Penanganan Mutakhir

Penyakit Jantung Koroner :

Sindroma Koroner Akut
Prof. dr. Harmani Kalim, MPH,Sp.JP (K), FIHA,
FASCC

Departemen Kardiologi dan Kedokteran Vaskuler FKUI

Pusat Jantung Nasional-RS Jantung Harapan Kita

Epidemiologi

Survei Kesehatan Rumah Tangga (SKRT)

Departemen Kesehatan menunjukkan,
penyakit jantung memberikan kontribusi
sebesar 19,8 % dari seluruh penyebab
kematian pada tahun 1993.
Angka tersebut meningkat menjadi 24,4
% pada tahun 1998
Hasil SKRT tahun 2001, PJK telah
menempati urutan pertama dalam deretan
penyebab utama kematian di Indonesia.

Atherosclerosis Timeline
Foam
Cells

Fatty
Streak

Intermediate
Atheroma
Lesion

Fibrous
Plaque

Complicated
Lesion/
Rupture

Endothelial Dysfunction
From First
Decade

From Third
Decade

From Fourth
Decade

Adapted from Pepine CJ. Am J Cardiol. 1998;82(suppl 10A):23S-27S.

Pathogenesis of
Atherosclerotic Plaques
Endothelial damage
Protective response results in production of
cellular adhesion molecules
Monocytes and T lymphocytes attach to
sticky surface of endothelial cells
Migrate through arterial wall to subendothelial space
Macrophages take up oxidised LDL-C
Lipid-rich foam cells
Fatty streak and plaque

The Activated Endothelium

activated

endothelium
cytokines (eg. IL-1, TNF-)
chemokines (eg.MCP-1, IL-8)
growth factors (eg. PDGF, FGF)
attracts monocytes and
T lymphocytes
which adhere to endothelial
cells

CELLULAR
ADHESION
MOLECULES

induces cell
proliferation and a
prothrombic state

Koenig W. Eur Heart J Suppl 1999;1(Suppl T);T1926.

Gambaran Robeknya Plak (Plaque)

disertai Proses Trombosis

Thrombus Forms and

Extends into the lumen

Unstable coronary
artery disease

Thrombus

Lipid core

Adventitia

Acute Coronary Syndrome :

Clinical Perspective
1772: Clinical description of progression of angina
symptoms to myocardial infarction and death
1910: Pre-infarction angina
1971: Introduction of terminology of unstable angina
1988: Concept of acute coronary syndrome
1990-1995: Risk stratification-Troponins

Milestones in Management of
Acute Coronary Syndrome
1983:Aspirin therapy
1985: Thrombolytic therapy
1988: Aspirin and heparin
1997: Low molecular weight heparin
1998: GPIIb/IIIa and aspirin and heparin
1999: Catheter based/ Invasive treatment
(PCI/CABG)
2001: Clopidogrel with aspirin
2005: Whats new??

Sindroma Koroner Akut

Angina Pektoris
terstabil
Infark miokard non
elevasi segmen ST
(STEMI)
Infark Miokard
dengan elevasi
segmen ST
(NSTEMI)

Patofisiologi sama
Persentasi sama
Aturan2
pengelolaan awal
sama
STEMI perlu
evaluasi untuk
intervensi
reperfusi akut

Clinical Classification of Myocardial

Infarction: Expert Consensus

Type I
Spontaneous MI related to ischemia due to a
primary coronary event such as a plaque
erosion and/or rupture, fissuring, or dissection

Type 2
MI secondary to ischemia due to either O2
demand or decreased supply (coronary artery
spasm, coronary embolism, anemia, HTN,
hypotension, arrhythmia)

Thygesen, K. et.al. Circulation 2007; 116: 2634 2653.

Clinical Classification of Myocardial

Infarction: Expert Consensus

Type 3
Sudden unexpected cardiac death, including
cardiac arrest, often with symptoms suggestive
of myocardial ischemia, accompanied by
presumably new ST elevation, or new LBBB, or
evidence of fresh thrombus in a coronary artery
by angiography and/or at autopsy, but death
occurring before blood tests could be obtained,
or at a time before the appearance of cardiac
biomarkers in the blood.

