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
Normal

Fatty
Streak

Fibrous
Plaque

Atherosclerotic
Plaque

Plaque
Rupture/
Fissure &
Thrombosis

Myocardial
Infarction
Ischemic
Stroke

Clinically Silent

Angina
Transient Ischemic Attack
Claudication/PAD

Critical
Leg
Ischemia

Cardiovascular Death

Increasing Age
3

Unstable
coronary
artery disease

Thrombus forms
forms
Thrombus
and extends
extends into
into
and
the lumen
lumen
the
Thrombus

Lipid core

Adventit
ia

RISK FACTORS FOR PLAQUE RUPTURE

Systemic Factors

Local Factors
Cap
Fatigue

Smoking
Cholesterol

Atheromatous Core
(size/consistency)
Cap
Thickness/
Consistency
Cap
Inflammation

Diabetes
Mellitus

Homocysteine

Fibrinogen

Impaired
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
Non-ST-Segment
Elevation MI
(NSTEMI)
ST-Segment
Elevation MI
(STEMI)

Similar pathophysiology
Similar presentation and
early management rules
STEMI requires
evaluation for acute
reperfusion intervention

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
CORONARYTHROMBUS
THROMBUS

Small
Smallthrombus
thrombus
(non-flow
(non-flowlimiting)
limiting)

Partially
Partiallyocclusive
occlusive
thrombus
thrombus
Transient
ischemia

No
NoECG
ECG
changes
changes

Healing
Healingand
and
Plaque
enlargement
Plaque enlargement

ST
STsegment
segment
Depression
Depressionand/or
and/or
TTwave
inversion
wave inversion

Negative
Serum
biomarkers

UNSTABLE
UNSTABLE
ANGINA
ANGINA

Positive
Serum
biomarkers
NON-ST
NON-STSEGEMENT
SEGEMENT
ELEVATION
ELEVATION

Occlusive
Occlusive
thrombus
thrombus
Prolonged
ischemia
ST
STelevation
elevation
(Q
(Qwave
wavelater)
later)

Positive
Serum
biomarkers
ST
STSEGMENT
SEGMENT
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
Angina
Non
occlusive
thrombus
Non specific
ECG
Normal
cardiac
enzymes

Occluding
thrombus
sufficient to
cause
tissue damage &
mild
myocardial
necrosis

NSTEMI

ST depression
+/T wave inversion
on
ECG
Elevated cardiac
enzymes

STEMI

Complete thromb
occlusion

ST elevations on
ECG or new LBBB
Elevated cardiac
enzymes
More severe
symptoms

Acute Management

Initial evaluation
& stabilization

Efficient risk
stratification

Focused cardiac
care

Evaluation

Efficient & direct history

Initiate stabilization
interventions

Occurs
simultaneo
usly

Plan for moving rapidly to

indicated cardiac
care
Directed Therapies
are
Time Sensitive!

Chest pain suggestive of

ischemia
Immediate assessment within 10
Initial
History
Minutes
Emergent

labs
and tests

12 lead ECG
Obtain initial
cardiac enzymes
electrolytes, cbc
lipids, bun/cr,
glucose, coags
CXR

care
IV access
Cardiac
monitorin
g
Oxygen
Aspirin
Nitrates

&
Physical
Establish
diagnosis
Read ECG
Identify
complicati
ons
Assess for
reperfusio

Focused History

Aid in diagnosis and

rule out other causes

Palliative/Provocative
factors
Quality of discomfort
Radiation
Symptoms associated
with discomfort
Cardiac risk factors
Past medical history
-especially cardiac

Reperfusion
questions

Timing of
presentation
ECG c/w STEMI
Contraindication
to fibrinolysis
Degree of STEMI
risk

Targeted Physical

Examination
Vitals
Cardiovascular
system
Respiratory
system
Abdomen
Neurological
status

Recognize factors
that increase risk
Hypotension
Tachycardia
Pulmonary rales, JVD
, pulmonary edema,
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, IAVL
Inferior
: II, III, AVF
Lateral
: I, AVL, V5-V6
Posterior
: V7-V9
Ventrikel Kanan
: V3R-V4R

Normal or nondiagnostic 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)

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 3648 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 Sa

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
Any prior
Intra Cranial
Haemoragic
acute
STEMI

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
STEMI
Historyacute
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:

<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 preferred if:

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

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 ACEI

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:

Review guidelines for specific

management of complications & other
specific clinical scenarios

recurrent ischemia, cardiogenic shock, ICH,

arrhythmias

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
Findings indicating
Findings indicating
Findings indicating
Acute Coronary
Syndrome
Assessment
HIGH likelihood of ACS

INTERMEDIATE

LOW likelihood of ACS

likelihood of ACS in
absence of highlikelihood findings

in absence of high- or
intermediate-likelihood
findings

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

Chest or left arm pain or

discomfort as chief
symptom
Age > 50 years

Probable ischemic
symptoms
Recent cocaine use

Physical
examination

New transient mitral

regurgitation, hypotension,
diaphoresis, pulmonary
edema or rales

Extracardiac vascular
disease

Chest discomfort
reproduced by palpation

ECG

New or presumably new

transient ST-segment
deviation (> 0.05 mV) or Twave inversion (> 0.2 mV)
with symptoms

Fixed Q waves
Abnormal ST segments or
T waves not documented
to be new

T-wave flattening or
inversion of T waves in
leads with dominant R
waves
Normal ECG

Serum cardiac
markers

Elevated cardiac troponin

T or I, or elevated CK-MB

Normal

Normal

ACS risk criteria

Low Risk ACS
No intermediate or high
risk factors

Intermediate Risk
ACS
Moderate to high likelihood
of CAD

<10 minutes rest pain

Non-diagnostic ECG
Non-elevated cardiac
markers
Age < 70 years

>10 minutes rest pain,

now resolved
T-wave inversion > 2mm
Slightly elevated cardiac
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
risk

Intermediate

risk

High
risk

Chest Pain
center

Conserva
tive
therapy

Invasive
therapy

Secondary Prevention

Disease

Behavioral

HTN, DM
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