STEMI

UA

Fox KAA et al. BMJ 2006;333:1091-1094


GRACE SCORE

Predictor Score Predictor Score Predictor Score

Age, years Systolic Blood Pressure (mmHg) Killip class

< 40 0 < 80 63 I 0
80 – 99 58 II 21
40 - 49 18
100 - 119 47 III 43
50 - 59 36
120 - 139 37 IV 64
60 - 69 55
140 - 159 26
70 - 79 73 160 - 199 11 Predictor Score
80 91 > 200 0 Cardiac arrest at 43
admission

Predictor Score Predictor Score Elevated cardiac 15


markers
Heart Rate , beats/min Creatinine (µmol/L)
ST Segment deviation 30
0 - 34 2
< 70 0
35 – 70 5
70-89 7 Risk category GRACE In-hospital
71 – 105 8 (tertile) Risk Score death (%)
90-109 13
106 – 140 11
Low ≤ 108 <1
110 - 149 23
141 – 176 14
150 - 199 36 Intermediate 109 - 140 1-3
177 – 353 23
> 200 46 ≥ 354 31 High > 140 >3

Khalill R et al. Exp Clin Cardiol.2009; 14(2): e25 – e30


NSTEMI shows greater number of coronary
lesions vs STEMI

LA Ferrara et al. Int J Cardiol. 2013;168(3):2905-6.


CRUSADE Bleeding Risk Score

Hamm CW et al. Eur Heart J 2011;32:2999 – 3054


Risk of In-Hospital Major Bleeding
Across The Spectrum of CRUSADE Bleeding Score
Short-Term Risk of death or non fatal MI in pts with UA/NSTEMI
Cath lab or later ?
Benefit of early intervention in
high risk patients

Kaplan–Meier Cumulative Risk of the Primary Outcome (death, myocardial infarction, or stroke), Stratified According
to GRACE Risk Score at Baseline.
18
Mehta, SR et al. N Engl J Med 2009;360:2165-75.
Initial Treatment when an ACS diagnosis appears likely
based on ESC NSTEACS Guideline1,2

Aspirin Initial dose of 150 – 300 mg non-enteric formulation followed by 75-100 mg/day (I.v.
administration is acceptable)
P2Y12 inhibitor Loading dose of ticagrelor or clopidogrel

Anticoagulation Choice between different options depends on strategy:


• Fondaparinux 2.5 mg/daily subcutaneously
• Enoxaparin 1 mg/kg twice daily subcutaneously
• UHF Lv. Bolus 60-70 IU/kg (maximum 5000 IU) followed by infusion of 12-15 IU/kg/h
(maximum 1000 IU/h) titrated to aPTT 1.5 – 2.5 × control
• Bivalirudin is indicated only in patients with a planned invasive strategy
Oral β-Blocker If tachycardic or hypertensive without signs of heart failure

P2Y12 inhibitor is recommended in initiation soon after the diagnosis of NSTE-


ACS irrespective of management strategy2

19 Reference: 1. Hamm CW et al. Eur Heart J. 2011; 32:2999-30354; 2. Roffi M et al. Eur Heart J 2016;37(3):267-315
In patients with acute chest pain, a-12 leads
Electrocardiogram has to be obtained in 10
minutes!
Normal Sinus Rhythm
ECG Presentation

• A 12-lead ECG should be obtained within


10 min after first medical contact
• This should be repeated in the case of
recurrence of symptoms, and after 6–9
and 24 h, and before hospital discharge.
• The initial ECG presentation is predictive of
early risk.

Hamm CW et al. Eur Heart J 2011;32:2999 – 3054


The best way to interpret an ECG is
to do it step by step
Rhythm
Rate
Cardiac Axis
P wave
PR interval
QRS complex
ST segment
QT interval (include T and U wave)
Other ECG signs
ST-Segment Elevation
Elevation of the ST segment may be an indicator of acute MI.

ST-Segment Elevation
T-Wave Inversion
Normal ECG Segments

ST-Segment Depression

25
EKG at a Glance. Medtronic Academia Medical Education.
Electrocardiogram Evaluation
An electrocardiogram (ECG) is a measurement of the electrical activity of the heart and
can be used to diagnose MI or other heart pathologies.

Example: Normal 12-Lead ECG

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

ECG Perspectives

26
EKG at a Glance. Medtronic Academia Medical Education.
ECG Regions
The various electrical leads of the ECG convey information about different regions of the heart.

l V1 V1 V4

ll aVL V2 V2 V5

III aVF V3 V3 V6

Lateral Territory
Inferior Territory
Posterior Territory
Anterior Territory
27
EKG at a Glance. Medtronic Academia Medical Education.
Coronary artery distribution
ECG 12 Leads Interpretation

29
ECG in STEMI

In the absence of LVH and LBBB In the presence LBBB or ST depression


• New LBBB, and symptoms suggestive of ACS
New ST elevation at the J point in 2 • ST depression in leads V1–V3 indicate
contiguous leads with ≥0.2 mV in men inferobasal myocardial ischemia (especially
(>40 years old) or ≥ 0.15 mV in women in when the terminal T-wave is positive)
leads V2-V3 and/or ≥0.1 mV in other leads

