Acute Coronary Syndrome

(ACS)
dr M. Arman Nasution SpPD
Coronary Artery
 Hospital

Hx Ventricular systolic dysfunction (LV/RV)

PE
EKG
Electrical instability
Recurrent ischemia/infarct
Inhospital admission ACS
ACS VT/VF
Heart Block
After discharged Atrial arrhythmia

Mechanical complication
Myocardial rupture
MR
VSD
 Ventricular
dysfunction
VT/VF
In-hospital admission
ACS Heart Block
After discharged Atrial arrhythmia

mechanical
Myocardial rupture
MR
VSD
Sequence of Events in Ischemic Heart
Disease

Arrythmias
Lost of muscle
Angina MI
Silent Ischemia
Remodeling

CAD
Progresif dilatation

Endothelial dysfunction
Heart Failure
Death
Risk Factor
 Acute coronary syndrome
Unstable angina

Acute non ST-elevation myocardial infarction

Acute ST-elevation myocardial infarction

Chronic coronary artery disease : chronic stable

angina
 Spectrum of CAD/ACS
No ST elevation ST elevation
Stable Unstable NSTEMI STEMI
angina angina

ACUTE CORONARY SYNDROMES

CAD = coronary artery disease; NSTEMI = non-ST-segment elevation myocardial infarction;

STEMI = ST-segment elevation myocardial infarction.
Source (Photos): Davies MJ. Heart. 2000;83:361-366.
 Pathophysiology of ACS

Subtotal artery occlusion Complete total occlusion

Non ST elevation ACS ST elevation ACS

(UA/NSTEMI) (STEMI)
 Structure of thrombus
following plaque disruption
UA/NSTEMI STEMI
Non-occlusive thrombus Occlusive thrombus
(platelets, some fibrins) (platelets, fibrins, red cell)

Plaque core

Intra-plaque thrombus
(platelet dominated)
Understanding Myocardial Ischemia

Imbalan
ce
 Understanding Myocardial Ischemia

DECREASE O2 SUPPLY INCREASE DEMAND

Mechanical Dec. Oxygenated Increase cardiac
Obstruction Blood Flow output..
Atheroma Anemia
(Thyrotoxicosis)
Myocardial Hypertrophy
Thrombosis Carboxyhemoglo- (AS,HTN)
binemia
Spasm Hypotension CAUSING DEC
CORONARY PERFUSION PRESSURE

Embolus

Coronary arteritis

Coronary trauma
Plaque
Fissure or
Rupture
Platelet
Adhesion

Platelet
Activation

Platelet
Aggregation

Thrombotic
Occlusion
 Consequence of
Acute Coronary Occlusion
TYPICAL ECG INC CARDIAC
HISTORY CHANGES ENZYMES
 Clinical
Presentation
Of
ACS
 Focused History
Aid in diagnosis and rule Reperfusion questions
out other causes
Timing of presentation
Palliative/Provocative ECG c/w STEMI
factors
Contraindication to
Quality of discomfort
fibrinolysis
Radiation Degree of STEMI risk
Symptoms associated
with discomfort
Cardiac risk factors
Past medical history
-especially cardiac
 Symptom
Acute chest pain
Nausea/ vomiting
Sweating
Dyspnea
Palpitation
Syncope
Pulmonary edema
Epigastric pain
Post-op hypotension
Oliguria
Acute confusional state
Stroke
Diabetic hyperglycemia
state
 ACS Clinical Presentation

Substernal chest pain or pressure (>20-30 min)

Localization or radiation to arms, back, throat, jaw
Accompanying features
Dyspnea
Nausea/vomiting
Diaphoresis
Weakness
Atypical: syncope
Risk Factor for Acute Coronary Syndrome

Non-modifiable

Modifiable
 Risk Factor

Age
Incidence increase with age.

Male gender
Men > premenupausal
women
After menupause ,
incidence is almost same

Family History of IHD

 Modifiable
Risk Factors
Smoking
Hyperlipidemia
Hypertension
Diabetes mellitus
Lack of exercise
Blood coagulation factors
Personality
Obesity
 Targeted Physical Examination

Vitalsigns Recognize factors that

Cardiovascular increase risk
system Hypotension
Respiratory Tachycardia
system Pulmonary rales, JVP,
pulmonary edema,
Abdomen
New murmurs/heart sounds
Neurological Diminished peripheral
status pulses
Signs of stroke
 Acute coronary syndromes
Aortic dissection

Esophageal reflux Pneumothorax

Chest pain
Myocarditis Acute pulmonary embolism

Acute pericarditis
Costochronditis
Psychosomatic
 Acute Coronary Syndromes

ST-elevation MI

Cardiac marker +ve Non-ST elevation ACS Unstable angina

Cardiac marker +ve Cardiac marker - ve

 Normal Repeat EKG when
ST-depression patient is in pain
T-wave inversion Continuous ST
ST-elevation or segment monitoring
LBBB
Cardiac Markers
 Timing of Release of Various Biomarkers After Acute
Myocardial Infarction

