ACUTE CORONARY SYNDROME

dr. H.M. Saifullah Napu, SpJP,FIHA

 Acute Coronary Syndrome
 The spectrum of clinical conditions ranging
from:
 unstable angina
 No ST segment elevation (NSTEMI) ---> non-Q
wave MI
 ST segmant elevation (STEMI) ---> Q-wave MI
 characterized by the common
pathophysiology of a disrupted atheroslerotic
plaque
 ACS in ED is frequent, often difficult to
recognize, a major cause of morbidity and
mortality with prognosis related to early
treatment
high risk of suboptimal care with
poor outcome
high need for management strategy
 Mr. DX. 38

 Chest pain – Atypical

 Risk factors: Diabetes, prior smoker

 Exam, ECG & blood tests: Normal

 Diagnosis: Indigestion

 Discharge for follow-up

 Went to zoo with kids

 Mr. DX. 38 Following day

 Recurrent Chest Pain

 Collapsed – unconscious

 Bystander CPR commenced

 VF- Unable to defibrillate

 Died in ED
CHEST PAIN
 Assessing Chest pain

 Character
 Time of onset, duration, frequency
 Changes in tempo
 Exacerbating and alleviating factors
 Pain during situation associated with increased
myocardial O2 demand ( e.g. exertion, stress )
 Unstable Angina / Myocardial Infarction
Symptoms

 new onset angina

 increase in frequency, duration or severity
 decrease in exertion required to provoke
 any prolonged episode (>10-15min)
 failure to abate with >2-3 S.L. NTG
 onset at rest or awakening from sleep
 Stable Angina - Symptoms
 mid-substernal chest pain
 squeezing, pressure-like in quality (closed fist = Levine’s
sign)
 builds to a peak and lasts 2-20 minutes
 radiation to left arm, neck, jaw or back
 associated with shortness of breath, sweating, or nausea
 exacerbated by exertion, cold, meals or stress
 relieved by rest, NTG
 Presentation Chest Pain
 54% pasien yang menunjukan gejala khas untuk ACS.
 34% “burning”, atau “indigestion”
 32% nyeri dada
 20% nyeri menusuk, tajam.
 42% tak dapat mendeskripsikan nyerinya.
 Nyeri yang tajam, menusuk, pleuritik, posisional,
betambah dengan penekanan dada tanpa adanya
riwayat CAD hampir selalu bukan iskemia.
 Pada orang tua, diabetes, wanita, nyeri dada tidak
khas (atipikal)
 Patifisiologi SKA
Perubahan yg tjd pd pembuluh darah koroner
Oleh karena penumpukan plak

Aterosklerosis

Gangguan pasokan darah koroner ke miokard

Area miokard kekurangan pasokan darah

Iskemia

Perubahan Metabolisme
Manifestasi klinis
Repolarisasi listrik anaerob
Perubahan Metabolisme Manifestasi
Repolarisasi listrik anaerob Klinis

ST Segment Non ST Segment Metabolisme

Elevasi Infark Elevasi Infark Nyeri
Anaerob
Miokard Miokard

Pelepasan Enzim Asam Laktat

Troponin T CKMB

Evolusi akan
Menjadi Infark
 3 Komponen dalam mendiagnosa
SKA

 Keluhan sakit dada yg berupa

APTS/UAP

 Perubahan EKG, STEMI atau Non

STEMI dengan atau tanpa Q patologik

 Dengan / tanpa peningkatan Enzim

jantung
 Psn Nyeri Dada SINDROM KORONER AKUT
Rwyat nyeri dada Aspirin 300 mg dikunyah dan Nitrat s.l.
khas
EKG 12 sandapan*
Petanda biokimia

•EKG Non diagnostik •Perubahan ST/T Elevasi seg

•Petanda biokimia (-) •Petanda biokimia (+)
ST
•Nyeri dada (-) •Nyeri dada menetap