Thygesen, K. et.al. Circulation 2007; 116: 2634 2653.

Clinical Classification of Myocardial

Infarction: Expert Consensus

Type 4a
MI associated with PCI

Type 4b
MI associated with stent thrombosis as
documented by angiography or at autopsy

Type 5
MI associated with CABG

Thygesen, K. et.al. Circulation 2007; 116: 2634 2653.

Faktor Penentu Luas Infark

1.

1.
2.
3.
4.

Lama oklusi
(Ingat: door to balloon < 90 menit dan
door to needle < 30 menit )
Kolateral
Tingkat konsumsi oksigen miokard
Keadaan metabolik
Keseimbangan fibrinolitik

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 Unstable Angina

Patients with typical angina - An episode of

angina
Increased in severity or duration
Has onset at rest or at a low level of exertion
Unrelieved by the amount of nitroglycerin or
rest that had previously relieved the pain

Patients not known to have typical angina

First episode with usual activity or at rest
within the previous two weeks
Prolonged pain at rest

Diagnosis of Acute MI
STEMI / NSTEMI

At least 2 of the
following
Ischemic

symptoms
Diagnostic ECG
changes
Serum cardiac
marker elevations

Unstable
Angina
Non occlusive
thrombus
Non specific
ECG
Normal cardiac
enzymes

NSTEMI
Occluding thrombus
sufficient to cause
tissue damage & mild
myocardial necrosis
ST depression +/T wave inversion on
ECG
Elevated cardiac
enzymes

STEMI
Complete thrombus
occlusion
ST elevations on
ECG or new LBBB
Elevated cardiac
enzymes
More severe
symptoms

Sasaran Perawatan Kardiak

1.
2.
3.

4.

5.

Mengurangi luasnya infark

Mempertahankan fungsi ventrikel kiri
Mencegah kejadian kardiak atau
komplikasi major
Mengatasi komplikasi yang mengancam
jiwa
Mulai melakukan pencegahan sekunder

Acute Management

Initial evaluation
& stabilization

Efficient risk
stratification

Focused cardiac
care

Evaluation

Efficient & direct history

Initiate stabilization
interventions

Occurs
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
and tests

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

Emergent
care
IV access
Cardiac
monitoring
Oxygen
Aspirin
Nitrates

History &
Physical
Establish
diagnosis
Read ECG
Identify
complications
Assess for
reperfusion

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

Rekaman EKG harus secepatnya

dilakukan dan diinterpretasi
saat pasien tiba di IGD
Standar waktu 10 menit

Hamm Lancet 358:1533,2001

Presentation
Working Dx

Ischemic Discomfort
Acute Coronary Syndrome

Davies MJ
Heart 83:361, 2000

ECG

No ST Elevation
NSTEMI

Biochem.
Marker
Final Dx Unstable Angina

ST Elevation

Myocardial Infarction
NQMI
Qw MI

Normal or non-diagnostic EKG

ST Depression or
Dynamic T wave Inversions

ST-Segment Elevation MI

New LBBB

QRS > 0.12 sec

L Axis deviation
Prominent S wave V1-V3
Prominent R wave 1, aVL, V5-V6

Use of Cardiac Markers in ACS

URL = 99th %tile of Reference Control Group

Multiples of the URL

50
20

Cardiac troponin after

classical AMI

10

CK-MB after AMI

Cardiac troponin after

microinfarction

2
Upper reference limit

1
0

2
3
4
5
6
Days After Onset of AMI

Modified from:
ESC/ACC Comm MI redefined JACC 36: 959,2000 Wu AH et al. Clin Chem 1999;45:1104.