Anderson, J. L. et al. J Am Coll Cardiol 2007;50:e1-e157

Copyright 2007 American College of Cardiology Foundation. Restrictions may apply.
 Cardiac Markers
Troponin ( T, I)
Very specific and more
sensitive than CK
Rises 4-8 hours after injury
May remain elevated for up
to two weeks
Can provide prognostic
information
Troponin T may be elevated
with renal dz,
poly/dermatomyositis
CK-MB isoenzyme
Rises 4-6 hours after injury
and peaks at 24 hours
Remains elevated 36-48 hours
Positive if CK/MB > 5% of total
CK and 2 times normal
Elevation can be predictive of
mortality
False positives with exercise,
trauma, muscle dz,
 Chest pain
Assess 12 lead ECG Goal = 10 min

Non Chronic Possible Definite

Cardiac Stable ACS ACS
Diagnosis Angina
Initial assesment
Hx
PE
 Chest Pain Suggestive of Ischemia

Immediate assessment within 10 Minutes

Initial labs Emergent History &
and tests care Physical
12 lead ECG IV access Establish
Obtain initial Cardiac
diagnosis
cardiac enzymes Read ECG
monitoring
Electrolytes, CBC, Identify
Oxygen
lipids, BUN/Cr, complications
glucose, Coags Aspirin Assess for
CXR Nitrates reperfusion
 ACS
Prevent plaque rupture : Statins
Decrease O2 need
Decrease platelet activation and aggregation
Open blocked vessel
Acute ST Elevation Myocardial Infarction
Assessments and treatments to consider for
patients who present with ACS

Initial general treatment (M O N A C)

M orphine 2-4 mg q 5-10 min
O xygen 4 L/min
N TG sublingual or spray, followed by infusion for persistent chest
pain
A spirin 160 -325 mg chew and swallow or/and
C lopidogrel 300mg oral
Specific Treatment : Reperfusion Therapy

Fibrinolysis vs primary PCI

Time is muscle
 Treatment of ASTEMI

Open coronary artery within 12 hr

Reperfusion Therapy
Fibrinolytic agents : Streptokinase, tPA
Primary PTCA
 Reperfusion Therapy
STEMI
Door to needle time
( First medical contact-to-needle time)
fibrinolytic therapy 30
Door to balloon time
( First medical contact-to-balloon time )
PCI 90
Contraindications and Cautions for Fibrinolysis in STEMI
Any prior intracranial hemorrhage

Absolute Known structural cerebral vascular lesion

Contraindications (e.g., arteriovenous malformation)
Known malignant intracranial neoplasm
(primary or metastatic)
Ischemic stroke within 3 months EXCEPT
acute ischemic stroke within 3 hours
Suspected aortic dissection
Active bleeding or bleeding diathesis
(excluding menses)
Significant closed-head or facial trauma
within 3 months
ACC/AHA Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction 2004
 Contraindications and Cautions
for Fibrinolysis in STEMI

History of chronic, severe, poorly controlled

Relative
hypertension
Contraindications
Severe uncontrolled hypertension on
presentation (SBP > 180 mm Hg or DBP >
110 mm Hg)
History of prior ischemic stroke greater than
3 months, dementia, or known intracranial
pathology not covered in contraindications
Traumatic or prolonged (> 10 minutes) CPR
or major surgery (< 3 weeks)
ACC/AHA Guidelines for the Management of Patients with ST-Elevation Myocardial Infarction 2004
 ST-Elevation MI New LBBB
ST elevation new LBBB

< 12 hour > 12 hour

Thrombolytic is Persistent symptom

contra-indicated
Eligible for
reperfusion Rx Not candidate for
reperfusion Rx No Yes
1 PCI

Other medical treatment

Thrombolytic Rx B-blocker Consider
: Streptokinase ACEI / ARB reperfusion Rx
: rt-PA Nitrate
Statin
 Door to <30 MIN
needle Reperfusion Goals

Door to
balloon <90 MIN
REPERFUSION

SYMPTOM ONSET TO-

REPERFUSION
<120 MIN

ONSET OF EMS HOSP ECG

SYMPYOMS ARRIVAL ARRIVAL

INCREASING LOSS OF MYOCYTES

 Door to Needle Time and Mortality

In hospital
mortality (%)

Door to Balloon Time and Mortality

Thai ACS registry

 Comparison of Approved Fibrinolytic Drugs
Feature SK t-PA
Fibrin-specific - ++
Half-life (minutes) 20 5
Antigencity Y N
90 minutes patency 60 84
Rate of ICH 0.34 0.69
Requires concomitant heparin +/- Y

Weight adjusted dosing N Y

Dose 1.5 mL units IV over 60 15 mg IV /1-2min
minutes 0.75 mg/kg IV/30 min
(max 50 mg)
0.5 mg/kg IV/60 min
SK (max 35 mg)

