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ACUTE CORONARY SYNDROME

Acute Coronary Syndrome


• Acute coronary syndrome (ACS) refers to the
constellation of clinical diseases occurring as a
result of acute myocardial ischemia.
clinical presentations ranging
• from unstable angina (UA)
• non-ST segment elevation MI (NSTEMI)
• ST segment elevation MI (STEMI)
• Acute myocardial infarction (AMI)
Incidence of Acute Coronary Syndromes (ACS):
Statistics From Various Studies

• 1.4 million hospitalizations each year for ACS


• 944,000 hospitalizations for unstable angina;
1994
• 121,000 hospitalizations for non–Q-wave MI;
1994
• 60% patients with unstable angina >65 years old
• 46% of patients with unstable angina are women
Hochman JS et al. J Am Coll Cardiol. 1997;30:141-148; Vital and Health Statistics. Hyattsville, Md:
1994: Series 13, No. 127; Clinical Practice Guidelines. AHCPR publication No. 94-0602.
Differentiation of ACS
Coronary
thrombus Pathophysiology
Small Occlusive
thrombus Partially occlusive
thrombus
(non-flow- thrombus
limiting) Transient Prolonged
ischemia ischemia

No ECG ST segment
depression and/or T ST elevation
changes (Q waves later)
wave inversion

+ Serum
- Serum + Serum biomarkers
Healing and plaque biomarkers biomarkers
enlargement

Unstable Non-ST-segment ST segment


angina elevation MI elevation MI

Adapted from Lilly, LS. Pathophysiology of Heart Disease, 3rd Edition.


Unstable
NSTEMI STEMI
Angina
Occluding thrombus Complete thrombus
Non occlusive sufficient to cause occlusion
thrombus tissue damage & mild
myocardial necrosis ST elevations on
Non specific ECG or new LBBB
ECG ST depression +/-
T wave inversion on Elevated cardiac
Normal cardiac ECG enzymes
enzymes
Elevated cardiac More severe
enzymes symptoms
Diagnose ACS
Stable Angina
• Stable angina pectoris is transient, episodic
chest discomfort resulting from myocardial
ischemia
• Trigger factor : Physical or psychological stress
(physical exertion, emotional stress, anemia,
dysrhythmias, or environmental exposures)
• Attack of angina resolves spontaneously with
rest or nitroglycerin (NTG)
Canadian Cardiovascular Society classification
for angina
Class Description
Class I no angina with ordinary physical activity
Class II slight limitation of normal activity as angina occurs with walking,
climbing stairs, or emotional stress
Class III severe limitation of ordinary physical activity as angina occurs on
walking one or two blocks on a level surface or climbing one flight of
stairs in normal conditions
Class IV inability to carry on any physical activity without discomfort
as anginal symptoms occur at rest
Unstable Angina
• Is defined as angina occurring with minimal
exertion or at rest, new-onset angina, or a
worsening change in a previously stable
anginal syndrome in terms of frequency or
duration of attacks, resistance to previously
effective medications, or provocation with
decreasing levels of exertion or stress.
Braunwald Classification of UA
Criteria of UA

Rest angina angina occurring at rest, >= 20 minutes, and occurring


within 1 week of presentation.
New-onset angina at least class II severity with onset within the last 2 months
Increasing or a previously known angina becomes more frequent, longer
progressive angina in duration, or increased 1 class within the last 2 months of
at least class III severity
diagnosis of UA Symptoms that last longer than 20 minutes despite
cessationof activity are consistent with angina at rest and
indicate
pathophysiologic of UA :
• Plaque rupture accompanied by thrombus
formation and vasospasm
• characterized by an electrocardiographic
abnormality, including T wave and ST segment
changes
Variant angina / Prinzmetal’s angina
• caused by coronary artery vasospasm at rest
with minimal fixed coronary artery lesions; it
may be relieved by exercise or NTG.
• The ECG reveals ST segment elevation
Acute Myocard Infarct
• AMI : myocardial cell death and necrosis of
the myocardium.
the diagnosis for an acute, evolving, or recent MI:
1. Typical rise and gradual fall (troponin) or more rapid rise and fall (isoenzyme of
creatine kinase with muscle and brain subunits [CK-MB]) of biochemical markers of
myocardial necrosis with at least one of the following:
a. Ischemic symptoms;
b. Development of pathologic Q waves on the ECG;
c. ECG changes indicative of ischemia (T wave changes or ST segment elevation or
depression); and/or
d. Coronary artery intervention.
2. Pathologic findings of an AMI.
Etiology & Risk Factors
• Atherosclerosis
• Nonmodifiable risk factors for atherosclerosis include
the following:
– Age, Sex, Family history of premature coronary heart
disease, Male-pattern baldness
• Modifiable risk factors for atherosclerosis include the
following:
– Smoking or other tobacco use, Diabetes mellitus,
Hypertension, Hypercholesterolemia and
hypertriglyceridemia, including inherited lipoprotein
disorders, Dyslipidemia, Obesity, Sedentary lifestyle and/or
lack of exercise, Psychosocial stress, Poor oral hygiene,
Type A personality
Regional Infarction
STEMI

