Screenshot 2564-11-07 at 02.18.49

Save Thais from Heart Diseases 2021
Acute Coronary Syndrome

Orawan Anupraiwan, MD.
Central Chest Institute of Thailand

Outline
• Definition of Acute MI
• ACS
• Revascularization
• Risk stratification
• Medication
Fourth Universal Definition of Myocardial Infarction
MI caused by atherothrombotic CAD and usually precipitated by
Type 1
atherosclerotic plaque rupture or erosion.
MI secondary ischemia due to myocardial injury due to mismatch

Type 2
between oxygen supply and demand.
Patients who suffer cardiac death, with symptoms suggestive of

Type 3 MI accompanied by presumed new ischaemic ECG changes or VF
Type 4 Myocardial infarction associated with PCI
Type 5 Myocardial infarction associated with CABG

Fourth universal definition of myocardial infarction 2018.
European Heart Journal (2019) 40, 237–269

Myocardial Infarction Type 1 Myocardial Infarction Type 2
ACS
Fourth universal definition of myocardial infarction 2018. European Heart Journal (2019) 40, 237–269
PRESENTATION
WORKING
DIAGNOSIS
12-LEADS ECG
&
SERIAL
CARDIAC
BIOMARKER
FINAL DIAGNOSIS
NSTEMI / UA (NSTE-ACS) STEMI
N Engl J Med 2017;376:2053-64.
Diagnostic
algorithm and
triage in ACS
©ESC 2020
2020 ESC Guidelines for the management of acute
coronary syndromes in patients presenting without
persistent ST-segment elevation
Diagnostic
algorithm and
triage in ACS
©ESC 2020
2020 ESC Guidelines for the management of acute
coronary syndromes in patients presenting without
persistent ST-segment elevation
Typical angina
✤ Chest discomfort: diffuse, not localized, not affected by movement
✤
!แห$ง&'อาการ: chest, upper extremity, mandible, epigastrium
✤
อาการมาก-นเ0อ Exertion/stress
✤ Ischemic equivalent: dyspnea, fatigue
✤
ระยะเวลา&'อาการ > 20 นา5
✤
อาการ&เ6ด8วมไ:: diaphoresis, nausea, syncope
✤ Relieved by rest or nitrate

Atypical presentation
•HF
•Typical angina with shorted episode
•Atypical location of pain
•Cardiac arrest
•CNS presentation: stroke (low CO), alteration of consciousness
•Peripheral embolization
•Fatigue
การ;กประ=>?@วย
การ$กประ'()*วย
1.อาการเAบหCอแ$นหDาอก (character), ความFนแรง (severity/pain score), และ
เวลา&เGม'อาการ (onset)
2.อาการ8วม: N/V, เHนลม, เIยนศKษะ, เหMอออก
3.NจPยเQยง: HT, DM, DLP, smoking, FH of CAD
4.RอSามในการใS fibrinolytic therapy เUน
ความเHนไปไ:ของ aortic dissection
ความเQยงWอการเ6ด GI bleeding
ประ=> cerebrovascular disease

การตรวจ/างกายเ2อง4น
การตรวจ8างกายYนแรก& ER
• Airway, Breathing, Circulation (ABC)
• Vital signs, general observation
• Jugular venous distension
• Lungs: rales
• CVS: pulse, heart murmur/gallop
• CNS: consciousness, weakness
• Systemic hypoperfusion
Table 4 Differential diagnoses of acute coronary syndromes in the
setting of acute chest pain
Bold = common and/or important differential diagnoses.

aDilated, hypertrophic and restrictive cardiomyopathies may cause angina or chest discomfort.
©ESC
2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without
www.escardio.org/guidelines
persistent ST-segment elevation (European Heart Journal 2020 - doi/10.1093/eurheartj/ehaa575)
ECG Changes
in STEMI
European Heart Journal 2019;40: 237-269

J-point elevation
1 mm = 0.1 mV
Isoelectric Line
ECG in STEMI
LM
RCA
LCX
LAD
Myocardial ischemia, injury, and infarction
Ischemia:
T inversion
Injury:
ST elevation
Infarction:
Q wave
Reciprocal:
ST depression
Acute inferior wall MI (+ RV infarction)
• ST elevation in II, III, aVF, and V1

• Reciprocal ST depression in I, aVL, V4-6
V3R
Standard Precordial Leads Right Ventricular Leads
V4R
V3R
Acute Myocardial Infarct- Inferior wall, with
Advanced Heart Block-likely Mobitz type I
Inferior wall MI
ST elevation in lead II, III, aVF
Z[า' AV-block หCอ bradycardia 8วม:วยหCอไ\ ]า'ใSเตKยม>ด

external pacemaker
ใS^ Right ventricular lead _กราย (V3R, V4R)
]า' RV infarction `ก' cardiogenic shock จาก RV failure
- ]า' cardiogenic shock และไ\' sign of left side HF (crepitation)

ใS load IV fluid aอน อbาเcงKบใS inotropic agent
- SามใS nitrate เdดขาด จะ^ใS cardiogenic shock เHนมาก-น