Bolus administration N N
Cost per dose (Baht) 9,606 49,857 51
ACS : Unstable angina or NSTEMI
 chest pain
(CAD) EKG
 nonfatal MI chest pain ischemia
ACS
ACS :: NSTEMI
NSTEMI or
or UA
UA
ACS : NSTEM or UA

Antithrombin
Fibrinolytic UFH, LMWH

Stabilized
Severe
stenosis ASA, clopidogrel,
Antiplatelets
Subtotal G2b3a inhibitors

occlusion
 Assessments and treatments to consider for
patients who present with ACS

Initial general treatment ( M O N A C )

M orphine 2-4 mg q 5-10 min
O xygen 4 L/min
N TG sublingual or spray, followed by infusion for persistent
chest pain
A spirin 160 -325 mg chew and swallow or/and

C lopidogrel 300mg oral

ACS
ACS :: NSTEACS
NSTEACS or
or UA
UA

PCI

Initial Conservative Strategy : Early Hospital Care
ASA; clopidogrel if intolerant (I, A)
Anticoagulant therapy should be added to antiplatelet
therapy as soon as possible after presentation (I, A)
Enoxaparin or UFH (I, A)
Fondaparinux (I, B)
Enoxaparin or fondaparinux preferable (IIa, B)

Initiate clopidogrel, loading dose + maintenance dose (I,

A)

ACC/AHA 2007 Guidelines for the Management of

Patients With Unstable Angina/NonST-Elevation Myocardial Infarction
 Adjunctive Therapies
Beta-blocker

IV nitroglycerine
recurrent ischemia, large anterior MI, heart
failure, antihypertensive effects
ACE inhibitor
large anterior wall MI, heart failure

24 .
Secondary Prevention and Long Term Management

Goals Recommendations

Smoking Assess tobacco use.

Goal:
Complete Strongly encourage patient and family to
Cessation stop smoking and to avoid secondhand
smoke.

Provide counseling, pharmacological

therapy (including nicotine replacement and
bupropion), and formal smoking cessation
programs as appropriate.

62
Secondary Prevention and Long Term Management
Goals Recommendations

Blood pressure
If blood pressure is 120/80 mm Hg or greater:
control:
Goal: < 140/90
Initiate lifestyle modification (weight control, physical
mm Hg or
activity, alcohol moderation, moderate sodium restriction, and
<130/80 mm Hg
emphasis on fruits, vegetables, and low-fat dairy products) in
if chronic kidney
all patients.
disease or
diabetes
If blood pressure is 140/90 mm Hg or greater or 130/80
mm Hg or greater for individuals with chronic kidney
disease or diabetes:

Add blood pressure-reducing medications, emphasizing the

use of beta-blockers and inhibitors of the renin-angiotensin-
aldosterone system.

63
Secondary Prevention and Long Term Management

Goals Recommendations

Physical activity: Assess risk, preferably with exercise test, to guide

Minimum goal: prescription.
30 minutes 3 to 4
days per week;
Optimal daily Encourage minimum of 30 to 60 minutes of activity,
preferably daily but at least 3 or 4 times weekly (walking,
jogging, cycling, or other aerobic activity) supplemented by
an increase in daily lifestyle activities (e.g., walking breaks
at work, gardening, household work).

Cardiac rehabilitation programs are recommended for

patients with STEMI.

64
Secondary Prevention and Long Term Management
Goals Recommendations

Lipid Start dietary therapy in all patients (< 7% of total calories as

management: saturated fat and < 200 mg/d cholesterol). Promote physical
(TG less than activity and weight management. Encourage increased
200 mg/dL) consumption of omega-3 fatty acids.
Primary goal:
LDL-C << than Assess fasting lipid profile in all patients, preferably within
100 mg/dL 24 hours of STEMI. Add drug therapy according to the
following guide:

LDL-C < 100 mg/dL (baseline or on treatment):

Statins should be used to lower LDL-C.

LDL-C 100 mg/dL (baseline or on

treatment):
Intensify LDL-Clowering therapy with drug treatment,
giving preference to statins.

65
Secondary Prevention and Long Term Management
Goals Recommendations

Lipid If TGs are 150 mg/dL or HDL-C is < 40 mg/dL:

management: Emphasize weight management and physical
(TG 200 mg/dL activity. Advise smoking cessation.
or greater)
Primary goal: If TG is 200 to 499 mg/dL:
NonHDL-C << After LDL-Clowering therapy, consider adding
130 mg/dL fibrate or niacin.

If TG is 500 mg/dL:
Consider fibrate or niacin before LDL-Clowering
therapy.
Consider omega-3 fatty acids as adjunct for high
TG.