•EKG tdk Observasi

berubah •EKG serial
Evaluasi utk
•Petanda(-) •Ulang petanda
6-12 jam stlh
reperfusi
•Nyeri dada(-)
onset nyeri dada* Rawat Terapi
Pulang • Nitrat
•Perubahan seg ST • ASA
Risiko rendah Risko tinggi •Petanda (+) APTS/NSTEMI •Clopidogrel
Periksa di Periksa •Nyeri dada •UFH/LMWH
Rawat jalan segera •(+/- Antagonis
menetap
Receptor GPIIb/IIIa
 Differential Diagnosis
of Chest Pain

Cardiac Gastrointestinal
 ACS : Infarct,angina •Reflux esofagus
 MVP •Ruptur esofagus
 Aortic Stenosis •Gall bladder disease
 Hypertrophic cardio- •Peptic Ulcer
myopathy •Pancreatitis
 Pericarditis
Lungs Vascular
•Aortic dissection/aneurysma
 Lung Emboli



Pnemonia
Pneumothorax
Others
•Musculoskeletal
 Pleuritis
•Herpes zoster
Difficulties in Chest Pain Triage

 Chest pain – precursor to sudden death

 Attend Emergency – 7% of all presentation
 No evidence of heart damage – misdiagnosis common
 Junior Drs – frequently underestimate the risk
 Hospitals crowded – pressure to discharge
“Could this patient be another Mr. DX?”
 Missed MI – commonest cause for litigation in US
 Suboptimal Outcome for Most
Chest Pain Patient

 Patients wait too long to seek medical care.

 Delay in the diagnosis of AMI and in the
implementation of treatment in the ED.
 Physician failure to correctly diagnose AMI in
patients with atypical signs and symptoms
 Failure to give proven effective therapy
Aggressive intervention, including aspirin,
clopidogrel, low molecular weight heparin,
glycoprotein IIb/IIIa inhibitor, fibrinolytic
therapy and revascularization, has been
demonstrated to reduce mortality and
minimized left ventricular damage when
initiated early after the onset of ACS.
Therefore, it is important to perform rapid
screening of chest pain patients in ED with
chest pain
 Atherothrombosis: a Generalized and
Progressive Process
Unstable
Plaque
angina

Normal
Fatty
streak
Fibrous
plaque
Athero-
sclerotic
plaque
rupture/
fissure &
thrombosis MI
}ACS
Ischemic
stroke/TIA

Critical leg
ischemia
Clinically silent
Stable angina Cardiovascular
Intermittent death
claudication

Increasing age
ACS, acute coronary syndrome; TIA, transient ischemic attack
 Risk Factors
 family history
 sex
 cigarette smoking
 diabetes mellitus
 hypertension
 hyperlipidemia
 sedentary life-style
 obesity
 elevated homocysteine.
 Incidence of ACS in the US
Number of people with ACS discharged from US hospitals in 2002
(including secondary discharges)

ACS
1,673,0001

UA MI
728,0001* 973,0001*

NSTEMI STEMI
55–70% of ACS patients2 30–45% of ACS patients2

*28,000 hospitalizations received both diagnoses for UA and MI

1. American Heart Association. Heart Disease and Stroke Statistics 2005 Update.
2. NRMI-4. J Am Coll Cardiol 2003; 41: 365A–366A.
FOR INTERNAL USE ONLY
Algorithm for Initial Assessment and Evaluation
of the Patient with Acute Chest Pain

Chest pain consistent with coronary ischemia

Within 10 minutes
• Initial evaluatioon • 12 lead ECG
• Establish IV • Aspirin 160-325 mg - chewed
• Establish continuous ECG monitoring
• Blood for baseline serum cardiac markers

Therapeutic/Diagnostic tracking
according 12-lead ECG results

Nondiagnostic/ ECG suggestive of ischemia - ST segment elevation or

normal ECG T wave inversion or ST depression New bundle branch block

ACC/AHA Pocket Guideline 2000

 ESC Recommended Strategy in ACS Patients1
Clinical suspicion of ACS

Physical examination
ECG monitoring, blood samples

Persistent No persistent Undetermined

ST-segment elevation ST-segment elevation diagnosis

Thrombolysis ASA, LMWH, ASA

PCI clopidogrel*, beta-blockers, nitrates

*Omit clopidogrel if
High risk Low risk
the patient is likely to
go to CABG within 5 Second troponin measurement
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.

