CORONARY ARTERY DISEASE

NON ST ELEVATION MYOCARDIAL INFARCTION

SUPERVISOR

DR. IDAR MAPPANGARA SP.PD,SP.JP, FIHA

BAGIAN KARDIOLOGI DAN PEMBULUH
DARAH FAKULTAS KEDOKTERAN
UNIVERSITAS HASANUDDIN

PATIENT IDENTITY
Name

: Mrs. H

Age

: 70 years old

Address

: Jl. Prof. Dr IR Sutami

MR

: 781676

Date of Admission

: 7th December 2016

HISTORY TAKING
Chief complaint

: Chest pain

Present Illness History :

Chest pain experienced since approximately 5 months ago and

worsen earlier this morning.
Pain described as penetrating to the back and radiated to the left
arm accompanied with numbness sensation on the arm
continuously, duration of pain more than 2 hours.

Shortness of breath (+), and nausea (-), Cough (-), Paroxysmal

Nocturnal Dyspnea (-), Dyspnea on Effort (-) , Orthopnea (-)
Prior admission to the hospital patient consumed Isosorbid dinitrate
5mg and was relieved from the chief complaint

HISTORY TAKING
Personal Life History :
Patient was diagnosed with Heart disease approximately 5 years
ago with routine medication.
Patient was recommended to undergo bypass but refused.

History of hypertension since 2 years ago with routine medication.

No history of diabetes mellitus.

History of high cholesterol previously.

No history alcohol consumption and smoking
No history of heart disease in the family

RISK FACTOR

Hypertension
Obese
dyslipidemia

Gender
Age

: Female
: 70 years

PHYSICAL
EXAMINATION
General Status

Moderate illness / Overweight / Compos mentis

Weight

: 67 kg

Height

: 164 cm

BMI

: 24,91 kg/m2

Vital Status
Blood pressure

:153/92 mmHg

Heart rate

: 99 bpm

Respiratory rate

: 28 rpm

Temperature

: 36,5 oC

PHYSICAL EXAMINATION
Conjunctiva anemic (-/-), icteric (-/-)

JVP R+1 cmH2O

Vesicular breath sound, rhonchi (-/-), wheezing (-/-)

Heart sound 1/2 reguler, murmur (-)

Peristaltic (+) normal, Ascites (-)
Extremity edema (-/-) warm acral.

ELECTROCARDIOGRAM

Sinus rhythm
Heart rate : 87 bpm
Axis : Between -30*
aand 90*(normo axis)
P wave : 0.2 s
R wave: Poor R wave
& not visible in lead
v3
PR interval : 0,12 s
Q wave: Q pathologis
at V1 and V2
QRS comples :0,08 s
ST segment : ST
depression on lead I,
II, Avf, V3,V4,V5,V6

Conclusion :
Sinus rhythm, Heart
rate 87 beats per
minute
Normoaxis,Old
miocardial infarction
anteroseptal
ischemic
anterolateral

LABORATORY RESULTS
TEST

RESULT

NORMAL VALUE

WBC

5.1 x 103/uL

4.0 10.0 x

RBC

4,04 x 106/uL 4.0 10

6.03 x 106

HGB

12.2 g/dL

12 18

HCT

38%

37 48

PLT

274 x 103/uL

150 400 x

PT

9.7 s

APTT

24.6 s

1010
- 314
22,0 - 30,0

INR

1,04

TEST

RESULT

NORMAL VALUE

GDS

170 mg/dL

<140

SGOT
SGPT

96 u/L
127 u/L

<38
<41

Ureum

35 mg/dL

10-50

Kreatinin

0.93 mg/dL

0,5-1,2

CK

123,00 u/L

<190

CKMB

17.6 u/L

<25

Trop I

0.08

<0.01

Natrium

145 mmol/L

136 - 145

Kalium

3.6 mmol/L

3,5 - 5,1

Klorida

105 mmol/L

97 - 111

Asam Urat

6.8 mg/dL

3,4-7,0

LABORATORY
RESULTS
TEST

RESULT

NORMAL VALUE

Total Cholesterol

295 mg/dl

200

HDL

43 mg/dl

> 55

LDL

216 mg/dl

< 130

TRIGLYCDERIDE

121 mg/dl

200

CHEST X-RAY
Result :
Cor membesar
(CTI index : 0.55)
Pinggang jantung melurus
Apex tertanam.
Aorta dilatasi dan elongasi
Kesan :
Cardiomegaly with dilatatio
Et elongatio aortae

DIAGNOSIS
Non - ST Elevation Myocardial Infarction (STEMI)
Coronary Artery Disease
Hypertension on treatment

TREATMENT
Bed rest
Oxygen 4 lpm via nasal cannula
IVFD NaCl 0,9% 500 cc/24 hours
Anti Coagulant : Clopidogrel 4 tabs 75mg/oral
Statin

: Atorvastatin 40 mg 0-0-1

Nitrate

: Nitroglycerin 10mg/min/iv

ACEI

: Captopril 3x12.5mg tab

Lactulose

: Laxadine syr 0-0-2 tsp

Anti anxiety

: Alprazolam 0,5 mg 0-0-1

Fibrinolytic

: Fondaparinux 2.5mg/24hours/iv

Anti aggregation thrombosis : Aspilet 2 tabs/oral

PLANNING
Echocardiography

Coronary Angiography

DISCUSSION

ACUTE CORONARY SYNDROME

Definition
as a condition caused by impaired blood flow to the coronary partial to total
acute myocardial so that there is an imbalance in the need for blood and
blood supply.