66
Secondary Prevention and Long Term Management

Goals Recommendations

Weight
management: Calculate BMI and measure waist circumference
Goal: as part of evaluation. Monitor response of BMI
BMI 18.5 to 24.9 and waist circumference to therapy.
kg/m2
Start weight management and physical activity as
Waist appropriate. Desirable BMI range is 18.5 to 24.9
circumference: kg/m2.
Women: < 35 in.
Men: < 40 in. If waist circumference is 35 inches in women or
40 inches in men, initiate lifestyle changes and
treatment strategies for metabolic syndrome.

67
Secondary Prevention and Long Term Management

Goals Recommendations

Diabetes Appropriate hypoglycemic therapy to

management: achieve near-normal fasting plasma
Goal: glucose, as indicated by HbA1c.
HbA1c < 7%
Treatment of other risk factors (e.g.,
physical activity, weight management,
blood pressure, and cholesterol
management).

68
 Management Strategies in Acute Coronary syndrome(ACS)

Symptoms of Acute Coronary Syndrome

ST elevation No ST elevation
(STEMI) EKG (UA/NSTEMI)

Reperfusion approach All patients Antithrombotic approach

1. ASA 1. Anti-ischemic medications
2. Heparin(UFH or LMWH) Beta-blocker
3. Clopidogrel Nitrated
4. Choose reperfusion method+/-Ca++ channel blocker
a. Fibrinolytic drug 2. General measures
b. Primary PCI Oxygen
Pain control (morphine)
3. Additional therapies
ACE inhibitor
Statin
1. ASA
2. Heparin(UFH or LMWH)
3. Clopidogrel
4. For high risk patients
GP IIb/IIIa inhibitor
Proceed to cathlab
 ABCDE
A- antiplatelets, ACE-I
B- beta-blocker, blood pressure control
C- cholesterol lowering, cigarette smoking
cessation
D- diet, diabetes management
E- exercise
PENYAKIT JANTUNG
KORONER

dr M. Arman Nasution SpPD

Penyakit jantung
hingga kini masih
menjadi penyebab
kematian
nomor satu
di dunia.

72
PENYAKIT JANTUNG
KORONER
Pembunuh No. 1 di Dunia
PJK 15 JUTA

DIARE 5 JUTA

KANKER 4,8 JUTA

TBC 3 JUTA

Angka Kematian / Tahun

Laporan Organisasi Kesehatan Dunia (WHO) 2008:
Angka kematian akibat penyakit kardiovaskular
diperkirakan akan meningkat jadi 17.5 juta hingga
20 juta pada 2015.
Selain itu, di Asia, penyakit ini lebih sering
menyerang yang berusia lebih muda ketimbang di
negara-negara belahan Barat. Hampir separuh dari
mereka yang meninggal karena penyakit kronis,
termasuk penyakit jantung dan stroke, berada
dalam usia produktif, yakni 15-69 tahun.
 WHO tahun 2005 : dari 58 juta kematian di
dunia , 17,5 (30%) disebabkan peny.jantung
& pemb. darah, terutama serangan jantung
(7,6 juta) dan stroke (5,7 juta). Diperkirakan
2015 mjd 20 juta.

RISKEDAS 2007 : prevalensi peny jantung &

pemb.darah sangat tinggi, spt : hipertensi 31,7 %,
penyakit jantung 7,2% dan stroke 8,3% per 1000
penduduk
penyakit jantung koroner
Penyakit Kardiovaskular
sering dijumpai
dialami pada usia
produktif
 Penyakit Jantung Koroner (PJK) adalah suatu
penyakit kronis akibat pengerasan
(atherosklerosis) dinding pembuluh darah
arteri jantung (koroner).

Atherosklerosis akan mengakibatkan

pembuluh arteri menjadi sempit dan kaku
yang berakibat timbulnya gangguan aliran
darah.
 Bila jantung berdenyut 70 kali / menit
Sekali denyut 70cc darah 5 liter
Curah Jantung
70cc darah mengitari 100.000 km
pembuluh
berdenyut 100.000 x/hari
2,5 milyar x/ sepanjang hidup
memompakan darah lebih dari 227 juta
liter
Atherosclerosis Timeline:
Endothelial Dysfunction
Foam Fatty Intermediate Fibrous Complicated
Cells Streak Lesion Atheroma Plaque Lesion/Rupture

Endothelial
From first decade Dysfunction
From third decade From fourth decade
Smooth muscle Thrombosis,
Growth mainly by lipid accumulation and collagen hematoma

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

84
Sequence of Events in Ischemic Heart
Disease

Arrythmias
Lost of muscle
Angina MI
Silent Ischemia
Remodeling

CAD
Progresif dilatation

Endothelial dysfunction
Heart Failure
Death
Risk Factor
Atherogenesis and Atherothrombosis:
A Progressive Process
Plaque
Athero- Rupture/ Myocardial
Fatty Fibrous sclerotic Fissure & Infarction
Normal Streak Plaque Plaque Thrombosis

Ischemic
Stroke

Critical
Leg
Clinically Silent Angina
Ischemia
Transient Ischemic Attack
Claudication/PAD
Cardiovascular Death
Increasing Age