Anamnesa
• Lihat faktor pencetus, aktifitas fisik berat,
stres, emosi, tindakan bedah, penyakit medis.
• Bedakan nyeri dada infark miokard dengan
penyebab nyeri dada yang lain*.
• Penderita STEMI yang tidak mempunyai
keluhan nyeri dada biasanya pada penderita
diabetes dan usia lanjut.
• Nyeri dada > 30 menit, bisa dipastikan STEMI.
Nyeri dada pada infark miokard
 Lokasi : substernal, retrosternal,
dan prekordial
 Sifat : rasa sakit tekan, terbakar,
tindih, tusuk, peras dan pelintir
 Penjalaran : lengan kiri, leher,
rahang bawah, gigi, punggung
perut dan lengan kanan
 Pencetus : latihan fisik, emosi,
dingin dan sesudah makan
 Gejala ikutan : mual, muntah,
sulit bernapas, keringat dingin
dan lemas
Acute Myocardial Infarction
– Laboratory Findings : – Differential
• CK-MB Diagnosis
– Elevate : 4-6 hr after onset • Aortic dissection
– Peak : 12-24 hr after onset • Pericarditis
– Return to baseline : 2-3 days after • Gastronintestinal
onset
disorders
• Troponin
– Elevate :2-6 hr after onset
– Peak : 12-24 hr after onset
– Stay elevated : 7-10 days
• Myoglobin
– Elevation : 1-3 hr after onset
– Peak : 4-12 hr after onset
– Stay elevated : 12-36 hr after onset
Cardiac Biomarkers in AMI

MARKER DETECTION PEAK DISAPPEARANCE

Myoglobin 1–4h 6–7h 24 h


CK-MB mass 3 – 12 h 12 – 18 h 2 – 3 days
Total CK 4–8h 12 – 30 h 3 – 4 days
cTnT 4 – 12 h 12 – 48 h 5 – 15 days
cTnI 4 – 12 h 12 – 24 h 5 – 7 days
IMA (ischaemia) few minutes 2–4h 6 hours

These values represent averages.


BIOCHEMICAL MARKERS IN AMI: RELEASE, PEAK
AND DURATION OF ELEVATION
Classic History Angina
• substernal or precordial left chest
pain/discomfort  radiate to the neck, jaw,
shoulders, or arms. If the discomfort does
extend down the arm involves the ulnar
aspect.
• Other symptoms : dyspnea, nausea, vomiting,
diaphoresis, weakness, dizziness, excessive
fatigue, or anxiety
Evaluation of ACS
• MONA : preadmission pharmacotherapeutic
interventions (morphine, oxygen, nitroglycerin, aspirin)
• Risk assessment tools: determine risk of death and
ischemia in NSTEMI and STEMI
– the PURSUIT (The Platelet Glycoprotein IIb-IIIa in Unstable
Angina: Receptor Suppression Using Integrilin Therapy)
– the GRACE (Global Registry of Acute Coronary Events)
– the TIMI (Thrombosis in Myocardial Infarction)
Diagnostic Investigation of ACS
• EKG
• Chest Radiography : heart size for chronic CHF
• Serum Markers
• Echocardiograph
• Myocardial Scintigraphy
• CT Scan
• Graded Excercise testing
Result of ECG
• Karena tjd ischaemic hasil ECG thd aktivitas ventrikel
mengalami perubahan (komplek QRST)
An acute anterolateral myocardial
infarction
An acute inferior wall myocardial
infarction
Management of ACS
• Treatment within the first hours after symptom
onset may result in substantial myocardial
salvage
• the average time to fibrinolysis ranges from 45 to
90 minutes
• The AHA recommends : AMI receive fibrinolytic
therapy within 30 minutes of arrival.
• AMI patients who undergo primary PCI : therapy
initiated no later than 90 min after arrival
Pharmacologic Th/
• Nitroglycerins • ACE Inhibitor (Captopril,
sublingual NTG tablet enalapril, lisinopril,
(0.4 mg or 400 μg) ramipril)
• morphine sulfate (2 to 5 • CCB
mg IV, repeated every 5 • Antiplatelet (aspirin,
- 30 minutes as GPI, clopidogrel
necessary) • Antithrombin (Heparin)
• Beta-Adrenergic
Blockers
Reperfusion Th/
• Fibrinolytics : t-PA
• PCI (percutaneus coronary interventions)
Terapi fibrinolisis Invasive Th/ (PCI)
Onset <3 hours Onset >3 hours
Contra Indication Efektif pada:
Perdarahan intrakranial kapanpun, Syok kardiogenik
stroke iskemik<3bulan, kecurigaan Usia >75 tahun
diseksi aorta, tumor intrakranial, Pasien KI fibrinolitik
AVM, gangguan sistem pembekuan
darah, cedera kepala tertutup
Streptokinase, reteplase, tenecplase
Penatalaksanaan Infark Miokard
• Istirahat total
• Diet makanan lunak serta rendah garam
• Pasang infus dekstrosa 5 % emergency
• Atasi nyeri :
Morfin 2,5 5 mg iv atau petidin 25 50 mg im
Lain - lain: nitrat , antagonis kalsium , dan beta bloker
• Oksigen 2 4 liter/menit
• Sedatif sedang seperti diazepam 3 dd 2 5 mg per oral
• Antikoagulan :
Heparin 20000 40000 U/24 jam atau drip iv atas
indikasi
Diteruskan dengan asetakumarol atau warfarin
• Streptokinase / trombolisis