SINDROM KORONER AKUT

(LK 3b)

Rendri Bayu Hansah

Modul Penyakit Jantung

Fakultas Kedokteran Universitas Baiturrahmah
Padang
 Scope of Problem
(2004 stats)
CHD single leading cause of
death in United States
452,327 deaths in the U.S. in 2004

1,200,000 new & recurrent

coronary attacks per year

38% of those who with

coronary attack die within a year
of having it

Annual cost > $300 billion

 Definitions
Acute coronary syndrome is defined as
myocardial ischemia due to myocardial
infarction (NSTEMI or STEMI) or unstable
angina
Unstable angina is defined as angina at rest, new
onset exertional angina (<2 months), recent
acceleration of angina (<2 months), or post
revascularization angina
Conditions that may mimic ACS include:

Musculoskeletal chest pain

Pericarditis (can have acute ST changes)
Aortic dissection
Central Nervous System Disease (may mimic
MI by causing diffuse ST-T wave changes)
Pancreatitis/Cholecystitis
 Expanding Risk Factors
Smoking
Hypertension
Diabetes Mellitus
Dyslipidemia
Low HDL < 40
Elevated LDL / TG
Family Historyevent in
first degree relative >55
male/65 female
Age-- > 45 for male/55
for female
Chronic Kidney Disease
Lack of regular physical
activity
Obesity
Lack of diet rich in fruit,
veggies, fiber
Atherogenesis and Atherothrombosis:
A Progressive Process
Plaque
Athero- Rupture/ Myocardial
Fatty Fibrous sclerotic Fissure &
Normal Streak Plaque Plaque Thrombosis Infarction

Ischemic
Stroke

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

3
 Thrombus forms and
Unstable coronary extends into the lumen
artery disease

Thrombus

Lipid core

Adventitia
 RISK FACTORS FOR PLAQUE RUPTURE
Local Factors Systemic Factors
Cap Smoking
Fatigue
Cholesterol
Atheromatous Core
(size/consistency)
Diabetes
Mellitus Fibrinogen
Cap
Thickness/
Consistency
Cap Homocysteine
Impaired
Inflammation
Fibrinolysis

Plaque
Rupture

Fuster V, et al. N Engl J Med. 1992;326:310-318.

Falk E, et al. Circulation. 1995:92:657-671.
 Acute Coronary Syndrome

Unstable Angina
Similar pathophysiology
Non-ST-Segment
Elevation MI Similar presentation and
(NSTEMI) early management rules

STEMI requires evaluation

ST-Segment for acute reperfusion
Elevation MI intervention
(STEMI)
 Diagnosis of Angina
Typical anginaAll three of the following
Substernal chest discomfort
Onset with exertion or emotional stress
Relief with rest or nitroglycerin

Atypical angina
2 of the above criteria

Noncardiac chest pain

1 of the above
 Diagnosis of Acute MI
STEMI / NSTEMI
At least 2 of the following
Ischemic symptoms
Diagnostic ECG
changes
Serum cardiac marker
elevations
 CONSEQUENCES OF CORONARY THROMBUS
CORONARY THROMBUS

Small thrombus Partially occlusive Occlusive

(non-flow limiting) thrombus thrombus
Transient
ischemia Prolonged
ischemia
No ECG
changes ST segment
Depression and/or ST elevation
T wave inversion (Q wave later)

Healing and
Plaque enlargement Negative
Serum Positive Positive
biomarkers Serum Serum
biomarkers biomarkers

UNSTABLE NON-ST SEGEMENT ST SEGMENT

ANGINA ELEVATION ELEVATION
 The Three Is
Ischemia= ST depression or T-wave inversion
Represents lack of oxygen to myocardial tissue
 The Three Is
Injury = ST elevation -- represents prolonged
ischemia; significant when > 1 mm above the baseline
of the segment in two or more leads
 The Three Is
Infarct = Q wave represented by first
negative deflection after P wave; must be
pathological to indicate MI
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
Acute Management

Initial evaluation &

stabilization

Efficient risk
stratification

Focused cardiac care

 Evaluation
Efficient & direct history
Occurs
Initiate stabilization interventions simultaneously