Extensive anterior wall MI
• ST elevation in aVR and I,aVR, V1-6

• Reciprocal ST depression in III, aVF, V3-6
ECG, Anatomy, and Pathology
LCX lesions
• Posterior MI (RCA/LCX)
STE: V7-9
ST E M I
EC Gi n STD: V1-2 (R:S≥1)
• Posterolateral MI (LAD/LCX)
STE: V7-9,I,aVL,V5-6
STD: V1-2
RCA lesions • Inferoposterior MI (RCA/LCX)
• Inferior MI (RCA distal to RV) STE: II,III,aVF,V7-9
STE: II, III, aVF STD: V1-2 (R:S≥1)
STD: aVL
• Inferior & RV MI (RCA proximal to RV) LAD lesions
STE: II, III, aVF, I, V4R
• Septal MI
• Inferolateral MI (LAD/LCX) STE: V1-2
STE: II, III, aVF, I,V5-6 ±V4R
• Anterior MI
• Inferoposterior MI (RCA/LCX) STE: V3-4
STE: II, III, aVF,V7-9
• Lateral MI
STD: V1-2 (R:S≥1)
STE: V5-6, I, aVL
Horizontal Down-sloping
Inverted T
ST-depression ST-depression
ECG
Changes in
NSTE-ACS
European Heart Journal 2019;40: 237-269

Illustration of early cardiac troponin kinetics in patients after acute
myocardial injury including AMI
Very early
sampling Early sampling Later sampling Very late sampling
Rising cTn values

from below to
>99th percentile
Delta is
detectable
cTn values
>99th percentile
Delta may not
be seen over a Acute
Downloaded from https://academic.oup.com/eur

short period cTn values myocardial
Cardiac >99th percentile infarction
Declining delta
Troponin Chronic
(cTn) myocardial
injury
Low
cTn
values
Hard to
detect
delta
99th
SC/ACC/AHA/WHF 2018
percentile
URL
Time from onset of symptoms (hours) European Heart Journal (2019) 40, 237–269
Fathil, M. F. et al. “Diagnostics on acute myocardial infarction: Cardiac troponin biomarkers.” Biosensors & bioelectronics 70 (2015): 209-20 .
Table 1 Clinical implications of high-sensitivity cardiac troponin
assays (cTn) (2)
Levels of hs-cTn should be interpreted as quantitative markers of cardiomyocyte damage

(i.e. the higher the level, the greater the likelihood of MI):
• Elevations beyond 5-fold the upper reference limit have high (>90%) PPV for
acute type 1 MI.
• Elevations up to 3-fold the upper reference limit have only limited (50–60%) PPV
for AMI and may be associated with a broad spectrum of conditions.
• It is common to detect circulating levels of cTn in healthy individuals.
Rising and/or falling cTn levels differentiate acute (as in MI) from chronic cardiomyocyte
damage (the more pronounced the change, the higher the likelihood of AMI).
©ESC
Value
Figure of of
2 Value high-sensitivity cardiac
high-sensitivity cardiac troponin
troponin.
hs-cTn assays (right) are reported in ng/L and provide identical

information as conventional assays (left, reported in μg/L) if the
concentration is substantially elevated, e.g. above 100 ng/L. In
contrast, only hs-cTn allows a precise differentiation between
‘normal’ and mildly elevated. Therefore, hs-cTn detects a relevant
proportion of patients with previously undetectable cardiac
troponin concentrations with the conventional assay who have hs-
cTn concentrations above the 99th percentile possibly related to
AMI.
??? = unknown due to the inability of the assay to measure in the
normal range
aThe limit of detection varies among the different hs-cTn assays
©ESC
between 1 ng/L and 5 ng/L. Similarly, the 99th percentile varies
among the different hs-cTn assays, mainly being between 10 ng/L
and 20 ng/L.
Table 1 Reasons for the elevation of cardiac troponin Increased .. myocardial oxygen demand, e.g.
• .
.
Sustained the discomfort
tachyarrhythmia is diffuse; not localized, nor positi
Reasons for the elevation of cardiac troponin values
values because of myocardial injury .. movement
• Severe because
hypertension of the
withof myocardial
region.
or without However,
left ventricular theseinjury sympt
..hypertrophy
.. for myocardial ischaemia and can be observed
Myocardial injury related to acute myocardial ischaemia Other
.
.. causes such as of gastrointestinal,
myocardial injury neurological, pulmonary
.. complaints. MI may occur with atypical symptom
Atherosclerotic plaque disruption with thrombosis. Cardiac .
. conditions, e.g.
12
• Heart .. orfailure cardiac arrest, or even without symptoms.
Myocardial injury related to acute myocardial ischaemia
.
.. of ischaemia too short to cause necrosis can als
• Myocarditis
because of oxygen supply/demand imbalance .
• Cardiomyopathy
. and
(any type)
elevations. The involved myocytes can subs
..
• Takotsubo syndrome
Reduced myocardial perfusion, e.g.
• Coronary .
. apoptosis. 42
revascularization procedure
• Cardiac .. procedure other than revascularization
If myocardial ischaemia is present clinically o
• Coronary artery spasm, microvascular dysfunction • Catheter .
. ablation
• Coronary embolism .
.. changesshocks
• Defibrillator together with myocardial injury, manife
• Coronary artery dissection • Cardiac .. or falling contusion pattern of cTn values, a diagnosis of acu
• Sustained bradyarrhythmia .. If myocardial ischaemia is not present clinically, th
• Hypotension or shock Systemic .
.. els conditions, e.g.
• Respiratory failure
• Sepsis, . may be
infectious indicative
disease of acute myocardial injury if
• Chronic .. kidneyand/or
diseasefalling, or related to more chronic
• Severe anaemia . is rising
• Stroke, .. subarachnoid haemorrhage
©ESC/ACC/AHA/WHF 2018
14
• Pulmonary . pattern is unchanging. Similar
embolism, pulmonary hypertension considerations
Increased myocardial oxygen demand, e.g. .
.. evaluating
• Infiltrative events
diseases, that are potentially
e.g. amyloidosis, sarcoidosisrelated to p
• Sustained tachyarrhythmia • Chemotherapeutic .. agents
. cause myocardial injury and/or MI. Additional eva
• Severe hypertension with or without left ventricular • Critically .. ill patients
hypertrophy • Strenuous .. a needexercise
for the initial diagnosis to be revised.
.. Patients with suspected acute coronary syndr
Other causes of myocardial injury . European Heart Journal (2019) 40, 237–269
Initial Assessment & Management in ACS
1. Triage to an ACS pathway
2. Initiate general care
3.Assess risk of CV death or recurrent ischemia
4. Choose invasive or noninvasive initial strategy
5. Select a second antiplatelet agent to add to aspirin
6. Choose an anticoagulant agent