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

Prognosis with Troponin

7.5 %

8
Mortality at 42 Days

6.0 %

6
5
4
3
2
1
0

1.0 %
831

3.4 %

3.7 %

148

134

1.7 %
174

50

0 to <0.4 0.4 to <1.0 1.0 to <2.0 2.0 to <5.0 5.0 to <9.0

Cardiac troponin I (ng/ml)

67
9.0

SPEKTRUM KLINIS SKA

Current definitions and

prognosis of ACS
12hr serum troponin T concentration (ug/L)
< 0.01

0.1 and < 1.0

1.0

BCS

ACS with unstable

angina

ACS with myocyte

necrosis

ACS with clinical

MI

ESC/ACC

Unstable angina

MI

MI

WHO

Unstable angina

Unstable angina

MI

30-day mortality

4.5%

10.4%

12.9%

6-month mortality

8.6%

18.7%

19.2%

Acute Coronary Syndrome

No ST Elevation

ST Elevation

Risk Stratification
Purposes
Triage / Transfer for Tertiary Care
Resource Allocation
Selection of Rx Strategy

Prognosis

Continuous Process
Presentation: History, ACS features, Biomarkers, PEx
In Hospital:
Events, Response to Rx
Discharge:
LV Function, Arrhythmias, Ischemia

Risk Stratification

YES

STEMI
Patient?

- Assess for reperfusion

- Select & implement
reperfusion therapy
- Directed medical
therapy

Based on initial
Evaluation, ECG, and
Cardiac markers

NO

UA or NSTEMI
- Evaluate for Invasive
vs. conservative
treatment
- Directed medical
therapy

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 ICH

Known structural cerebral vascular lesion (e.g.,
AVM)
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

Advantages of
Fibrinolytic Therapy

More universal access

Shorter time to treatment
Greater clinical trial evidence of:

reduction in infarct size

improvement of LV function

Results less dependent on physician

experience
Lower system costs
42

Advantages of primary PCI over

thrombolysis
Clinical indices

Event rate
Thrombolysis

PCI

Absolute
RR

Relative
RR

NNT

Short term mortality

(4-6weeks)

8%

5%

3%

36%

33

Long term mortality

(6-18months)

8%

5%

3%

38%

33

Stroke

2%

<1%

2%

64%

50

Re-infarction

8%

3%

5%

59%

20

Recurrent ischaemia

18%

7%

11%

59%

20

Death or non-fatal
re-infarction

12%

7%

5%

44%

20

Need for CABG

13%

8%

5%

38%

20

Comparing outcomes

STEMI cardiac care

STEP 1: Assessment
Time since onset of symptoms

Is this high risk STEMI?

KILLIP classification
If higher risk may manage with more invasive rx

Determine if fibrinolysis candidate

90 min for PCI / 12 hours for fibrinolysis

Meets criteria with no contraindications

Determine if PCI candidate

Based on availability and time to balloon rx

Medical Therapy
MONA + BAH

Morphine (class I, level C)

Analgesia
Reduce pain/anxietydecrease sympathetic
tone, systemic vascular resistance and oxygen
demand
Careful with hypotension, hypovolemia,
respiratory depression
Oxygen (2-4 liters/minute) (class I, level C)
Up to 70% of ACS patient demonstrate
hypoxemia
May limit ischemic myocardial damage by
increasing oxygen delivery/reduce ST elevation

Nitroglycerin (class I, level B)

Analgesiatitrate infusion to keep patient
pain free
Dilates coronary vesselsincrease blood
flow
Reduces systemic vascular resistance and
preload

Aspirin (160-325mg chewed & swallowed) (class

I, level A)
Irreversible inhibition of platelet
aggregation
Stabilize plaque and arrest thrombus
Reduce mortality in patients with STEMI

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
Reassess for therapy as contraindications
resolve

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

Start in patients with anterior MI,
pulmonary congestion, LVEF < 40%
Start in first 24 hours
ARB as substitute for patients unable to use
ACE-I

Heparin (class I, level C to class IIa, level C)

LMWH or UFH (max 4000u bolus, 1000u/hr)
Indirect inhibitor of thrombin
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

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

Unstable angina/NSTEMI
cardiac care

Evaluate for conservative vs. invasive

therapy based upon:
Risk

of actual ACS
TIMI risk score
ACS risk categories per AHA
guidelines
Low

Intermediate

High

High Risk ACS (UA/NSTEMI)