Annual Patient Admissions for
Acute Coronary Syndromes

Remember 3 IS

ST-elevation MI Non-ST elevation ACS

 The Three I’s
 Ischemia= ST depression or T-wave inversion
Represents lack of oxygen to myocardial tissue
 The Three I’s
 Injury = ST elevation -- represents prolonged
ischemia; significant when > 1 mm above the baseline of
the segment in two or more leads
 The Three I’s
 Infarct = Q wave — represented by first negative
deflection after P wave; must be pathological to
indicate MI
Inferior Wall MI
Anterior Wall MI
GAMBARAN EKG ACS
 ST segmen depresi (  30 %)
 Gelombang T terbalik (20-30%)
 ST elevasi temporer (2-5%)
 Sering saat direkam di UGD gambaran
EKG normal
TREATMENT OF ACUTE CORONARY SYNDROME
 Atasi simptoms :
- Menurunkan kebutuhan oksigen (B bloker, nitrat, antagonis
kalsium)
- Memperbaiki perfusi koroner (trombolisis, PCI, CABG)
- Perbaiki metabolisme miokard (trimetazedin, nivabradine)
 Perbaiki Prognosis :
- Aspirin
- Thienopyridine (Clopidogrel, Ticlopidin)
- Cilostazol, Ace inhibitor, Statin
 Unstable Angina: Treatment Goals
 Acute
– Relieve angina
– Prevent MI
– Preserve viable myocardium if there is an infarction
– Prevent death
 Chronic
– Cardiac rehabilitation
– Identify and treat coronary risk factors / underlying
disease
– Prevent recurrent admissions
White. Unstable angina: Ischemic syndromes. In: Topol EJ (ed). Textbook of Cardiovascular Medicine.
Lippincott-Raven, Philadelphia, Pennsylvania: 1998:365–393
 Unstable Angina -
High Risk Features
 prolonged rest pain
 dynamic EKG changes (ST depression)
 age > 65
 diabetes mellitus
 left ventricular systolic dysfunction
 angina associated with congestive heart failure, new
murmur, arrhythmias or hypotension
 elevated Troponin I or T
 TIMI risk score
1 point each for presence of :
 Age > 65 years
 Documented prior coronary artery stenosis > 50%
 Three or more conventional cardiac risk factors (e.g. age, sex, family
history, hyperlipidemia, diabetes, smoking, obesity)
 Use of aspirin in the preceding 7 days
 Two or more anginal events in the preceding 24h
 ST-segment deviation (transient elevation or persistent depression)
 Increased cardiac biomarkers

Score 5 – 7 : Score 3 – 4 : Score 0 – 2 :

high risk intermediate risk low risk

(Pollack et al, 2003)

 Medications Recommended for Long-Term
Therapy in Patients with ACS
Agent Comments Class/Level
of Evidence*
aspirin antiplatelet I/A
clopidogrel antiplatelet when aspirin is contraindicated I/B
in addition to aspirin for at least one month I/B
and up to 9 months
beta blockers anti-ischemic I/A

ACEI EF <40% or heart failure I/A

EF >40% IIa/B
CCB antianginal when beta blockers are not I/B
successful
antianginal when beta blockers are I/C
contraindicated
 Medications Recommended for Long-Term
Therapy in Patients with ACS
Agent Comments Class/Level
of Evidence*
warfarin low intensity with or without aspirin IIb/B
Dipyridamole antiplatelet III/A
statins LDL cholesterol >130 mg/dlI/A I/A
LDL cholesterol 100-130 mg/dl IIa/C
gemfibrozil HDL cholesterol <40 mg/dl IIa/B
niacin HDL cholesterol <40 mg/dl IIa/B
niacin or triglycerides >200 mg/dl
gemfibrozil
folate elevated homocysteine IIb/C
antidepressant depression IIb/C
treatment of blood pressure >135/85 mm Hg I/ A
hypertension
 Acute Myocardial Infarction (STEMI)
 total thrombotic occlusion of epicardial coronary artery 
onset of ischemic cascade
 prolonged ischemia  altered myocardial cell structure and
eventual cell death (release of enzymes - CPK, LDH,
Troponin)
 altered structure  altered function (relaxation and
contraction)
 consequences of altered function often include exacerbation
of ischemia (ischemia begets ischemia)
 Acute Myocardial Infarction (STEMI)