N Engl J Med 2017;376:2053-64.
STEMI
Time is Muscle
คําแนะนําในการดูแลรักษาเบืองต้ น STEMI
*ในสถานพยาบาลทีมีอปุ กรณ์พร้อม
** ข้อห้ามสําคัญ เช่น RV infarction ได้รบั ยากลุ่ม PDE-5 inhibitors ความดันโลหิตตําอยู่แล้ว
7
Importance of Time-to-Treatment
Mortality at 6 months in 10 RCT’s Meta-analysis
Primary PCI Thrombolysis
Zijlstra at al. EHJ 2002

Reperfusion Therapy
2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation
STEMI Treatment Guidelines
Reperfusion
Strategies
2017 ESC Guidelines for the
management of acute myocardial
infarction in patients presenting with
ST-segment elevation
คําแนะนําการรักษาโดยการเปิ ดหลอดเลือดหัวใจ STEMI
8
“Important Time Target”
Modes of Patient presentation, components of ischemic time and flowchart for reperfusion strategy selection
Non-PCI Center
Maximum expected delay from
STEMI Dx-PPCI ≤ 120 min ? Transferred Patient:
Maximum time from STEMI Dx-
PPCI (wire crossing) ≤ 90 min
Maximum time from
Downloaded from https://academic.oup.com/eurheartj/article

Door-in-door-out time < 30 min
FMC-ECG diagnosis
≤ 10 min
Maximum time from

STEMI Dx-lytic bolus ≤ 10 min
PCI Center
PCI Center:
Maximum time from STEMI Dx-
PPCI (wire crossing) ≤ 60 min
9
Maximum target times according to repercussion strategy selection in patients presenting via EMS or non-PCI center
“Fibrinolysis
Strategy”
Downloaded from https://academic.oup.com/eurheartj/article-abstract/39/2/1

Time delay from start of
fibrinolysis to evaluation
(success/failure) 60-90 min
Time delay from start of

fibrinolysis to angiography
(if success fibrinolysis)
2-24 hours

Successful Reperfusion
Relief of symptoms, maintenance or restoration of

Symptom
hemodynamic and electrical stability
Reduction of at lease 50% in the initial ST segment

ECG elevation
• Ventricular arrhythmias
Reperfusion
arrhythmias
• Accelerated idioventricular rhythm (AIVR)
• Non-sustained bradycardia
• Patency of Infarct-related artery (IRA)

CAG • Distal TIMI flow/myocardial blush score/TIMI
frame count
ECG evolution during acute ST elevation myocardial infarction
Acute Coronary
Occlusion
Reperfusion
Accelerated idioventricular rhythm (AIVR)
Wide complex tachycardia

Ventricular rate เeวก[า atrial rate,VR 60-125 bpm
“Fibrinolysis Strategy”
Desirable features of ideal Thrombolytic drug

TABLE
Circulation. 2004;110:e82.
Comparison of Approved Fibrinolytic Agents
Parameter Streptokinase (SK) TNK t-PA Alteplase (t-PA) Reteplase (rPA)
30-50 mg
Up to 100 mg in 90 min 10 U × 2 (30 min apart)
Dose 1.5. MU in 30-60 min
(based on weight) (based on weight) each over 2 min
Bolus administration No Yes No Yes
Antigenic allergic reaction

Yes No No No
(hypotension)
Systemic fibrinogen
Marked Minimal Mild Moderate
depletion
90-min potency rate (%) ~ 50 ~ 75 ~ 75 ~ 75
TIMIgrade III flow (%) 32 63 54 60
Cost/dose (USD) 568 2,750 2,750 2,750

Circulation. 2004;110:e82.
การประเมินผู้ปว่ ยก่อนให้ Fibrinolysis
Onset of angina
Check list contraindication for SK
Inform consent:
• Disease
• SK/TNK: Indication, mechanism, side effect, and

complication (worse situation)
• Outcome and prognosis
Evaluate pain score
Vital signs
Absolute contraindication for fibrinolysis
Prior intracranial hemorrhage (ICH)
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Ischemic stroke within 3 months
Suspected aortic dissection
Active bleeding or bleeding diathesis (excluding menses)
Significant closed head trauma or facial trauma within 3 months
Intracranial or intraspinal surgery within 2 months
Severe uncontrolled hypertension (unresponsive to emergency therapy)
For streptokinase, prior treatment within the previous 6 months