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

Conservative
therapy

Invasive
therapy

Invasive therapy option

UA/NSTEMI

Coronary angiography and

revascularization within 12 to 48 hours
after presentation to ED
For high risk ACS (class I, level A)
MONA + BAH (UFH)
Clopidogrel

20% reduction death/MI/Stroke CURE trial

1 month minimum duration and possibly up to 9 months

Glycoprotein IIb/IIIa inhibitors

Conservative Therapy for

UA/NSTEMI

Early revascularization or PCI not planned

MONA + BAH (LMW or UFH)
Clopidogrel
Glycoprotein IIb/IIIa inhibitors

Only in certain circumstances (planning PCI, elevated

TnI/T)

Surveillence in hospital

Serial ECGs
Serial Markers

Medication Use at Discharge

and 1-year Mortality

After adjusting for age, previous MI, CHF, Killip

class, abnormal biomarker, ST deviation/BBB on
presentation, the discharge use of the following
medications was associated with lower 1-year
mortality *:
ASA [OR=0.48 (0.36 to 0.63), P<0.001]
Beta-blocker [OR=0.72 (0.56 to 0.92), P<0.01]
ACE inhibitor [OR=0.76 (0.60 to 0.96), P=0.02]
Lipid lowering agent [OR=0.72 (0.57 to 0.92),
P<0.01]
* OR= odds ratio (95% confidence interval)

Comprehensive Medical Therapy For 2nd Prevention for

Patients with CHD or Other Vascular Disease
Risk Reduction

ASA*
Beta Blockers*
ACE inhibitors*
Statins*
Smoking Cessation

20-30%
20-35%
22-25%
25-42%
50%

*The four medications every atherosclerosis patient should be

treated with, unless contraindications exist and are documented

Pencegahan Sekunder
A : ASA, antikoagulan, ACE-I/ARB (LVD, HF, HTN,
DM)
B : Beta-blocker, BW reduction, BP Control
(BP< 130/80 mmHg)
C : Cigarette smoking cessation
Cholesterol control (K-LDL<70 mg/dl)
D : Diet ( AHA step 2 diet )
Diabetes management ( Ac<7%)
E : Exercise regularly
Education
F : Family Support
G : Go to Hospital

Secondary Prevention of Coronary

Disease
Secondary
Prevention

CAD
Non-Coronary
Atherosclerosis

Primary
Prevention

Population
Wellness

Subclinical
Atherosclerosis
Multiple Risk
Factors
Environmental,
Genetic Factors that
Produce Risk

Prevention news
From 1994 to 2004 the death rate from
coronary heart disease declined33%...
But the actual number of deaths declined
only18%

Getting better with treatment

But more patients developing disease
need for primary prevention focus

Kesimpulan

SKA mencakup APTS, NSTEMI, dan STEMI

Fokus penatalaksanaan
- penilaian dan intervensi segera ( MONA + BAH )
- stratifikasi resiko ( APTS/NSTEMI VS STEMI )
- reperfusi cepat pada STEMI (Fibrinolitik vs PCI )
- strategi konservatif vs invasif dini pada APTS/
NSTEMI
Pencegahan sekunder agresif pada pasien SKA
- BB, ACE-1/ARB, ASA, statin

FarahMutiaraSariHarmani

Objectives

Define & delineate acute coronary

syndrome

Review Management Guidelines

Unstable Angina / NSTEMI

STEMI

Review secondary prevention initiatives

Acute Coronary Syndromes

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 Acute MI
STEMI / NSTEMI

At least 2 of the
following
Ischemic

symptoms
Diagnostic ECG
changes
Serum cardiac
marker elevations

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

Diagnosis of Unstable Angina

Patients with typical angina - An episode of

angina
Increased in severity or duration
Has onset at rest or at a low level of exertion
Unrelieved by the amount of nitroglycerin or rest
that had previously relieved the pain

Patients not known to have typical angina

First episode with usual activity or at rest within
the previous two weeks
Prolonged pain at rest

Unstable
Angina
Non occlusive
thrombus
Non specific
ECG
Normal cardiac
enzymes

NSTEMI
Occluding thrombus
sufficient to cause
tissue damage & mild
myocardial necrosis
ST depression +/T wave inversion on
ECG
Elevated cardiac
enzymes