Major cardiovascular problems

based on statistics for hospital care and a high mortality rate.
The main cause of the acute coronary syndromes is obstruction in
the coronary arteries.
Consequences arising from the arterial obstruction depends on
the degree and location of the obstruction range from
unstable angina,
myocardial infarction without ST segment elevation (NSTEMI)
myocardial infarction with ST-segment elevation (STEMI).

ACS CATEGORIES
Unstable Angina
Pectoris

NSTEMI

STEMI

Manifestations :
Typical angina, without
enzyme elevations
cardiac biomarkers, with
or without ECG changes
indicate ischemia

Manifestations :
typical angina,
accompanied by an
increase in cardiac
marker enzymes in the
absence of ST elevation
on ECG picture.

Manifestations :
typical angina,
accompanied by an
increase in cardiac
marker enzymes, with the
description ST elevation
on ECG.

Rupture of unstable
plaque

Unstable thrombus
formation on plaque
rupture

Thrombus in plaque
rupture

Thrombus begins to form. Transient or incomplete

vascular occlusion.

Complete vascular
occlusion.

EPIDEMIOLOGY AND ETIOLOGY

United States
myocardial infarction occurred in approximately 1.5 million cases,
Results in death for 400,000 to 500,000 people.

Acute coronary syndrome mostly occurs when there is an acute

thrombus formed in the coronary arteries.
Artheromatous plaque can sometimes be unstable and eventually
rupture causing thrombus and cause blockage in the end.

RISK FACTORS
Unmodified
Age

Modifiable
in lipid serum

Sex
Race

hypertension
Cholesterol

Family history

Smokers

Pathogenesis of Atherosclerosis: is primarily an

inflammatory process, and it is asymptomatic until it
produces:
Narrowing of the lumen sufficient narrowing of the
vessel produces symptoms of ischemia (intermittent
claudication, angina, gangrene)
Sudden occlusion caused by plaque rupture followed
by thrombosis (eg: myocardial infarction)
Emboli these may have an impact in other vessels
(eg: stroke)
Aneurysms resulting from wall weakening

PATHOGENESIS

Atherosclerosis is the major cause of CAD : focal deposits of

cholesterol and lipids in the intimal wall of the artery.

Although several risk factors are present, endothelial injury is caused by

an inflammatory response in the intimal layer of the artery and the
deposition of the lipids in the wall.

SIGNS AND SYMPTOMS

The most common symptom of CAD : ANGINA

Other symptoms that may occur with CAD include:

Shortness of breath (SOB)
Palpitations (irregular heartbeats, skipped beats or a flip
flop feeling in chest)
A faster heartbeat
Dizziness
Nausea
Extreme weakness
Sweating
Some people dont have symptoms. In rare cases, a person can
have a silent heart attack, without symptoms.

DIAGNOSING
There are 2 or 3 criterias:
1. Chest Pain, more than 20 minutes and not cured even
with nitrates
2. Increased Biochemical markers
3. Changed Electrocardiography (ECG)
ST Segment depression 0,5 mm in V1-V3 and in
other leads
Non persistent ST-Segment elevation (<20
minutes),
with lower amplitude of ST Segment elevation in
STEMI
Symmetrical T wave inversion 2 mm reinforce
alleged NSTEMI

CARDIAC BIOMARKERS
Cardiac troponins are the reference
markers of MI because they are more
specific and sensitive than other
marker.
Troponin
Rises 4-6 hours after MI
Can remain elevated for up to two
weeks!
Very specific for cardiac damage
Elevated in many other conditions
than ACS
Hypotension of any cause
(~80% patients)
Renal failure
Congestive heart failure
Many others
Always predicts worse outcomes

CARDIAC BIOMARKERS
CK

Rises 4-6 hours after MI

Peaks and falls by 36-48 hours after MI
Total CK is non-specific
CK-MB is more specific for cardiac tissue
(but there is still some in skeletal muscle!!)