2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.
Relative Contraindication
• History of chronic, severe, poorly controlled HT
• Severe uncontrolled HT on presentation (SBP> 180 or DBP > 110 mmHg)
• History of prior ischemic stroke > 3 month, dementia, or known intracranial

pathology not covered in contraindications
• Traumatic or prolonged (>10 min) CPR or major surgery (< 3 wk)
• Recent (within 2-4 wk) internal bleeding
• Noncompressible vascular punctures
• For streptokinase/anistreplase: prior exposure (> 5 days) or prior allergic

reaction to thoses agents
• Pregnancy
• Active peptic ulcer
• Current use of anticoagulants: the higher the INR (INR > 1.7 or PT > 15 sec)
ระหว่างให้ Fibrinolysis during เตรียมอะไรบ้าง
Medical team: doctor, nurse (ACLS)
Set emergency (prepare for resuscitation)
Defibrillator, AED
Monitor & record clinical, V/S, ECG
Ambulance (Telemetry), refer team
How to manage hypotension during SK infusion
• Notknown pathophysiology: allergy (antistreptokinase Ab),

bradykinin, prostacyclin (vasodilatation)
• Severe hypotension in patients with severe left ventricular dysfunction
• Slowing or stopping the infusion (slow rate ≤ 200-250 U/kg/min)
• Placing the patient in the Trendelenburg position
• Administering an infusion of low-dose norepinephrine or dopamine

การเ6ด ICH ใน?@วย&ไ: fibrinolysis
• อุบัติการณ์ของ ICH ~ 0.6% (เกิด stroke ทั้งหมด 1.34%)
• 65-75% เกิดภายใน 24 ชม.
• ตำแหน่งที่เกิดบริเวณ
Lobar/subcortical 77%
Parenchyma hemorrhage 15-33%
Subdural hematoma 15%
• ปัจจัยที่มีผลต่อการเกิด ICH ได้แก่
อายุ > 65 ปี
น้ำหนักตัวน้อย (ผู้ชาย < 70, ผู้หญิง < 65 kg)
SBP > 160, DBP > 95 mmHg
NTEMI
UA
Diagnosis
Figure 13
Central illustration.
Choice of Figure
Management strategy for
non-ST-segment elevation
antithrombotic acute coronaryCentra
syndrome
treatment patients. Manag
non-ST
Invasive vs acute c
Selective invasive
strategy
patien
2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting wit
persistent ST-segment elevation (European Heart Journal 2020 - doi/10.1093/eurheartj/ehaa
D/C & post D/C

2020 ESC Guidelines for the management
management of acute coronary syndromes in patients
presenting without persistent ST-segment
elevation
for non-ST-segment elevation acute coronary syndrome
Diagnosis
patients.
Figure 13 (1) Central illustration. Management strategy
patients.
©ESC
2020 ESC Guidelines for the management
2020ofESC
acute coronary syndromes
Guidelines in patients presenting
for the management of acutewithout
coronarypersistent ST-segment
syndromes elevation
in patients presenting
withou
persistent ST-segment elevation (European Heart Journal 2020 - doi/10.1093/eurheartj/ehaa575
Figure 3 (1)
0 h/1 h rule-out and
rule-in algorithm using
high-sensitivity cardiac
troponin assays in
haemodynamically stable
patients presenting with
suspected non-ST-
segment elevation acute
coronary syndrome to the
emergency department.
aOnly applicable if CPO >3 h.

Figure 4 (1) Timing of the
blood draws and clinical
decisions when using
the European Society
of Cardiology
0 h/1 h algorithm.
2020 ESC Guidelines for the management of acute coronary syndromes

in patients presenting without persistent ST-segment elevation
Recommendations on biomarker measurements for prognostic
stratification (2)
Recommendations Class Level
Score to risk stratify in NSTE-ACS
GRACE risk score models should be considered for estimating prognosis. IIa B
The use of risk scores designed to evaluate the benefits and risks of
IIb A
different DAPT durations may be considered.
To estimate bleeding risk, the use of scores may be considered in patients
IIb B
undergoing coronary angiography.
©ESC
Supplementary Figure 3
Global
Clinical Registry
scores for risk of
assessment.
Acute Coronary
Syndrome (GRACE)
©ESC
The figure shows a nomogram for calculation of the GRACE
risk score and was adapted by Granger et al.
207
Selection of NSTEMI treatment strategy & time according to initial risk stratification
Invasive vs Selective
invasive strategy
PCI center EMS or Non-PCI center
Figure 9
non-ST-s
elevatio
coronar
treatme
timing a
initial
risk stra
คําแนะนําการฉีดสี หลอดเลือดหัวใจในผ้ ูป่วย NSTE-ACS
* ภายใน 72 ชัวโมง ในสถานพยาบาลมีความพร้อม

31
คําแนะนําการฉีดสี หลอดเลือดหัวใจในผ้ ูป่วย NSTE-ACS (ต่ อ)
** โดยเร็ว ในสถานพยาบาลทีมีความพร้อม
32
Initial Assessment & Management in ACS
1. Triage to an ACS pathway
2. Initiate general care
3.Assess risk of CV death or recurrent ischemia
4. Choose invasive or noninvasive initial strategy
5. Select a second antiplatelet agent to add to aspirin
6. Choose an anticoagulant agent
N Engl J Med 2017;376:2053-64.