3
 Nyeri dada
Tidak ada
Penyempitan Kematian Otot Jtg
Penyempitan
Kematian Mendadak

Proses Penyempitan /
Normal Pengerasan
Sindroma Koroner Akut
(STEMI)
Normal Atherosclerosis Plaque Rupture ACS

Decades Minutes/Seconds
Angina klasik :
Tidak Dapat Dimodifikasi

Usia
Jenis kelamin
Riwayat keluarga
Ras
faktor resiko PJK
Dapat Dimodifikasi
Lipid/lemak dan
lipoprotein
Diabetes mellitus
Hipertensi
Kebiasaan merokok
Obesitas
Kurang olahraga
stress
 Riwayat Penyakit
Pemeriksaan fisik
Pemeriksaan Laboratorium penunjang
Elektrokardiogram (EKG)
Treadmil Test
Ekokardiogram
Angiografi Koroner
Myocardial Perfusion Imaging
Pada sindrom koroner akut :

Aritmia/Block ---- Kematian Mendadak

Disfungsi Ventrikel Gagal Jantung

Hipotensi ---- Shock Cardiogenic

Mekanikal : Ruptur Ventrikel/Septum

Pericarditis
 ANTIANGINA
ANTIPLATELET
ANTIKOAGULAN/ANTITROMBIN
Terapi tambahan :
- ACE-I
- PREPARAT STATIN
 Dengan Obat-obatan :
* Aspilet / antiplatelet
* Nitrat
* Beta-bloker
* Ace-Inhibitor
* Antagonis kalsium
* Statin
Dengan Tindakan :
* Angioplasti dengan balon dan stent (PTCA)
* Operasi pintas koroner (CABG)
 Merubah gaya hidup
Mengkonsumsi makanan sehat
Mengontrol kadar kolesterol darah
Mengontrol kadar gula darah
Stop merokok
Berolahraga secara teratur
Mencegah obesitas / kegemukan
Menghindari stress
 Faktor Resiko untuk PJK
Hiperkoagubilitas Gaya Hidup (merokok dll)

Hemosisteinemia Hiperlipidemia

Hipertensi
Jenis Kelamin
Infeksi?
Umur
Diabetes
Genetik
Aterosklerosis Obesitas

Manifestasi Aterotrombosis
Pengenalan dini, Kenali Faktor Resiko !!!
PENYAKIT JANTUNG
KORONER
 Penyakit Jantung Koroner (PJK) adalah suatu
penyakit kronis akibat pengerasan
(atherosklerosis) dinding pembuluh darah
arteri jantung (koroner).

Atherosklerosis akan mengakibatkan

pembuluh arteri menjadi sempit dan kaku
yang berakibat timbulnya gangguan aliran
darah.
 Kadar LDL dan Trigliserida darah tinggi
Kadar HDL darah rendah
Hipertensi
DM, Obesitas /kegemukan
Genetik / faktor keturunan
Merokok
Kurang olah raga, stress
Mengkonsumsi makanan berlemak tingi
 Perjalanan : Leher, lengan kiri, mandibula, gigi, punggung, dan
dapat juga lengan kanan
Nyeri membaik atau hilang dengan istirahat
Faktor pencetus : Latihan fisik, stres emosi, udara dingin, dan
sesudah makan
Gejala yang menyertai: Mual, muntah, sulit bernafas, keringat
dingin, dan lemas
Lokasi : Substermal (dibawah tulang dada), retrostermal
(belakang tulang dada), dan prekordial
Sifat Nyeri : Rasa sakit, seperti ditekan, rasa terbakar, ditindih
benda berat, seperti ditusuk, rasa diperas, dan dipelintir
 Riwayat Penyakit
Pemeriksaan fisik
Pemeriksaan Laboratorium penunjang
Elektrokardiogram (EKG)
Treadmil Test
Ekokardiogram
Angiografi Koroner
Myocardial Perfusion Imaging
 WHO tahun 2005 : dari 58 juta kematian di
dunia , 17,5 (30%) disebabkan peny.jantung
& pemb. darah, terutama serangan jantung
(7,6 juta) dan stoke (5,7 juta). Diperkirakan
2015 mjd 20 juta.

RISKEDAS 2007 : prevalensi peny jantung &

pemb.darah sangat tinggi, spt : hipertensi 31,7 %,
penyakit jantung 7,2% dan stroke 8,3% per 1000
penduduk
 Prevalensi Nasional NAD
Penyakit Jantung 7,2 % 12,6 %

Stroke 0,8 % 16,6

1,7 %
DM 1,1 %
14,1 %
Ggn Mental Emosional 11,6 %
18,5
Gangguan Jiwa Berat 0,5%
53,3 %
Kurang Aktivitas Fisik 48,2%.
 Penyebab kematian utama
pd wanita usia > 65 thn

Diseluruh dunia, 8,6 juta

wanita meninggal per tahun
akibat penyakit jantung.