Remember this is one component in the diagnosis

of NSTEMI
CK alone cannot be used to diagnose NSTEMI

CARDIAC BIOMARKERS

ELECTROCARDIOGRAPHY

ELECTROCARDIOGRAPHY

VASCULARISATION OF HEART

DIFFERENTIAL DIAGNOSIS

PHARMOCOLOGY
Anti Ichemic

Beta Blocker

(to myocardial
oxygen demand
or myocardial
oxygen supply)

Nitrate
Calcium Channel Blocker (CCB)

Perhimpunan Dokter Spesialis Kardiovaskular Indonesia. Pedoman Tatalaksana Sindrom Koroner Akut.2014

PHARMOCOLOGY
Anti
Platelet

ASA : Aspirin : loading dose 150-300 mg,

maintenance dose 75-100 mg

( platelet
aggregation
and inhibit
thrombus
formation)

P2Y12 inhibitor : Ticagrelor: loading dose

180 maintenance dose 2x90 mg
P2Y12 inhibitor : Clopidogrel: loading dose
300 mg, maintenance dose 75 mg/hari

Common side effects : gastritis, peptic ulcer disease, GI bleeding; use with PPI

Perhimpunan Dokter Spesialis Kardiovaskular Indonesia. Pedoman Tatalaksana Sindrom Koroner Akut.2014

PHARMOCOLOGY
ACE
Inhibitor

Captopril : 2-3 x 6,25-50 mg

(prevent
remodelling)

Ramipril : 2,5-10 mg/day in 1 or 2

dose
Lisinopril: 2,5-20 mg/day in 1 dose

Common side effects : hyperkalaemia,

dry cough (build up of bradykinin)

Perhimpunan Dokter Spesialis Kardiovaskular Indonesia. Pedoman Tatalaksana Sindrom Koroner Akut.2014

PHARMOCOLOGY
Statin

Atorvastatin : 80 mg /day single dose

(Anti
inflammation
and plaque
stabilisation)

targeted LDL<100 mg/dL

Perhimpunan Dokter Spesialis Kardiovaskular Indonesia. Pedoman Tatalaksana Sindrom Koroner Akut.2014

PHARMOCOLOGY
Fundaparinuks : 2,5 mg subcutan

Anti
Coagulation
(inhibit thrombin
generation and/or
activity thereby
reducing thrombusrelated events)

Enoksaparin : 1 mg/kg, 2 times/day

UFH :Bolus i.v 60 u/g, max doses 4000 U, Infus i.v

12 U/kg for 24-48 hours with max dose of 1000
U/hour, Targeted aPTT 1,5 2x control

Perhimpunan Dokter Spesialis Kardiovaskular Indonesia. Pedoman Tatalaksana Sindrom Koroner Akut.2014

REPERFUSION THERAPY FOR NSTEMI

Terapi konservatif

-Angiografi elektif
-Stress test
CABG
PCI- stenting: kelainan single vessel
Penyakit arteri koroner kompleks
Kelainan koroner left main dengan triple vessel
Oklusi total
Kelainan difus

PREDISCHARGE AND
SECONDARY PEVENTION
Lifestyle modification
Weight loss
Management of hypertension
Management of diabetes
Lipid intervention
Antiplatelet
Beta blocker
ACEI/ARB

Penatalaksanaan NSTEMI secara

skematis. (Sari Harahap,2014)

PROGNOSIS
Mortality rate 15-30%

The risk of death depends on many factors, including patient

age, previous history of coronary disease, presence of other
illnesses and the extent of infarction.
In 25% of episodes of acute myocardial infarction, sudden
death occurs within a few minutes after the attack.
Acute attacks increased mortality by age. Death of
approximately 10-20% in those under 50 years and 20% in the
elderly.
Six-months mortality rate in Global Registry of Acute Coronary
Events (GRACE ), were 13% for patient with non-ST elevation
myocardial infarction acute coronary syndrome and 8% for
those with unstable angina.

GRACE

(GLOBAL REGISTRY OF ACUTE CORONARY EVENTS)

INTERPRETATION
Hospitalisation mortality risk :

108 low risk (<1%)

109-140 moderate risk (1-3%)
>140 high risk (>3%).

Mortality risk 6 months after discharge :

88 low risk (<3%).
89-118 moderate risk (3-8%)
>118 high risk (>8%).

KILLIP CLASSIFICATION
Tabel 5 : Mortalitas 30 hari berdasarkan kelas Killip

(dikutip dari Killip T, Kimball JT (Oct 1967). Treatment of myocardial infarction in a

coronary care unit. A two year experience with 250 patients. Am J Cardiol. 20 (4): 457
64.)

REFERENCES
1.[Internet]. http: //jki.or.id. 2016 [cited 12 December 2016].
Available from:
http://www.inaheart.org/upload/file/Pedoman_tatalaksana_Sin
drom_Koroner_Akut_2015.pdf
2.Roffi M, Patrono C, Collet J, Mueller C, Valgimigli M,
Andreotti F et al. 2015 ESC Guidelines for the management of
acute coronary syndromes in patients presenting without
persistent ST-segment elevation. European Heart Journal.
2015;37(3):267-315.

3.Fakultas Kedokteran Universitas Indonesia, (2014) Kapitas

Selekta Kedokteran Edisi ke-4, Media Aesculapius, Jakarta,
Indonesia.
4.Roy D. Russ, PhD, (2006) Crash Course Cardiovascular
System, Mosby Elsevier, Philadelphia.

THANK YOU