 wavefront phenomenon of ischemic evolution - endocardium

to epicardium
 If limited area of infarction  homeostasis achieved
 If large area of infarction (>20% LV )  Congestive
heart failure
 If larger area of infarction (>40% LV) 
hemodynamic collapse
 Initial Management in ED
 Aspirin 165 - 325 mg (chew and swallow)
 Sublingual NTG unless:
• systolic pressure < 90 mm Hg or ≥ to 30 mm Hg below
baseline
• severe bradycardia (< 50 bpm)
• tachycardia (> 100 bpm) or
• suspected RV infarction.

 O2 by nasal prongs, first 2 - 3 h in all; continue if PaO2

<90%
 Analgesia: small doses of morphine (2-4 mg) as needed
 Fibrinolysis or PCI if ST elevation > 1mV or LBBB
(Goal: door-needle < 30 min or door-dilatation < 60-90
min)
 Management of Patients with ST Elevation

ST elevation

Aspirin
Beta-blocker

 12 h > 12 h

Eligible for Fibrinolytic therapy Not a candidate for Persistent

fibrinolytic therapy contraindicated reperfusion therapy symptoms ?

No Yes
Primary
Fibrinolytic therapy
PTCA or CABG
Other medical therapy: Consider
ACE inhibitors Reperfusion
? Nitrates Therapy
Anticoagulants
 Treatment of Acute Myocardial
Infarction
 aspirin, NTG, heparin, analgesia, oxygen
 reperfusion therapy
 thrombolytic therapy (t-PA, SK, n-PA, r- PA)

 new combinations ( t-PA, r-PA + 2b / 3a inhib)

 cath lab (PTCA, stent)

 decrease MVO2
 nitrates, beta blockers and ACE inhibitors

 for high PCWP - diuretics

 for low Cardiac Output - pressors (dopamine, levophed,

dobutamine; IABP; early catheterization)
 Assessing Reperfusion Options for
Patients with STEMI1
STEP 1: Assess time and risk (time from symptom onset, risk of STEMI, risk of
thrombolysis, time for transport to PCI lab)

STEP 2: Determine whether fibrinolysis or invasive strategy is preferred*

Fibrinolysis preferred if: Invasive strategy preferred if:

• Early presentation (<3 hours) • Skilled PCI lab with surgical backup
• Invasive strategy not an option available
• Delay to invasive strategy • High risk (i.e. cardiogenic shock)
• Contraindications to fibrinolysis
• Late presentation (>3 hours)
• Diagnosis of STEMI is in doubt
*If presentation is <3 hours from onset and there is no delay to an invasive strategy,
there is no preference for either strategy

1. Antman EM et al. Circulation 2004; 110: 588–636. FOR INTERNAL USE ONLY
 Door - to - Needle
Chest pain, arrived at EMG: anamnesis, O2, infuse

10 minute
Record ECG, evaluate ST elevation

10 minute
Present/ absent contraindication thrombolytic:
- Bleeding
- BP persist > 180/110 mmHg
- History stroke
- Mayor operation< 2 mo
- Severe disease (e.g. Cancer)
10 minute
Consider primary PTCA:
No Yes - Patient with stroke & bleeding
risk
- Shock cardiogenic
Thrombolytic therapy
Intra Coronary Thrombus
Angiogram in unstable angina: Angiogram in unstable angina: after
eccentric, ulcerated plaque stent deployment