3 juta wanita meninggal akibat

stroke per tahun ( 11 %, pria
hanya 8,4 %)

Dalam 20 thn terakhir menunjukkan peningkatan serangan

jantung pada usia 35 s/d 54 thn.
Mortalitas dalam minggu minggu pertama setelah
serangan jantung 2 x dibandingkan pria
 38 % wanita dan 25 % pria akan meninggal dalam 1 tahun
sejak serangan jantung yang pertama.

46 % wanita dan 22 % pria yg selamat setelah serangan

jantung akan mengalami gagal jantung dalam 6 tahun.

Mortalitas wanita yg menjalani CABG 2 3 x pria.

62,6% dari seluruh penderita gagal jantung yang meninggal

adalah wanita.

Kematian akibat serangan jantung pd wanita 4 - 6 x lebih

tinggi dibandinggkan kanker payudara.
Hospitalizations in the U.S. Due to Acute
Coronary Syndromes (ACS)
Acute Coronary
Syndromes*

1.57 Million Hospital Admissions - ACS

UA/NSTE STEMI
MI
1.24 million .33 million
Admissions per year Admissions per year

Heart Disease and Stroke Statistics 2007 Update. Circulation 2007; 115:69-171. *Primary and secondary
diagnoses. About 0.57 million NSTEMI and 0.67 million UA.
 Yang tidak dapat di ubah :
1. usia
2. jenis kelamin
Yang Dapat di ubah : 3. riwayat keluarga
1. Merokok 4. tipe kepribadian
2. Hipertensi
3. Diabetes
4. Hiperkolesterol
5. Obesitas
6. kurang olah raga
7. stres
Sequence of Events in Ischemic Heart
Disease

Arrythmias
Lost of muscle
Angina MI
Silent Ischemia
Remodeling

CAD
Progresif dilatation

Endothelial dysfunction
Heart Failure
Death
Risk Factor
Atherogenesis and Atherothrombosis:
A Progressive Process
Plaque
Athero- Rupture/ Myocardial
Fatty Fibrous sclerotic Fissure & Infarction
Normal Streak Plaque Plaque Thrombosis

Ischemic
Stroke

Critical
Leg
Ischemia
Clinically Silent Angina
Transient Ischemic Attack Cardiovascular Death
Claudication/PAD
Increasing Age

3
Sindroma Koroner Akut
(STEMI)
1. Trombus tidak oklusif pada plak yang sudah ada

2. Obstruksi dinamik (spasme koroner / vasokonstriksi )

3. Obstruksi mekanik yang progresif

4. Inflamasi dan atau infeksi

5. Faktor atau keadaan pencetus ( mis : anemia,

hipoksemia, tirotoksikosis, takikardia, demam dll)
Angina klasik :
Angina Equivalent :

Tidak ada nyeri / rasa tidak

enak di dada yang khas,
namun pasien menunjukkan
gejala gagal jantung
mendadak (sesak napas),
atau aritmia ventrikular
(palpitasi, presinkop, sinkop)
 Treatment Delayed is Treatment Denied

Symptom Call to PreHospital ED Cath Lab

Recognition Medical System

Increasing Loss of
Myocytes
Delay in Initiation of Reperfusion Therapy
ACC/AHA, 2007
1. Angina saat istirahat : terjadi saat istirahat dan
terus menerus, biasanya lebih dari 20 menit.

2. Angina pertama kali : angina pertama dengan

CCS III.

3. Angina yang Meningkat : semakin lama makin

sering, semakin lama waktunya atau lebih
mudah tercetus
 HISTORICAL POINTS RISK OF CARDIAC EVENTS (%)
BY 14 DAYS IN TIMI 11B*
Age 65 1 RISK DEATH DEATH, MI OR
3 CAD risk factors 1 SCORE OR MI URGENT REVASC
(FHx, HTN, chol, DM, active smoker)
0/1 3 5
Known CAD (stenosis 50%) 1
2 3 8
ASA use in past 7 days 1
3 5 13
PRESENTATION
Recent ( 24H) severe angina 1 4 7 20
cardiac markers 1 5 12 26
ST deviation 0.5 mm 1 6/7 19 41
RISK SCORE = Total Points (0 - 7)
*Entry criteria:UA or NSTEMI defined as ischemic pain
Low = 0-2 points, Medium = 3-4 points
at rest within past 24H, with evidence of CAD (ST segment
High = 5-7 points deviation or +marker)
Antman et al JAMA 2000; 284: 835 - 842
Intervensi koroner
perkutan ( PCI )
 Sakit dada khas IMA 12 jam

EKG : 1 mm elevasi seg ST pada 2 sandapan yg

bersebelahan
2mm elevasi seg ST pada 2 sandapan
prekordial
Bundle branch block yg baru
Syok kardiogenik pd IMA ( bila kateterisasi dan
revaskularisasi tdk dapat dilakukan )

Trombolisis door to needle time < 30 menit !!