Thrombosis after rupture of
atherosclerotic plaque
Figure 6
Antithrombotic
treatments in non-ST-
segment elevation acute
coronary syndrome
patients: pharmacological
targets. Drugs with oral
administration are shown
in black letters and drugs
with preferred parenteral
administration in red.
Abciximab (in brackets) is
not supplied anymore.
2020 ESC Guidelines for the management of acute coronary syndromes

in patients presenting without persistent ST-segment elevation
Figure 13 (2) Central illustration.elevation
for non-ST-segment Management strategysyndrome
acute coronary
patients.
Choice of
patients. antithrombotic
treatment Management strategy for NSTEMI
2020 ESC Guidelines for the management of acute coronary syndromes in patients pr
persistent ST-segment elevation (European Heart Journal 2020 - doi/10.1093/eu
2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation
Algorithms for Reperfusion Therapy of ACS: Initiate DAPT & Anticoagulant Therapy
STEMI NSTE-ACS
Fibrinolytic PPCI Ischemia-Guided
Invasive Stratigy
Strategy Strategy Strategy
1. ASA (Class I, A) 1. ASA (Class I, A)

1. ASA (Class I, A)
1. ASA (Class I, A) 2.P2Y12 Inhibitor (Class I, A) 2.P2Y12 Inhibitor (Class I, A)
2.P2Y12 Inhibitor (Class I, A)
2.P2Y12 Inhibitor - Ticagrelor (Class I, A) - Ticagrelor (Class I, B)**
- Ticagrelor (Class I, B)*
- Clopidogrel (Class I, A) - Prasugrel (Class I, A) - Prasugrel (Class I, B)
- Clopidogrel (Class I, B)
3.Anticoagulant - Clopidogrel (Class I, A) - Clopidogrel (Class I, C)
3.Anticoagulant
3.Anticoagulant 3.Anticoagulant
-Enoxaparin (Class I, A) or
- UFH (Class I,C)
- UFH (Class I,C) or - Fondaparinux with UFH - Fondaparinux or
-UFH (Class I, B) or
- Enoxaparin (Class IIa, A) or

bolus (Class I, B)
- Enoxaparin or
-Fondaparinux (Class IIa,B)
Until revascularization or duration

- Bivalirudin (Class IIa, A) - Enoxaparin (Class IIa, B)
- UFH
of hospital stay up to 8 days.

During PPCI - Bivalirudin (Class IIb, A)
5-8 days (Class I, B)
During PCI
** All patients at moderate-to-high risk of ischaemic events * Low bleeding risk
Dose of Antiplatelet in ACS
Oral Antiplatelet Loading Dose Maintenance Dose Caution
2017 ESC Guidelines for the management of acute myocardial infarction in patients presentingwithST-segmentelevation
Aspirin 150-300 mg 75-100 mg/day
600 mg
(PPCI)
Clopidogerl 75 mg/day
300 mg
• Loading dose 75 mg in patients ≥ 75 years

(Fibrinolysis)
Ticagrelor 180 mg 90 mg bid
• Contra-indicated in patients with previous

stroke.
10 mg/day
Prasugrel 60 mg
(5 mg in BW ≤ 60 kg) • Generally not recommended in patients ≥ 75
years (but dose 5 mg/d should be used if
necessary)
Dose of Anticoagulant Co-therapies in ACS
Anticoagulant Bolus dose Maintenance Dose Caution
In patients < 75 years:

1 mg /kg SC every 12 hr
• Until revascularization or hospital
30 mg IV bolus (followed 15 min after bolus dose) discharge (maximum of 8 days)
• In patients with eGFR < 30 ml/min/1.73
Enoxaparin m2, regardless of age, the SC dose are
given once every 24 hr
In patients ≥ 75 years:
0.75 mg/kg every 12 hr
• Not recommend if eGFR <15 ml/min/
No IV bolus dose (start with first SC dose) 1.73 m2
• Only with streptokinase

• Not recommended for PPCI
Fondaparinux 2.5 mg IV bolus 2.5 mg SC once daily • Not recommend if eGFR < 20 ml/min/
1.73 m2
60 IU IV bolus
12 IU/kg IV infusion
• Target aPTT 50-70 sec or 1.5-2.0 times
UFH (maximum 4000 IU) (maximum 1000 IU/hr) for 24-48 hr (monitored at 3, 6, 12, and 24 hr)
Table 7 P2Y12 receptor inhibitors for use in non-ST-segment
elevation acute coronary syndrome patients (3)
Oral administration i.v. administration
Clopidogrel Prasugrel Ticagrelor Cangrelor
Delay to 5 days 7 days 5 days No significant delay
surgery
Kidney No dose No dose No dose No dose
failure adjustment adjustment adjustment adjustment
Dialysis Limited data Limited data Limited data Limited data

or CrCl
<15 mL/min
©ESC
for non-ST-segment
patients. elevation acute coronary syndrome
patients.
D/C & post D/C
management
2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation
2020 ESC Guidelines for the management of acute coronary syndromes in patients prese
Long Term Therapy
Long Term Therapy
Medication
Antiplatelets (DAPT for 12 months if no bleeding)
Statin (±Ezetimibe, ±PCSK9i)
RAAS Inhibitors
Beta-blockers
Life style intervention & risk factor control