STEMI
Complete thrombus
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

Occurs
Initiate stabilization interventions simultaneousl
y

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
and tests

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

Emergent
care
IV access
Cardiac
monitoring
Oxygen
Aspirin
Nitrates

History &
Physical
Establish
diagnosis
Read ECG
Identify
complicatio
ns
Assess for
reperfusion

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

Modified from Libby P

Circ 104:365,2001

Acute Coronary
Syndrome

Superficial
Erosion

Ruptured
Fibrous Cap

Hamm Lancet 358:1533,2001

Presentation

Ischemic Discomfort

Working Dx

Acute Coronary Syndrome

Davies MJ
Heart 83:361, 2000

ECG

No ST Elevation
NSTEMI

Biochem.
Marker
Final Dx Unstable Angina

ST Elevation

Myocardial Infarction
NQMI
Qw MI

Use of Cardiac Markers in

ACS

URL = 99th %tile of Reference Control Group

Multiples of the URL

50
20

Cardiac troponin after

classical AMI

10

CK-MB after AMI

Cardiac troponin after

microinfarction

2
Upper reference limit

1
0

2
3
4
5
6
Days After Onset of AMI

Modified from:
ESC/ACC Comm MI redefined JACC 36: 959,2000 Wu AH et al. Clin Chem 1999;45:1104.

Acute Coronary Syndrome

No ST Elevation

ST Elevation

Risk Stratification
Purposes
Triage / Transfer for Tertiary Care
Resource Allocation
Selection of Rx Strategy

Prognosis

Continuous Process
Presentation: History, ACS features, Biomarkers, PEx
In Hospital:
Events, Response to Rx
Discharge:
LV Function, Arrhythmias, Ischemia

Symptoms suggestive of ACS

Rapid Triage
Obtain Biomarkers

Non
Cardiac
Diagnosis

As Per
Other Dx

Assess 12 lead ECG

Chronic
Stable
Angina

Medical
Rx

Goal = 10 min

Possible
ACS

Definite
ACS
ASA
Antithrombin
Beta Blocker

ACS Protocol

Symptoms Suggestive of ACS

Definite ACS

Possible ACS
No ST elev.

ST elev.

< 12h
Lytic
eligible
Lytic
(D-N < 30 m)

Lytic
ineligible

> 12h
Not a reperfusion
candidate
Consider
Reperfusion
for Symptoms

PCI*
(D-B < 90)
Consider:
GP IIb/IIIa + stent

*Skilled Oper./Team Rapidly Available

Medical Rx
(ACEI)

Symptoms Suggestive of ACS

Possible ACS

Definite ACS
No ST elev.

Non dx ECG
Neg. card. markers
Observe
f/u studies
Neg
Neg
Outpt f/u

Stress

ST-Tw changes
Ongoing pain
Positive card markers
Hemodynamic abnl.

ST elev.
Evaluate for
reperfusion

Pos
Pos

Dx of ACS confirmed
Admit to hospital
Acute ischemia pathway

Chronology of
Atherosclerotic Vascular Disease
Process

Development of
atherosclerosis and
vulnerable plaque

Acute Coronary Syndrome

Secondary Prevention

Ischemic
Heart Disease
Cerebrovascular
Disease
Peripheral Vascular
Disease

Modified from Libby P

Circ 104:365,2001

Troponins for Evaluation and

Management of ACS
Disadvantages

Advantages

Risk Stratificaton
Sens/Spec > CKMB
Detect Recent MI
Selection of Rx
Detect Reperfusion

Low sens. early (< 6h)

Repeat at 8-12 h if neg.
Limited ability to
detect late minor
reinfarction

Recommendation
Useful as single test to efficiently Dx NSTEMI
Clinicians should familiarize themselves with Dx
cutoffs in local lab

ECG assessment
ST Elevation or new LBBB
STEMI
ST Depression or dynamic
T wave inversions

NSTEMI
Non-specific ECG

Unstable Angina

Normal or non-diagnostic EKG

ST Depression or Dynamic T wave

Inversions

ST-Segment Elevation MI

New LBBB

QRS > 0.12 sec

L Axis deviation
Prominent R 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 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

Prognosis with Troponin

7.5 %

8
Mortality at 42 Days

6.0 %

6
5
4
3
2
1
0

1.0 %
831

3.4 %

3.7 %

148

134

1.7 %
174

50

0 to <0.4 0.4 to <1.0 1.0 to <2.0 2.0 to <5.0 5.0 to <9.0

Cardiac troponin I (ng/ml)

67
9.0

Risk Stratification

YES

STEMI
Patient?

