Acute Coronary Syndrome

Dr. Infan Ketaren SpJP(K),FIHA,FAsCC

SMF Kardiologi & Vaskular
RSUD Dr. Soedarso Pontianak
 Introduction
 Acute coronary syndrome (ACS) is a broad term encompassing
a spectrum of acute myocardial ischemia and injury ranging
from unstable angina (UA) and non–ST-segment elevation
myocardial infarction (NSTEMI) to ST-segment elevation
myocardial infarction (STEMI)
 ACS accounts for approximately 1.2 million hospital admissions in
the US annually
 It is a type of coronary heart disease (CHD), which is responsible
for one-third of total deaths in people older than 35
 Some forms of CHD can be asymptomatic, but ACS is always
symptomatic
 Definitions

 ACS is a syndrome defined by the presence of symptoms,

electrocardiographic (ECG)changes, and/or biochemical
markers consistent with myocardial ischemia or injury
 Typical symptoms include chest pain or pressure, but ACS
can also manifest with symptoms such as shortness of
breath, nausea, or malaise
 Acute Coronary Syndrome
( ACS )

ST-segment ST-segment
Depression Elevation

Biomarkers of Biomarkers of Biomarkers of

Cardiac Injury ( - ) Cardiac Injury ( + ) Cardiac Injury ( + )

UA NSTEMI STEMI
( Unstable Angina ) ( Non ST-Elevation ( ST-Elevation
Myocardial Infarction ) Myocardial Infarction )
European Heart Journal (2007) 28,882
 Etiology

 ACS is a manifestation of CHD (coronary heart disease) and

usually a result of plaque disruption in coronary arteries
(atherosclerosis)
 The common risk factors for the disease are smoking,
hypertension, diabetes, hyperlipidemia, male sex, physical
inactivity, family obesity, and poor nutritional practices.
 Atherosclerosis Timeline

Foam Fatty Intermediate Fibrous Complicated

Cells Streak Lesion Atheroma Plaque Lesion/Rupture

Endothelial dysfunction

From first decade From third decade From fourth decade

Smooth muscle Thrombosis,
Growth mainly by lipid accumulation and collagen haematoma

Adapted from Stary HC et al. Circulation 1995;92:1355-1374.

 Atherogenesis and Atherothrombosis:
A Progressive Process to Cardiovascular Events
Plaque
Athero- Rupture/ Myocardial
Fatty Fibrous sclerotic Fissure & Infarction
Normal Streak Plaque Plaque Thrombosis

Ischemic
Stroke

Periferal
Ischemia

Clinically Silent Angina

Transient Ischemic Attack
Claudication/PAD Cardiovascular Death

Increasing Age

3
Coronary Artery
PATHOPHYSIOLOGY
 Arterial Thrombosis

Endothelial Erosion Plaque Rupture

25% fatal coronary thrombosis 75% major coronary thrombosis

Activation of Platelets

Activation of Coagulation System

Release Vasoactive Substances

ACUTE CORONARY SYNDROME

( ACS )
European Heart Journal (2007) 28,882
Hyperacute phase of extensive anterior
myocardial infarction
 Clinical presentation of ACS

 Prolonged (>20 min) anginal pain at rest

 New onset (de novo) severe angina (CCS class III)
 Recent destabilization of previously stable angina
with at least CCS III (crescendo angina) or
 Post MI angina
 Pain patterns with myocardial ischemia

Usual distribution of pain with Less common sites of pain with

myocardial ischemia myocardial ischemia

Right side Jaw

Epigastrium Back
 Admission CHEST PAI N

Working
Suspicion of Acute Coronary Syndrome ( ACS )
Diagnosis

Persistent Normal /
ECG ST-Elevation
ST/T-abnormalities
Undetermined ECG

Biochemistry Troponin (+) Troponin 2x (-)

Risk High Risk Low Risk

Stratification

Diagnosis STEMI NSTEMI UA

Treatment Reperfusion Invasive Non-Invasive

Guideline for the diagnosis and treatment of NSTEMI ACS, ESC Guidelines June 14 th, 2007
STEMI
‘Time is muscle/
myocardium’
Door to needle
(trombolitik) < 30 menit
Door to balloon (primary
PCI) < 60-90 menit
System Delay and Mortality in STEMI Patients

35
30,8
30 28,1

25 23,3

20
Mortality, % 15,4
15

10

0
0 to 60 min 61 to 120 121 to 180 181 to 360
min min min

Terkelsen CJ JAMA 2010;304:763-771

Wave-front Phenomenon of
Ischemic Cell Death
 ESC : Management Strategy in ACS
Patients Clinical suspicion of ACS

Physical examination
ECG monitoring, blood samples

Persistent No persistent Undetermined

ST-segment elevation ST-segment elevation diagnosis

Thrombolysis ASA, Fonda/Enox/UHF ASA

PCI clopidogrel*, beta-blockers, nitrates

*Omit clopidogrel if
the patient is likely High risk Low risk
to go to CABG Second troponin measurement
within 5 days GPIIb/IIIa,
coronary angiography
Positive Twice negative

PCI, CABG or medical management Stress test,

depending upon clinical and angiographic features coronary angiography

1. Bertrand ME et al. Eur Heart J 2002; 23; 1809−1840.

 ESC : Management Strategy in ACS Patients
Clinical suspicion of ACS

Physical examination
ECG monitoring, blood samples

Persistent No persistent Undetermined

ST-segment elevation ST-segment elevation diagnosis

Thrombolysis ASA, Fonda/Enox/UHF ASA

PCI clopidogrel*, beta-blockers, nitrates

*Omit clopidogrel if
the patient is likely High risk Low risk
to go to CABG Second troponin measurement
within 5 days GPIIb/IIIa,
coronary angiography
Positive Twice negative

PCI, CABG or medical management Stress test,

depending upon clinical and angiographic features coronary angiography

1. Bertrand ME et al. Eur Heart J 2002; 23; 1809−1840.

Therapeutic Approach to STEMI

Antman et al. Circulation 2004;110:e82-292

ESC Guidelines 2008
 REPERFUSION
CLASS I
1. STEMI patients presenting to a hospital with PCI
capability should be treated with primary PCI within 90
minutes of first medical contact as a system goal
(Level of Evidence : A)

2. STEMI patients presenting to a hospital without PCI

capability and who cannot be transferred to a PCI
center and undergo PCI within 90 minutes of first
medical contact, should be treated with fibrinolytic
therapy within 30 minutes of hospital presentation as a
system goal unless fibrinolytic therapy is
contraindicated
(Level of Evidence : B)

European Heart Journal (2007) 28,882