2017 ESC Focused Update on DAPT in Coronary Artery Disease, developed in collaboration with EACTS
Algorithm for
Figure 7 (1)
antithrombotic
Algorithm for antithro
therapy in NSTEMI
without AF
therapy in non-ST-seg
undergoing PCI
elevation acute coron
syndrome patients wi
atrial fibrillation unde
percutaneous coronar
intervention.
2020 ESC Guidelines for the management of

acute coronary syndromes in patients presenting
without persistent ST-segment elevation
Very HBR is defined as recent bleeding in t
Recommendations for pharmacological long-term management
after non-ST-segment elevation acute coronary syndrome
(excluding antithrombotic treatments) (1)
Lipid-lowering drugs
Statins are recommended in all NSTE-ACS patients. The aim is to reduce LDL-C
I A
by ≥50% from baseline and to achieve LDL-C <1.4 mmol/L (<55 mg/dL) .
If the LDL-C goala is not achieved after 4–6 weeks with the maximally
tolerated statin dose, combination with ezetimibe is recommended.
I B
If the LDL-C goalc is not achieved after 4–6 weeks despite maximally tolerated
Recommendations
statin therapy and ezetimibe, the addition of a PCSK9 inhibitor is Class Level
I B
recommended.
Lipid-lowering drugs (continued)
If the
aFor
current
patients at very highNSTE-ACS episode
cardiovascular risk is awithrecurrence
(such as patients within
ACS), an LDL-C reduction of at less than
least 50% 2 years
from baseline and anof a goal <1.4 mmol/L (<55
LDL-C
mg/dL) are recommended.
first ACS, while taking maximally tolerated statin-based therapy, an LDL-C IIb B
©ESC
goal of <1.0 mmol/L (<40 mg/dL) may be considered.
ACE inhibitors or ARBs
ACE inhibitors (or ARBs in cases of intolerance to ACE inhibitors) are

(see Table 4)
2019 ESC/EAS Guidelines for the management
B
Downloaded from https://academic.oup.com/eurheartj/advance-article-abstract/doi/10.1093/eurheartj/ehz455/5556353 by guest on 14 November 2019

Treatment goal of dyslipidaemias: lipid modification to reduce
LDL-C goal
for LDL-C • SCORE <1%
cardiovascular risk
The Task Force for the management of dyslipidaemias of the
European Society of Cardiology (ESC) and European
• SCORE ≥1% and <5% Atherosclerosis Society (EAS)
• Young patients (T1DM <35 years;
T2DM <50 years) with DM durationAuthors/Task Force Members: François Mach* (Chairperson) (Switzerland),
3.0 mmol/L Colin Baigent* (Chairperson) (United Kingdom), Alberico L. Catapano1*
(116 mg/dL)
Low <10 years without other risk factors(Chairperson) (Italy), Konstantinos C. Koskinas (Switzerland),
1
Manuela Casula1
(Italy), Lina Badimon (Spain), M. John Chapman (France), Guy G. De Backer
(Belgium), Victoria Delgado (Netherlands), Brian A. Ference (United Kingdom),
Ian M. Graham (Ireland), Alison Halliday (United Kingdom), Ulf Landmesser
(Germany), Borislava Mihaylova (United Kingdom), Terje R. Pedersen (Norway),
• SCORE ≥5% and <10%
Gabriele Riccardi1 (Italy), Dimitrios J. Richter (Greece), Marc S. Sabatine (United
2.6 mmol/L • Markedly elevated single risk factors, in
States of America), Marja-Riitta Taskinen1 (Finland), Lale Tokgozoglu1 (Turkey),
(100 mg/dL) Moderate Olov Wiklund1 (Sweden)

particular TC >8 mmol/L (310 mg/dL) or
LDL-C >4.9 mmol/L (190 mg/dL) or
The three chairpersons contributed equally to the document.
*Corresponding authors: François Mach, Cardiology Department, Geneva University Hospital, 4 Gabrielle-Perret-Gentil, 1211 Geneva, Switzerland. Tel: þ41 223 727 192,
BP ≥180/110 mmHg
Fax: þ41 223 727 229, Email: francois.mach@hcuge.ch. Colin Baigent, Nuffield Department of Population Health, University of Oxford, Richard Doll Building, Roosevelt Drive,
Oxford OX3 7LF, United Kingdom. Tel: þ44 1865 743 741, Fax: þ44 1865 743 985, Email: colin.baigent@ndph.ox.ac.uk. Alberico L. Catapano, Department of Pharmacological
and Biomolecular Sciences, University of Milan, Via Balzaretti, 9, 20133 Milan, and Multimedica IRCCS, Milan, Italy. Tel: þ39 02 5031 8401, Fax: þ39 02 5031 8386,
• FH without other major risk factors

Email: alberico.catapano@unimi.it.
ESC Committee for Practice Guidelines (CPG), National Cardiac Societies document reviewers and Author/Task Force Member affiliations: listed in the Appendix.
• Moderate CKD (eGFR 30–59 mL/min)