- Assess for reperfusion

- Select & implement
reperfusion therapy
- Directed medical
therapy

Based on initial
Evaluation, ECG, and
Cardiac markers

NO

UA or NSTEMI
- Evaluate for Invasive vs.
conservative treatment
- Directed medical therapy

Cardiac Care Goals

Decrease

amount of myocardial

necrosis
Preserve LV function
Prevent major adverse cardiac events
Treat life threatening complications

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 ICH

Known structural cerebral vascular lesion (e.g., AVM)
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)

Relative contraindications for fibrinolysis..

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
STEMI dx in doubt

Comparing outcomes

Medical Therapy
MONA + BAH

Morphine (class I, level C)

Analgesia
Reduce pain/anxietydecrease sympathetic tone,
systemic vascular resistance and oxygen demand
Careful with hypotension, hypovolemia, respiratory
depression
Oxygen (2-4 liters/minute) (class I, level C)
Up to 70% of ACS patient demonstrate hypoxemia
May limit ischemic myocardial damage by increasing
oxygen delivery/reduce ST elevation

Nitroglycerin (class I, level B)

Analgesiatitrate infusion to keep patient pain free
Dilates coronary vesselsincrease blood flow
Reduces systemic vascular resistance and preload

Aspirin (160-325mg chewed & swallowed) (class I, level A)

Irreversible inhibition of platelet aggregation
Stabilize plaque and arrest thrombus
Reduce mortality in patients with STEMI

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
Reassess for therapy as contraindications resolve

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

Start in patients with anterior MI, pulmonary
congestion, LVEF < 40%
Start in first 24 hours
ARB as substitute for patients unable to use ACE-I

Heparin (class I, level C to class IIa, level C)

LMWH or UFH (max 4000u bolus, 1000u/hr)
Indirect inhibitor of thrombin
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

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

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

Unstable angina/NSTEMI
care

cardiac

Evaluate for conservative vs. invasive

therapy based upon:
Risk

of actual ACS
TIMI risk score
ACS risk categories per AHA guidelines
Low

High
Intermediate

TIMI Risk Score

Predicts risk of death, new/recurrent MI, need for

urgent revascularization within 14 days

ACS risk criteria (UA/NSTEMI)

Low Risk ACS
No intermediate or high
risk factors
<10 minutes rest pain
Non-diagnositic ECG
Non-elevated cardiac
markers
Age < 70 years

Intermediate Risk ACS

Moderate to high likelihood
of CAD
>10 minutes rest pain,
now resolved
T-wave inversion > 2mm
Slightly elevated cardiac
markers

High Risk ACS (UA/NSTEMI)

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

Conservative
therapy

Invasive
therapy

Secondary prevention
behavioral intervention

Smoking cessation

Physical Activity

Cessation-class, meds, counseling

Goal 30 - 60 minutes daily
Risk assessment prior to initiation

Diet

DASH diet, fiber, omega-3 fatty acids

<7% total calories from saturated fats

Or maybe just move.

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

Lipid lowering agent

Aspirin* and/or Clopidorgrel

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 (MONA+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

Cardiovascular disease and

diabetes
~65% of deaths are
to CV disease

Coronary heart
disease deaths
2- to 4-fold

Cardiovascular
complications of
T2DM

due

Stroke risk
2- to 4-fold

Heart failure
2- to 5-fold
T2DM = type 2 diabetes mellitus

Bell DSH. Diabetes Care. 2003;26:2433-41.

Centers for Disease Control (CDC). www.cdc.gov.