PCI pd IMA lebih unggul bila dilakukan dlm 90 30 menit
 Riwayat stroke hemoragik,kapanpun terjadinya
Riwayat stroke iskemik dalam 3 bulan kecuali stroke iskemik
dengan onset < 3 jam
Neoplasma intrakranial
Perdarahan internal aktif(tidak termasuk menstruasi)
Kecurigaan suatu diseksi aorta
Luka kepala tertutup yg signifikan atau trauma facial dalam 3
bulan
Kelainan struktural atau pembuluh darah cerebral

ACC/AHA guideline of STEMI 2004

 Fibrinolitik :Kontra Indikasi Relatif
Hipertensi berat saat datang ke UGD yaitu BP> 180 / 110 mmHg
Pungsi vaskuler yg tak dapat dikompresi
Perdarahan internal 2 4 mgg sebelumnya
Konsumsi antikoagulan oral
prolonged CPR ( > 10 minutes) or operasi mayor dlm jangka waktu 2-4 minggu
Untuk Streptokinase : pemberian sebelumnya ( 5 hari-2 tahun)
atau riwayat reaksi alergi
Kehamilan
Active peptic ulcer
Riwayat hipertensi kronis yg tak terkontrol
Riwayat stroke iskemik lebih dari 3 bulan,demensia atau
patologi serebral lainnya yg blm tercantum dalam indikasi kontra
 Streptokinase ( Streptase )
1.5 million Unit in 100 ml D5W or 0.9% saline
selama 30-60 mnt
without heparin : Inferior MCI
with heparin : anterior MCI
tPA
15 mg IV bolus kemudian 0.75 mg/Kg selama 30
mnt,dilanjutkan 0.5 mg/Kg selama 60 mnt
berikutnya
ACC/AHA, 2007
Operasi pintas koroner ( CABG )
Pada sindrom koroner akut :

Aritmia/Block ---- Kematian Mendadak

Disfungsi Ventrikel Gagal Jantung

Hipotensi ---- Shock Cardiogenic

Mekanikal : Ruptur Ventrikel/Septum

Pericarditis
 Strategi Tatalaksana Sindrom Koroner akut

Clinical suspicion
of ACS Thrombolysis
Persistent ST elevation Or
Physical exam
ECG PCI/Angioplasty
Blood samples
No persistent
ST elevation High Risk
Elevated troponin
Recurrent ischemia
Hemodynamic / rhythmic unstability
GPIIb/IIIa blocker
Aspirin,LMWH Early post-MI unstable angina
Clopidogrel Cor-angiography
Beta-blockers Low risk Positive
Normal troponin 2 nd
Nitrates on admission Troponin
Twice
Stress test
Before or after
negative discharge

ESC 2002
 Dengan Obat-obatan :
* Aspilet / antiplatelet
* Nitrat
* Beta-bloker
* Ace-Inhibitor
* Antagonis kalsium
* Statin
Dengan Tindakan :
* Angioplasti dengan balon dan stent (PTCA)
* Operasi pintas koroner (CABG)
 Merubah gaya hidup
Mengkonsumsi makanan sehat
Mengontrol kadar kolesterol darah
Mengontrol kadar gula darah
Stop merokok
Berolahraga secara teratur
Mencegah obesitas / kegemukan
Menghindari stress
 ANTIANGINA
ANTIPLATELET
ANTIKOAGULAN/ANTITROMBIN
Terapi tambahan :
- ACE-I
- PREPARAT STATIN
 NITRAT
PENYEKAT BETA
ANTAGONIS KALSIUM
Nama generik Nama Paten/Dagang

Isosorbid mononitrat (ISMO) IMDUR, ISMO-20, PENTACARD,

CARDISMO, ELANTAN, DLL
Isosorbid dinitrat (ISDN) CEDOCARD/CEDOCARD
RETARD,
ISOMACK RETARD, FARSORBID,
ISOKET, ISORBID, ISORDIL, DLL
Glyseryl trinitrat NITROMACK RETARD,
NITROCINE,
NITROMACK RETARD FORTE
 CARA KERJA : Mengakibatkan vasodilatasi / pelebaran pembuluh darah
perifer dan koroner
EFEK TERHADAP JANTUNG : Mengurangi kebutuhan oksigen
miokard/jantung dan meningkatkan suplai oksigen miokard/jantung
INDIKASI : Antiangina, gagal jantung
EFEK SAMPING : Sakit kepala, pusing, muka merah, dll
KONTRA INDIKASI : VIAGRA
PERHATIAN :
- Untuk angina pektoris/sakit dada tablet 5 mg letakan di bawah lidah
(sublingual)
- Digunakan 3-4 kali sehari sesuai dosis yang dianjurkan dokter
- Tab. Sublingual tdk boleh dibelah atau digerus
- Tab. Retard 2 x sehari pada pagi hari dan malam seb. Tidur
- 15 menit setelah menggunakan obat sublingual tdk ada efek, harus
segera ke rumah sakit
Nama generik Nama paten/dagang