1
Representing the EAS.
ESC entities having participated in the development of this document:
• DM w/o target organ damage, with DM

Associations: Acute Cardiovascular Care Association (ACCA), Association of Cardiovascular Nursing & Allied Professions (ACNAP), European Association of Cardiovascular
Imaging (EACVI), European Association of Preventive Cardiology (EAPC), European Association of Percutaneous Cardiovascular Interventions (EAPCI).
duration ≥10 years or other additional risk factor

Councils: Council for Cardiology Practice, Council on Hypertension, Council on Stroke.
Working Groups: Aorta and Peripheral Vascular Diseases, Atherosclerosis and Vascular Biology, Cardiovascular Pharmacotherapy, e-Cardiology, Thrombosis.
The content of these European Society of Cardiology (ESC) Guidelines has been published for personal and educational use only. No commercial use is authorized. No part of
1.8 mmol/L
the ESC Guidelines may be translated or reproduced in any form without written permission from the ESC. Permission can be obtained upon submission of a written request to
High
Oxford University Press, the publisher of the European Heart Journal and the party authorized to handle such permissions on behalf of the ESC (journals.permissions@oxfordjour-
nals.org).
• ASCVD (clinical/imaging)
(70 mg/dL)
Disclaimer. The ESC/EAS Guidelines represent the views of the ESC and EAS, and were produced after careful consideration of the scientific and medical knowledge, and the
• SCORE ≥10%
evidence available at the time of their publication. The ESC and EAS is not responsible in the event of any contradiction, discrepancy, and/or ambiguity between the ESC/EAS
& ≥50%
Guidelines and any other official recommendations or guidelines issued by the relevant public health authorities, in particular in relation to good use of healthcare or therapeutic
• FH with ASCVD or with another

strategies. Health professionals are encouraged to take the ESC/EAS Guidelines fully into account when exercising their clinical judgment, as well as in the determination and the
implementation of preventive, diagnostic, or therapeutic medical strategies; however, the ESC/EAS Guidelines do not override, in any way whatsoever, the individual responsibil-
ity of health professionals to make appropriate and accurate decisions in consideration of each patient’s health condition and in consultation with that patient and, where appro-
reduction major risk factor

priate and/or necessary, the patient’s caregiver. Nor do the ESC/EAS Guidelines exempt health professionals from taking into full and careful consideration the relevant official
updated recommendations or guidelines issued by the competent public health authorities, in order to manage each patient’s case in light of the scientifically accepted data pur-
• Severe CKD (eGFR <30 mL/min)

suant to their respective ethical and professional obligations. It is also the health professional’s responsibility to verify the applicable rules and regulations relating to drugs and
from
medical devices at the time of prescription.
• DM & target organ damage: ≥3

C The European Society of Cardiology and the European Atherosclerosis Association 2019. All rights reserved.
V
1.4 mmol/L
For permissions please email: journals.permissions@oup.com.
baseline
(55 mg/dL)
Very High major risk factors; or early onset of
T1DM of long duration (>20 years)
European Heart Journal (2019) 00, 1-178 Low Moderate High Very high CV Risk
2018 AHA/ACC (updated): Secondary Prevention
Clinical ASCVD
Healthy Lifestyle
No Very high-risk ASCVD ? Yes

Initiate High-intensity
Age ≤ 75 Age > 75 Statin (Class I)
Initiate High- Initiate moderate or

intensity Statin high-intensity statin Add Ezetimibe (Class IIa)
(Class I) (Class IIa) • If on maximal statin & LDL-C ≥ 70 mg/dL
Add Ezetimibe Continuation of high-