In suspected posterior (circumflex artery- related)


or right ventricle-related infarction

• ST elevation in V7,V8 and V9 using a cut-point


>0.05 mV.
• ST elevation in V3R and V4R, using a cut-off point
>0.05 mV, and >0.1 mV in men <30 years.
ST Segment Elevation LBBB

Steg G et al. Eur Heart J. 2012;33:2569-619 30


Hamm CW et al. Eur Heart J 2011;32:2999 – 3054
ECG Changes of Injury Acute Myocardial Infarction

In early stage of AMI , ECG may be normal


or near normal

5- 30 min after onset of


infarction

Changes
< 1 mm - > 10 mm

1-2 hours of onset symptoms

• ST resolves - anterior up to 2 weeks; posterior


> 2 weeks
• T wave : many months

Morris F, Brady WJ. BMJ 2012;324;831-834 31


Classic appearance

• ST segment elevation
• Upwardly convex
• T wave inversion
• Q wave formation
• Pathologic Q wave:
• 0.04 sec
• > 1/3 R
STEMI: Diagnosis EKG
Diagnosis STEMI menurut terdapatnya perubahan akut EKG sebagai berikut:

Tanpa LVH dan LBBB:


• ST elevasi baru pada J point pada 2 sadapan yang bersebelahan
≥0,2 mV pada pria dan ≥0,15 mV pada wanita di sadapan V2-V3
dan/atau ≥0,1mV pada sadapan lainnya
Terdapatnya LBBB atau ST depresi:
• LBBB baru dan gejala sugestif SKA
• ST depresi di sadapan V1-V3 yang menandakan iskemia
miokardium inferobasal (terutama jika gelombang T terminal
positif)
Pada kecurigaan infark posterior atau ventrikel kiri
• ST elevasi di V7 (pada linea aksilaris posterior kiri), V8 (pada linea
midskapularis kiri) dan V9 (pada tepi kiri linea paraspinal),
menggunakan batasan > 0,05 mV → Menangkap gambaran sikumfleks
dominan kiri menggunakan sadapan posterior di sela iga kelima
• ST elevasi pada sadapan prekordial kiri (V3R dan
V4R),menggunakan batasan >0,05 mV dan >0,1 mV pada pria <30
tahun → Menangkap kecurigaan infark ventrikel kanan dengan menggunakan
sadapan prekordial

Referensi: Hamm CW et al. Eur Heart J. (2011); 32 (32): 2999-305


Inferior STEMI with total occlusion of proximal RCA
Anterior STEMI with total occlusion of proximal LAD
A-53 yo man with severe chest dyscomfort radiating to
the left arm since 6 hours
A-65 yo man with epigastric pain accompanied by nausea and
diaphoresis. Reported presyncope on her way to the hospital
Pedoman Tatalaksana Sindrom Koroner Akut PERKI 2017
Left Bundle Branch Block in STEMI

• Occurs when normal electrical activity in the His-


Purkinje system is interrupted → activation of the
left ventricle is delayed
• Criteria on ECG:
• QRS duration > 120 ms
• QS or rS complex in V1
• Notched (M-shaped) R wave in V6
• The presence of LBBB obscure ST segment shift →
LBBB in a patient with symptoms consistent with
MI should be treated as a STEMI
“Normal” LBBB pattern:
“Appropriate Discordance”

• Leads w/ positive QRS complex → ST segment depression


• Leads w/ negative QRS complex → ST segment elevation
LBBB in Acute MI:
Sgarbossa Criteria
A. Concordant ST elevation > 1 mm in any lead
B. Concordant ST depression > 1 mm in V1, V2, V3
C. Discordant ST elevation > 5 mm (less specific)

LOW SENSITIVITY
HIGH SPECIFICITY
LBBB in STEMI: Sgarbossa A
LBBB in STEMI: Sgarbossa B
LBBB in STEMI: Sgarbossa A and B
Right Bundle Branch Block
in STEMI
• RBBB is historically thought to be more ‘benign’
than LBBB thus not always listed as indication for
reperfusion
• RBBB usually do not mask the repolarization phase
changes or Q waves, therefore it is commonly
thought other ECG changes have to be present to
conclude the diagnosis
• Recent studies showed patients with MI and RBBB
also have poor prognosis → current guidelines
suggested primary PCI approach when persistent
ischemic symptoms occur in the presence of RBBB
“Normal” RBBB pattern
• QRS duration > 100 ms
(incomplete block) or more than
120 ms (complete block)
• A terminal R wave in lead V1 (eg.
R, rR’, rSR’ or qR)
• A slurred S wave in l and V6
“Normal” RBBB pattern

Remember to discern where the end of QRS


complex and measure ST segment deviation
from J point
STEMI with RBBB pattern

Complete RBBB with ST elevation in V2-V4, I, aVL and


reciprocal ST depression in II, III aVF

Acute extensive anterior STEMI


ECG IMPOSTOR OF STEMI
Acute pericarditis
• Diffuse ST elevation in all
leads except aVR
• Depression of PR segment
• No reciprocal changes
• The morphology of ST
segment in concave in
opposite of convex ST
elevation in STEMI
• Clinical presentation of
inflammation
Acute pericarditis
Early repolarization