Plan for moving rapidly to

indicated cardiac care
Directed Therapies
are
Time Sensitive!
 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 monitoring Read ECG

electrolytes, cbc Oxygen Identify

lipids, bun/cr, Aspirin complications

glucose, coags Nitrates Assess for

CXR reperfusion
 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
 Targeted Physical
Examination Recognize factors that
Vitals increase risk
Cardiovascular Hypotension
system Tachycardia
Respiratory system Pulmonary rales, JVD ,
Abdomen pulmonary edema,
Neurological status New murmurs/heart sounds

Diminished peripheral
pulses
Signs of stroke
 ECG assessment

ST Elevation or new LBBB

STEMI

ST Depression or dynamic
T wave inversions
NSTEMI

Non-specific ECG
Unstable Angina
Lokasi infark berdasarkan letak
perubahan gambaran EKG

Anterior : V1-V6
Anteroseptal : V1-V4
Anterior ekstensif : V1-V6, I-AVL
Inferior : II, III, AVF
Lateral : I, AVL, V5-V6
Posterior : V7-V9
Ventrikel Kanan : V3R-V4R
Normal or non-diagnostic EKG
ST-Segment Elevation MI
 New LBBB

QRS > 0.12 sec

L Axis deviation
Prominent Q wave V1-V3
Prominent S wave 1, aVL, V5-V6
with T-wave inversion
 Cardiac markers
Troponin ( T, I) CK-MB isoenzyme
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
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,
DM, PE
 Cardiac Care Goals

Decrease amount of myocardial necrosis

Preserve LV function

Prevent major adverse cardiac events

Treat life threatening complications

 Tatalaksana Pra Rumah Sakit
Petugas kesehatan/dokter umum di klinik
- Mengenali gejala sindrom koroner akut dan pemeriksaan EKG bila ada
- Tirah baring dan pemberian oksigen 2-4 L/menit
- Berikan aspirin 160-325 mg tablet kunyah bila tidak ada riwayat
alergi aspirin
- Berikan preparat nitrat sublingual misalnya isosorbid dinitrat 5 mg
dapat diulang setiap 5-15 menit sampai 3 kali
- Bila memungkinkan pasang jalur infus
- Segera kirim ke rumah sakit terdekat dengan fasilitas ICCU (Intensive
Coronary Care Unit) yang memadai dengan pemasangan oksigen dan
didampingi
dokter/paramedik yang terlatih
 STEMI cardiac care
STEP 1: Assessment
Time since onset of symptoms
90 min for PCI / 12 hours for fibrinolysis

Is this high risk STEMI?

KILLIP classification
If higher risk may manage with more invasive rx

Determine if fibrinolysis candidate

Meets criteria with no contraindications

Determine if PCI candidate

Based on availability and time to balloon rx
 Fibrinolysis Indications

ST segment elevation >1mm in two

contiguous leads
New LBBB
Symptoms consistent with ischemia
Symptom onset less than 12 hrs prior to
presentation
 Absolute contraindications for fibrinolysis
therapy in patients with acute STEMI

Any prior Intra Cranial Haemoragic

Known structural cerebral vascular lesion
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
 Relative contraindications for fibrinolysis
therapy in patients with acute STEMI
History of chronic, severe, poorly controlled hypertension
Severe uncontrolled hypertension on presentation (SBP greater than 180 mm Hg
or DBP greater than 110 mmHg)
History of prior ischemic stroke greater than 3 months, dementia, or known
intracranial pathology not covered in contraindications
Traumatic or prolonged (greater than 10 minutes) CPR or major surgery (less
than 3 weeks)
Recent (within 2-4 weeks) internal bleeding
Noncompressible vascular punctures
For streptokinase/anistreplase: prior exposure (more than 5 days ago) or prior
allergic reaction to these agents
Pregnancy
Active peptic ulcer
Current use of anticoagulants: the higher the INR, the higher the risk of
bleeding
 STEMI cardiac care
STEP 2: Determine preferred reperfusion strategy

Fibrinolysis preferred if: PCI preferred if:

<3 hours from onset
PCI not available/delayed
door to balloon > 90min
door to balloon minus
door to needle > 1hr
Door to needle goal <30min
No contraindications
PCI available
Door to balloon < 90min
Door to balloon minus
door to needle < 1hr
Fibrinolysis
contraindications
Late Presentation > 3 hr
High risk STEMI
Killup 3 or higher
STEMI dx in doubt
 Medical Therapy
MONACLO + BAH
Morphine
Analgesia
Reduce pain/anxietydecrease sympathetic tone, systemic
vascular resistance and oxygen demand
Careful with hypotension, hypovolemia, respiratory
depression

Oxygen (2-4 liters/minute)

Up to 70% of ACS patient demonstrate hypoxemia
May limit ischemic myocardial damage by increasing
oxygen delivery/reduce ST elevation
 Nitroglycerin
Analgesiatitrate infusion to keep patient pain free
Dilates coronary vesselsincrease blood flow
Reduces systemic vascular resistance and preload
Careful with recent ED meds, hypotension, bradycardia,
tachycardia, RV infarction

Aspirin (160-325mg chewed & swallowed)

Irreversible inhibition of platelet aggregation
Stabilize plaque and arrest thrombus
Reduce mortality in patients with STEMI
Careful with active PUD, hypersensitivity, bleeding
disorders
 Clopidogrel (class I, level B)
Irreversible inhibition of platelet aggregation
Used in support of cath / PCI intervention or if unable to
take aspirin
3 to 12 month duration depending on scenario
 Beta-Blockers (class I, level A)
14% reduction in mortality risk at 7 days at 23% long term
mortality reduction in STEMI
Approximate 13% reduction in risk of progression to MI
in patients with threatening or evolving MI symptoms
Be aware of contraindications (CHF, Heart block,
Hypotension)
Reassess for therapy as contraindications resolve

ACE-Inhibitors / ARB (class I, level A)

Start in patients with anterior MI, pulmonary congestion,
LVEF < 40% in absence of contraindication/hypotension
Start in first 24 hours
ARB as substitute for patients unable to use ACE-I
 Heparin
LMWH or UFH (max 4000u bolus, 1000u/hr)
Indirect inhibitor of thrombin
less supporting evidence of benefit in era of reperfusion

Adjunct to surgical revascularization and thrombolytic /

PCI reperfusion
24-48 hours of treatment

Coordinate with PCI team (UFH preferred)

Used in combo with aspirin and/or other platelet inhibitors

Changing from one to the other not recommended

 Additional medication therapy

Glycoprotein IIb/IIIa inhibitors

(class IIa, level B)
Inhibition of platelet aggregation at final common
pathway
In support of PCI intervention as early as possible
prior to PCI
 Additional medication therapy

Aldosterone blockers (class I, level A)

Post-STEMI patients
no significant renal failure (cr < 2.5 men or 2.0 for women)
No hyperkalemis > 5.0

LVEF < 40%

Symptomatic CHF or DM
 Rekomendasi pengobatan SKA
Rekomendasi terapi antitrombotik tanpa terapi
reperfusi
Rekomendasi terapi antirombotik pada pemberian
terapi fibrinolitik
Rekomendasi antitrombotik pada terapi angioplasti
koroner perkutan (PCI) primer
Dosis ACE-Inhibitor pada tatalaksana SKA
Dosis ARB pada SKA
Rekomendasi terapi untuk mengatasi nyeri, sesak dan
anxietas
 STEMI care CCU
Monitor for complications:
recurrent ischemia, cardiogenic shock, ICH, arrhythmias

Review guidelines for specific management of

complications & other specific clinical scenarios
PCI after fibrinolysis, emergent CABG, etc