Abnormal glucose metabolism in CAD

n = 2107 inpatients with acute CAD; n = 2854 outpatients with stable CAD
Known diabetes

OGTT*

60

Total
patients
(%)

40

58

60

32

30

20

Patients*
(%)

51

40

20

0
Inpatients

Outpatients

0
Inpatients
IGT

*n = 1920 without known diabetes

OGTT = oral glucose tolerance test;
IGT = impaired glucose tolerance; IFG = impaired fasting glucose

IFG

Outpatients
New DM

Bartnik M et al.
Eur Heart J. 2004;25:1880-90.

New-onset hyperglycemia linked to

highest rate of in-hospital mortality
N = 2030 hospital patients
40

30
Mortality
20
(%)

10
0
Normoglycemia

ICU patients
*P < 0.01 vs normoglycemia and
known diabetes

Known diabetes

New hyperglycemia

Non-ICU patients

Umpierrez GE et al. J Clin Endocrinol Metab. 2002;87:97882.

Stress hyperglycemia in AMI: Association

with mortality risk in patients without known
diabetes
Reference

Hyperglycemia
definition
(mg/dL)

OSullivan 1991

>144

Lewandowicz 1979

121

Soler 1981

110

Oswald 1986

144

Bellodi 1989

>121

Ravid 1975

>121

Sewdarsen 1989

144

Pooled
0

10 11 12 13

Unadjusted RR of in-hospital mortality after MI*

*vs patients with normoglycemia

Capes SE et al. Lancet. 2000;355:773-8.

Baseline fasting plasma glucose levels

predict HF hospitalization in high-risk
patients
ONTARGET/TRANSCEND; N = 31,546 with CVD or DM + end-organ damage
Normal low

0.06

23% in HF
hospitalization per
18 mg/dL glucose in
patients with no
known diabetes

Normal high

0.05

IFG
New DM

0.04
Proportion
with incident HF
hospitalization

DM

0.03
0.02
0.01
0.0
0

200

400

600

800

1000 1200

Follow-up (days)
Log rank P < 0.001

Held C et al. Circulation. 2007;115;1371-5.

Admission glucose and glucose change

within 24 hours predict mortality risk
N = 1469 with AMI (n = 1219 without DM)
12
10
30-day
mortality
(%)

9% in 30-day mortality
per 11 mg/dL glucose in
first 24 hr (P = 0.002)*

8
6
4
2
0

0
<125

125<140 140<170
Baseline glucose (mg/dL)

170

Glucose (24 hr vs baseline)

30 mg/dL decrease
No change to <30 mg/dL decrease
*Multivariate analysis

Increase

Goyal A et al. Eur Heart J. 2006;27:1289-97.

Modified from Libby P

Circ 104:365,2001

Acute Coronary
Syndrome

Superficial
Erosion

Ruptured
Fibrous Cap

Hamm Lancet 358:1533,2001

Presentation

Ischemic Discomfort

Working Dx

Acute Coronary Syndrome

Davies MJ
Heart 83:361, 2000

ECG

No ST Elevation
NSTEMI

Biochem.
Marker
Final Dx Unstable Angina

ST Elevation

Myocardial Infarction
NQMI
Qw MI

Troponins for Evaluation and

Management of ACS
Disadvantages

Advantages

Risk Stratificaton
Sens/Spec > CKMB
Detect Recent MI
Selection of Rx
Detect Reperfusion

Low sens. early (< 6h)

Repeat at 8-12 h if neg.
Limited ability to
detect late minor
reinfarction

Recommendation
Useful as single test to efficiently Dx NSTEMI
Clinicians should familiarize themselves with Dx
cutoffs in local lab

Acute Coronary Syndrome

No ST Elevation

ST Elevation

Risk Stratification
Purposes
Triage / Transfer for Tertiary Care
Resource Allocation
Selection of Rx Strategy

Prognosis

Continuous Process
Presentation: History, ACS features, Biomarkers, PEx
In Hospital:
Events, Response to Rx
Discharge:
LV Function, Arrhythmias, Ischemia

Symptoms suggestive of ACS

Rapid Triage
Obtain Biomarkers

Non
Cardiac
Diagnosis

As Per
Other Dx

Assess 12 lead ECG

Chronic
Stable
Angina

Medical
Rx

Goal = 10 min

Possible
ACS

Definite
ACS
ASA
Antithrombin
Beta Blocker

ACS Protocol

Symptoms Suggestive of ACS

Definite ACS

Possible ACS
No ST elev.