(Class IIb) intensity statin (Class Add PCSK9 inhibitor
• If on maximal statin IIa) (Class IIa)
therapy and LDL-C ≥70 • If on clinical judged maximal LDL-C
mg/dL lowering therapy and LDL-C ≥ 70 mg/
dL (or non-HDL ≥ 100 mg/dL)
Guidelines specify statin doses
High-intensity Moderate-intensity ↓ Low-intensity
↓ LDL-C by ≥50% LDL-C by 30–50% ↓ LDL-C by <30%*
Atorvastatin (40)–80 mg 10–20 mg –
Rosuvastatin 20–40 mg 5–10 mg –
Simvastatin – 20–40 mg 10 mg
Pravastatin – 40–80 mg 10–20 mg
Lovastatin – 40 mg 20 mg
Fluvastatin XL – 80 mg –
Fluvastatin – 40 mg bid 20–40 mg
Pitvastatin – 2–4 mg 1 mg
Bold: Statins and doses evaluated in RCTs
Italics: Statins and doses approved by US FDA but not tested in RCTs reviewed Stone NJ, et al. J Am Coll Cardiol 2013 Nov 7. Epub ahead of print
*Should be used in patients unable to tolerate moderate-to high-intensity therapy Reproduced with kind permission from American College of Cardiology Jan 2014
Asian ancestry may modify the statin dose prescribed
Lipid-lowering drugs (continued)
If the current NSTE-ACS episode is a recurrence within less than 2 years of a
first ACS, while taking maximally tolerated statin-based therapy, an LDL-C IIb B
recommended in patients with heart failure with reduced LVEF (<40%),
diabetes, or CKD unless contraindicated (e.g. severe renal impairment, I A
hyperkalaemia, etc.) in order to reduce all-cause and cardiovascular mortality
and cardiovascular morbidity.
©ESC
Recommendations
after non-ST-segment elevation acute coronary syndrome Class Level
(excluding
Beta-blockersantithrombotic treatments) (2)
Recommendations
Beta-blockers are recommended in patients with systolic LV dysfunction or Class Level
I A
heart failure with reduced LVEF
Lipid-lowering drugs (continued)(<40%).
In patients with prior MI, long-term oral treatment with a beta-blocker
If the current NSTE-ACS episode is a recurrence within less than 2 years of a
should be considered in order to reduce all-cause and cardiovascular
first ACS, while taking maximally tolerated statin-based therapy, an LDL-C IIa
IIb BB
mortality and cardiovascular morbidity.
recommended in patients with heart failure with reduced LVEF (<40%),
diabetes, or CKD unless contraindicated (e.g. severe renal impairment, I A
©ESC
hyperkalaemia, etc.) in order to reduce all-cause and cardiovascular mortality
and cardiovascular morbidity. persistent ST-segment elevation (European Heart Journal 2020 - doi/10.1093/eurheartj/ehaa575)
ESC
MRAs
MRAs are recommended in patients with heart failure with reduced LVEF
(<40%) in order to reduce all-cause and cardiovascular mortality and I A
cardiovascular morbidity.
Proton pump inhibitors
Concomitant use of a proton pump inhibitor is recommended in patients
receiving aspirin monotherapy, DAPT, DAT, TAT, or OAC monotherapy who
I A
are at high risk of gastrointestinal bleeding in order to reduce the risk of
gastric bleeds.
©ESC
Lifestyle Interventions & Risk Factor Control
Smoking cessation
Diet, alcohol and weight control
Exercise-based cardiac rehabilitation
Resumption of activities
Risk factor control: HT, DLP, DM, etc

Conclusion
Accurate diagnosis of ACS has life-saving implications and
requires a careful assessment.
The initial management involves both aggressive medical
therapy and revascularization.
Early risk stratification permits the identification of high-risk
patients who stand to gain the most from potent therapies.
Aggressive attention to secondary prevention initiatives for
ACS patients (longterm therapy and control risk factor).

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Save Thais from Heart Diseases 2021

Acute Coronary Syndrome

Central Chest Institute of Thailand

MI secondary ischemia due to myocardial injury due to mismatch

Patients who suﬀer cardiac death, with symptoms suggestive of

Type 4 Myocardial infarction associated with PCI

Type 5 Myocardial infarction associated with CABG

European Heart Journal (2019) 40, 237–269

✤ Ischemic equivalent: dyspnea, fatigue

✤ Relieved by rest or nitrate

•Typical angina with shorted episode

•Atypical location of pain

•CNS presentation: stroke (low CO), alteration of consciousness

2.อาการ8วม: N/V, เHนลม, เIยนศKษะ, เหMอออก

3.NจPยเQยง: HT, DM, DLP, smoking, FH of CAD

4.RอSามในการใS fibrinolytic therapy เUน

ความเHนไปไ:ของ aortic dissection

ประ=> cerebrovascular disease

• Vital signs, general observation

• Jugular venous distension

• CVS: pulse, heart murmur/gallop

• CNS: consciousness, weakness

Bold = common and/or important differential diagnoses.

European Heart Journal 2019;40: 237-269

• ST elevation in II, III, aVF, and V1

Z[า' AV-block หCอ bradycardia 8วม:วยหCอไ\ ]า'ใSเตKยม>ด

ใS^ Right ventricular lead _กราย (V3R, V4R)

]า' RV infarction `ก' cardiogenic shock จาก RV failure

- ]า' cardiogenic shock และไ\' sign of left side HF (crepitation)

- SามใS nitrate เdดขาด จะ^ใS cardiogenic shock เHนมาก-น

• ST elevation in aVR and I,aVR, V1-6

European Heart Journal 2019;40: 237-269

Rising cTn values

Downloaded from https://academic.oup.com/eur

Levels of hs-cTn should be interpreted as quantitative markers of cardiomyocyte damage

hs-cTn assays (right) are reported in ng/L and provide identical

2. Initiate general care

3.Assess risk of CV death or recurrent ischemia

4. Choose invasive or noninvasive initial strategy

5. Select a second antiplatelet agent to add to aspirin

6. Choose an anticoagulant agent

Primary PCI Thrombolysis

Zijlstra at al. EHJ 2002

Downloaded from https://academic.oup.com/eurheartj/article

Maximum time from

Downloaded from https://academic.oup.com/eurheartj/article-abstract/39/2/1

Time delay from start of

European Heart Journal (2018) 39, 119–177

Relief of symptoms, maintenance or restoration of

Reduction of at lease 50% in the initial ST segment

• Patency of Infarct-related artery (IRA)

Wide complex tachycardia

Desirable features of ideal Thrombolytic drug

Bolus administration No Yes No Yes

Antigenic allergic reaction

90-min potency rate (%) ~ 50 ~ 75 ~ 75 ~ 75

TIMIgrade III flow (%) 32 63 54 60

Cost/dose (USD) 568 2,750 2,750 2,750

Check list contraindication for SK

• SK/TNK: Indication, mechanism, side effect, and

• Outcome and prognosis

Evaluate pain score

Known structural cerebral vascular lesion

Known malignant intracranial neoplasm