Atenolol BETA BLOK, INTERNOLOL, NIF-

TEN
TENORET 50, TENORMIN, DLL
Metoprolol LOPRESOR, SELOKEN, CARDIOSEL
Propranolol INDERAL, FARMADRAL, DLL
Carvedilol DILBLOC, V-BLOC
Bisoprolol MAINTATE, CONCOR

INDIKASI : Antiangina, Hipertensi, Gagal jantung

EFEK SAMPING :
- Nausea, muntah, diare ringan, konstipasi
- Mimpi buruk, insomnia, halusinasi, depresi mental
- Rasa lelah, rash, demam, purpura
Nama generik Nama paten / dagang

Amlodipin NORVASK, TENSIVASK, DLL

Diltiazem DILTAN, FARMABES, HERBESSER, DLL
Nifedipin ADALAT, NIF-TEN,
VASDALAT, DLL
Verapamil ISOPTIN SR, CARDIOVER, DLL
Nimodipin NIMOTOP

INDIKASI : Antiangina, Anti-Hipertensi

CARA KERJA :
- Menghambat kontraksi miokard dan otot polos pembuluh darah
- Melambatkan konduksi AV dan depresi nodus SA
- Vasodilatasi, inotropik, dll
EFEK SAMPING :
- Hipotensi
- Nyeri kepala
- Muka merah
- dll
 TDD :
- ANTIPLATELET
- ANTIKOAGULAN
- TROMBOLITIK
ORAL :
Nama generik Nama dagang / paten
1. Aspirin ASPILET, ASCARDIA, ASTIKA,
APTOR, TROMBO ASPILET,
FARMASAL, RESTOR, DLL
2. Dipyridamol PERSANTIN
3. Ticlopidin AGULAN, TICLID, PICLODIN,
TICURING, CARTRILET, DLL
4. Clopidogrel PLAVIX
5. Cilostazol PLETAAL, AGGRAVAN,
CITAZ
6. Aspirin + dipiridamol AGGRENOX
Nama generik Nama dagang / paten
1. Abciximab ReOPro
2. Tirofiban AGGRASTAT
3. Eptifibatide INTEGRILIN
ORAL :
Nama generik Nama dagang / paten
1. Coumarin/warfarin SIMARC-2, WARFARIN EISAI
2. Melagatran

PARENTRAL :
Heparin HEPARIN SODIUM B. BRAUN,
INVICLOT
2. LMWH FRAXIPARIN, LOVENOX
3. Fondaparinux ARIXTRA
PARENTRAL :
Nama generik Nama dagang/ paten
1. Streptokinase FAMIKINASE, STREPTASE
2. Urokinase ABBOKINASE
3. Tpa ALTEPLASE
4. Rateplase RETAVASE
5. Tenecteplase -
Nama generik Nama dagang / paten
1. Captopril CAPOTEN, FARMOTEN, CAP
TENSIN, LOCAP, PRATEN,DLL
2. Fisinopril ACENOR-M, MONOPRIL
3. Lisinopril INTERPRIL, ZESTRIL
4. Perindopril PREXUM
5. Ramipril TRIATEC, TRIATEC PLUS

INDIKASI : Antihipertensi, Jantung

EFEK SAMPING : Batuk, hiperkalemia, dll
KONTRA INDIKASI : Hamil, gagal ginjal berat, dll
JANTUNG :
- Menurunkan afterload dan preload
- Menurunkan masa ventrikel kiri
- Menurunkan stimulasi simpatis
- Menyeimbangkan kebutuhan dan suplai oksigen miokard
VASCULAR :
- Antihipertensi
- Memperbaiki tonus dan kelenturan arterial
- Memperbaiki fungsi endotel
- Efek antitrombogenik langsung
- Efek antimigrasi dan anti-proliferasi thd sel otot polos, neutrofil
dan sel mononuclear
- Efek antitrombosit
- Meningkatkan fibrinolisis endogen
Nama generik Nama paten / dagang

Simvastatin CHOLESTAT, ZOCOR, ZOVAST,

SIMBADO, SIMCHOL, SIMCOR, DLL
Atorvastatin LIPITOR
Lovastatin LOFACOL, LIPOVAS, CHOLESTRA
Fluvastatin LESCOL
Rosuvastatin CRESTOR

INDIKASI : Penekan kolesterol

EFEK SAMPING : Hati, nyeri otot, dll
PERHATIAN : Gunakan malam hari, akan tidur
 Memperbaiki fungsi endotel
Mengurangi sel-sel radang
Menurunkan aktivitas matrix metalloproteinase
Mengurangi aktivitas platelet
Modulasi tissue factor pada plak
Mengurangi viscositas darah dan memperkuat
fibrinolitik action dengan mengurangi produksi PAI-I
Mengurangi peningkatan aktivitas c-RP
Ass WR WB