ST elev.

< 12h
Lytic
eligible
Lytic
(D-N < 30 m)

Lytic
ineligible

> 12h
Not a reperfusion
candidate
Consider
Reperfusion
for Symptoms

PCI*
(D-B < 90)
Consider:
GP IIb/IIIa + stent

*Skilled Oper./Team Rapidly Available

Medical Rx
(ACEI)

Symptoms Suggestive of ACS

Possible ACS

Definite ACS
No ST elev.

Non dx ECG
Neg. card. markers
Observe
f/u studies
Neg
Neg
Outpt f/u

Stress

ST-Tw changes
Ongoing pain
Positive card markers
Hemodynamic abnl.

ST elev.
Evaluate for
reperfusion

Pos
Pos

Dx of ACS confirmed
Admit to hospital
Acute ischemia pathway

Chronology of
Atherosclerotic Vascular Disease
Process

Development of
atherosclerosis and
vulnerable plaque

Acute Coronary Syndrome

Secondary Prevention

Ischemic
Heart Disease
Cerebrovascular
Disease
Peripheral Vascular
Disease

Modified from Libby P

Circ 104:365,2001

Electrocardiographic Changes

129

Causes of ST segment Elevation

Acute myocardial infarction

Benign early repolarization
Left bundle branch block
Left ventricular hypertrophy
Ventricular aneursym
Coronary vasospasm
Pericarditis
Brugada Syndrome
Subarachnoid hemorrhage
130

Initial Management in ED
1.

Initial evaluation with ECG in < 10 min

2.

O2 by nasal prongs, IV access, continual ECG

3.

Sublingal NTG unless SBP<90 or HR <50 or >100

4.

Analgesia (morphine or meperidine)

5.

Aspirin (325 mg po chewed)

6.

Lipid panel, electrolytes, magnesium, CIPs

7.

Thrombolysis or PCI if ST >1mV or LBBB

(door-needle < 30 min or door-balloon < 90 min)

Thrombolytics
Mechanism of Action
Streptokinase
Proactivator

Activator

Fibrin

Plasminogen
tPA
Reteplase
Tenecteplase
Plasmin

Activates
plasminogen
that is bound to
fibrin

Fibrin degradation
products

Thrombolytics
Mechanism of Action
Streptokinase
Proactivator

Activator

Fibrin

Plasminogen
tPA
Reteplase
Tenecteplase
Plasmin

Activates
plasminogen
that is bound to
fibrin

Fibrin degradation
products

Thrombolytics

Absolute
Contraindications

Previous hemorrhagic stroke

at any time; or other strokes
within one year
Known intracranial neoplasm
Active internal bleeding
Suspected aortic dissection

Precautions

Severe uncontrolled HTN

(BP>180/100mmHg)
Current use of anticoagulants in
therapeutic dose (INR 2-3)
Recent trauma (within 2-4
weeks), including head trauma
or traumatic or prolonged CPR or
major surgery(<3 weeks)
Noncompressible vascular
punctures
Recent internal bleeding (within
2-4 weeks)
Active PUD
H/O chronic severe HTN

Thrombolytics

Monitoring Parameters

EKG
BP
Sites of bleeding
CBC (H/H, platelets)

Pivotal Thrombolytic Clinical Trials

GISSI-1

GISSI-2

ASSENT-2

ASSENT-3

(1986)

(1990)

(1999)

(2001)

ISIS-2

GUSTO-I

GUSTO-III

GUSTO-V

(1988)

(1993)

(1997)

(2001)

136

Advantages of Fibrinolytic Therapy

More universal access

Shorter time to treatment
Greater clinical trial evidence of:

reduction in infarct size

improvement of LV function

Results less dependent on physician

experience
Lower system costs
137

Comparing outcomes