Decision making for risk stratification at hospital

discharge and/or need for CABG
 Risk Stratification to Determine the Likelihood of
Acute Coronary Syndrome
Assessment Findings indicating
HIGH likelihood of ACS
History Chest or left arm pain or
discomfort as chief
symptom
Reproduction of previous
documented angina
Known history of coronary
artery disease, including
myocardial infarction
Physical New transient mitral
regurgitation,
examination hypotension, diaphoresis,
pulmonary edema or rales
ECG New or presumably new
transient ST-segment
deviation (> 0.05 mV) or T-
wave inversion (> 0.2 mV)
with symptoms
Serum cardiac Elevated cardiac troponin
T or I, or elevated CK-MB
markers
Findings indicating Findings indicating
INTERMEDIATE LOW likelihood of ACS
likelihood of ACS in in absence of high- or
absence of high- intermediate-likelihood
likelihood findings findings
Chest or left arm pain or Probable ischemic
discomfort as chief symptoms
symptom Recent cocaine use
Age > 50 years
Extracardiac vascular Chest discomfort
disease reproduced by palpation
Fixed Q waves T-wave flattening or
Abnormal ST segments or inversion of T waves in
T waves not documented leads with dominant R
to be new waves
Normal ECG
Normal Normal
 ACS risk criteria
Low Risk ACS Intermediate Risk
No intermediate or high
ACS
risk factors Moderate to high likelihood
of CAD
<10 minutes rest pain
>10 minutes rest pain,
Non-diagnostic ECG now resolved

Non-elevated cardiac T-wave inversion > 2mm

markers
Slightly elevated cardiac
Age < 70 years markers
 High Risk ACS
Elevated cardiac markers
New or presumed new ST depression
Recurrent ischemia despite therapy
Recurrent ischemia with heart failure
High risk findings on non-invasive stress test
Depressed systolic left ventricular function
Hemodynamic instability
Sustained Ventricular tachycardia
PCI with 6 months
Prior Bypass surgery
 Low Intermediate High
risk risk risk

Chest Pain
center
Conservative Invasive
therapy therapy
 Secondary Prevention
Disease
HTN, DM

Behavioral
smoking, diet, physical activity, weight

Cognitive
Education, cardiac rehab program
 Secondary Prevention
disease management
Blood Pressure
Goals < 140/90 or <130/80 in DM /CKD
Maximize use of beta-blockers & ACE-I

Lipids
LDL < 100 (70) ; TG < 200
Maximize use of statins; consider fibrates/niacin first
line for TG>500; consider omega-3 fatty acids

Diabetes
A1c < 7%
 Secondary prevention
behavioral intervention
Smoking cessation
Cessation-class, meds, counseling
Physical Activity
Goal 30 - 60 minutes daily
Risk assessment prior to initiation

Diet
DASH diet, fiber, omega-3 fatty acids
<7% total calories from saturated fats
 Secondary prevention
cognitive
Patient education
In-hospital discharge outpatient clinic/rehab

Monitor psychosocial impact

Depression/anxiety assessment & treatment
Social support system
 Medication Checklist
after ACS
Antiplatelet agent
Aspirin* and/or Clopidorgrel
Lipid lowering agent
Statin*
Fibrate / Niacin / Omega-3

Antihypertensive agent
Beta blocker*
ACE-I*/ARB
Aldactone (as appropriate)
 Summary
ACS includes UA, NSTEMI, and STEMI
Management guideline focus
Immediate assessment/intervention (MONACLO + BAH)
Risk stratification (UA/NSTEMI vs. STEMI)
RAPID reperfusion for STEMI (PCI vs. Thrombolytics)
Conservative vs Invasive therapy for UA/NSTEMI

Aggressive attention to secondary prevention

initiatives for ACS patients
Beta blocker, ASA, ACE-I, Statin
 Conclusions: Treatment of
NSTEMI/UAP
ASA
NTG (consider MSO4 if pain not relieved)
Beta Blocker
Heparin/LMWH
ACE-I
+/- Statin
+/- Clopidogrel (dont give if CABG is a possibility)
+/- IIBIIIA inhibitors (based on TIMI risk score)
 Conclusions: Treatment of
STEMI
ASA
NTG (consider MSO4 if pain not relieved)
Beta Blocker
Heparin/LMWH
ACE-I
Clopidogrel (based on possibility of CABG)
IIB-IIIA
+/- Statin
Activate the Cath Lab!!!
Terima Kasih