• Common Benign ECG pattern in young healthy male, incidence 5-13%


• ST segment morphology similar with pericarditis
• Notched, slurred or otherwise well-demarcated J point
Left Ventricle Aneurysm
Ventricular-paced rhythm

• Pacemaker spikes
• Follow similar “appropriate discrodance” rule, as in LBBB
Hyperkalemia

• Narrow based, peaked T wave with symmetrical appearance


• May be accompanied by ST segment elevation due to ST segment being
“pulled” by the tall T wave
ECG in NSTEACS

• ST depression of >0.05 mV in V1-V3 and >0.1 mV in


other leads
• Symmetrical T wave inversion >0.2 mV
• Could be completely normal
ST depression 0.04 from J point < 0.05 mV

(A, B) Horizontal ST depression.


(C, D) Downsloping ST segment depression.
(D) Left ventricular strain frequently associated with left ventricular
hypertrophy.
(E) Scooping ST segment depression frequently from digitalis effect.
(F) Slow upsloping ST segment depression.
(G) Fast upsloping ST segment depression frequently a normal finding.

Note : arrows indicate the J point.


Myocardial Ischemia in NSTEACS
Myocardial Ischemia in NSTEACS
ELEKTROKARDIOGRAM YANG NORMAL TIDAK
MENGEKSKLUSI ADANYA SINDROMA KORONER AKUT

ANGINA TIDAK STABIL (UAP/APTS) ADALAH


DIAGNOSIS BERDASARKAN ANAMNESIS
Cardiac Biomarkers for
ACS Diagnosis
Cardiac troponin is the preferred biomarker because it is more sensitive and accurate than CK-MB.1,2

Cardiac Troponin1,2 CK-MB1,2

Nature of biomarker Nature of biomarker


• Troponin T and troponin I are proteins found • CK-MB is a muscle protein involved in energy
in cardiac muscle fibers transfer

Sensitivity of test Sensitivity of test


• Troponin tests have greater sensitivity and • CK-MB may also be released by damaged
specificity than CK-MB skeletal muscle

Abnormal Elevation of Biomarker Abnormal Elevation of Biomarker


• An increased cTn concentration is defined as • An increased CK-MB concentration is defined
any value exceeding the upper reference limit as any value exceeding the upper reference
of the assay limit of the assay

Timing of MI detection Timing of MI detection


• Detects MI 2-12 hours after onset; may • Rises 2-12 hours after MI, but falls much
remain elevated for 2 weeks after onset more quickly than cTn (2 days)

Upper Reference Limit = the 99th percentile of a normal reference population 61


1. Anderson JL, et al. J Am Coll Cardiol. 2007;50:e1-e157. 2. Thygesen K, et al. Eur Heart J. 2012;33:2251-2567.
Cardiac Biomarker

• Troponins are more specific and sensitive


than the traditional cardiac enzymes
• The test should be repeated 6–9 h after
initial assessment if the first measurement is
not conclusive
• Do not wait biomarker result in STEMI
patients

Kumar A; Cannon CP et al. Mayo Clin Proc. 2009;84(10):917-938; Steg G et al. Eur Heart J. 2012;33:2569-619; 62
Roffi M et al. European Heart Journal 2015. doi:10.1093/eurheartj/ehv320
Likelihood That Signs and Symptoms Indicate
an ACS Secondary to CAD

High likelihood Intermediate likelihood Low likelihood


Any of the following: Absence of high-likelihood features Absence of high- or intermediate-
Feature
and presence of any of the following likelihood features but may have

Chest or left arm pain or discomfort Chest or left arm pain or discomfort Probable ischemic symptoms in
as chief symptom reproducing as chief symptom absence of any of the intermediate
previously documented angina likelihood characteristics
History
Known history of CAD, including MIAge ≥70 y Recent cocaine use
Male sex
Diabetes mellitus
Transient MR murmur, hypotension, Extracardiac vascular disease Chest discomfort reproduced by
palpation
Examination diaphoresis, pulmonary edema, or
rales

New, or presumably new, transient Fixed Q waves T-wave flattening or inversion <1 mm
in leads with dominant R waves
ST-segment deviation (≥1 mm) or T- ST depression of 0.5-1.0 mm or Normal ECG tracing
ECG
wave
inversion in multiple precordial T-wave inversion >1.0 mm
leads
Elevated cardiac TnI, TnT, or CK-MB Normal Normal
Cardiac markers
levels
63
Kumar A; Cannon CP et al. Mayo Clin Proc. 2009;84(10):917-938
Take Home Message

Chest pain

ST elevation ST depression
ECG ST segment

Bio-chemistry Troponin rise / Troponin


fall normal

Diagnosis

STEMI NSTEMI UA
Adapted from Hamm CW et al. Eur Heart J 2011;32:2999 – 3054, Davies MJ. Heart 2000;83:361–366

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