Penyakit Jantung Koroner

Yofara Maulidiah Muslihah

1111103000047
Pembimbing:
dr. Achyar, SpJP

KEPANITERAAN KLINIK
ILMU KARDIOLOGI
FKUIN-RSUP FATMAWATI
JAKARTA 2016

HD (Heart Disease)
General term for a variety of heart conditions.
Most common form:

CHD or CAD

CHD (Coronary Heart Disease)

CAD (Coronary Artery Disease)
Others:
Hypertension, congestive heart failure, stroke, congenital
cardiovascular defects, atherosclerosis of the blood vessels,
and other diseases of circulatory system.

US Department of Health and Human Services. Cardiovascular Disease. 2012.

NIH Publication; 12(7680) p6

Coronary Artery Disease Epidemiology

Indonesia:
2008
17,3 million deaths due to heart diseases
More than 3 million of it affects people age < 60 years old
Prevalence in 2013 as much as 0,5% or 883.447 people
Highest prevalence found in West Java with 160.812 people

Pusat Data dan Informasi Kementerian

Kesehatan RI, 2014

Coronary Arteries

Coronary Arteries

CAD: Etiology

More than 90% of ACS result from

disruption of an atherosclerotic plaque with
subsequent platelet aggregation and
formation of an intracoronary thrombus.

Arterial Stenoses and Their Clinical

Implications
Initiation and evolution of plaque previously discussed generally last many years (affected
individuals have no symptoms).
Plaque burden > capacity of artery to remodel outward encroachment on the arterial lumen
begins.
Lesions producing stenoses > 60% cause flow limitations under conditions of increase demand and
produce chronic stable angina pectoris/ claudication.

Determinants of

Most Cases of Myocard Infarct

No History of Stable Angina

Result not from increase in stenoses grade, but from lesions

that do not limit flow mostly thrombosis.

Thrombosis and Atheroma Complication

Plaque Rupture and Thrombosis

Angina

Most often described as pressure, discomfort, tightness, burning, or

heaviness in the chest; rarely described as pain. It is neither sharp nor stabbing,
and does not vary significantly with inspiration or movement of the chest wall. It is
a steady discomfort lasts a few minutes, rarely more than 5 to 10 minutes.
It is precipitated by conditions that increase myocardial oxygen demand (e.g.
increased heart rate, contractility, or wall stress); this includes physical exertion,
anger, and other emotional excitement (also large meal or cold weater).

ACUTE
CORONARY
SYNDROME
Angina Pectoris
tidak stabil (UAP)

Infark Miokard
tanpa ST Elevasi
(NSTEMI)

Infark Miokard
dengan ST
Elevasi (STEMI)

Biomarker

Troponin: begin to rise 3-4 hours after onset discomfort, peak 1836hr, decline slowly 10-14 days
CK : start to rise 3-8 hours, peak 24 hr, return to normal 48-72 hr

In-Hospital Care
Within the first 10 minutes that the patient is in the Emergency
Department, work through the following:
1.

Check vital signs

2.

Evaluate O2 saturation

3.

Establish IV access

4.

Get or review a 12-leads ECG

5.

Look for risk factors of ACS, cardiac history, signs and symptoms of HF by taking a brief,
targeted history

6.

Perform physical exam

7.

Complete a fibrinolytic check list and check contra-indication

8.

Obtain a portable x-ray (< 30 minutes)

Rapid Initiation Therapy

1.

Total Bed rest

2.

Oxygen supplementation with O2 artery <95% or distress respiration

3.

Oxygen supplementation can be given to all patient with ACS in the first 6
hours, without consider the saturation

3.

Aspirin 160-320 mg sublingual can be given to all patient who doesnt have
intolerance with aspirin

4.

Receptor blocker ADP (adenosine diphosphate) clopidogrel 300 mg,

followed with maintenance dose 75 mg/day

Rapid Initiation Therapy (2)

7. Nitrogliserin (NTG) spray/tablet sublingual for the patient with chest pain
when arrive in emergency room and persistent: can be repeated each 5 minutes
max. 3 times

Still not responsive

Morfin sulfat 1-5 mg intravena, can be repeated each10-30 minutes

Therapy

REPERFUSION

PCI OR
Thrombolitic?

Keberhasilan reperfusi:
Nyeri dada berkurang
ST segmen normal
Puncak cardiac marker lebih cepat dari
seharusnya

STEMI

Terapi fibrinolitik direkomendasikan diberikan dalam 12 jam sejak

awitan gejala pada pasien-pasien tanpa indikasi kontra apabila IKP
primer tidak bisa dilakukan oleh tim yang berpengalaman dalam 120

FIBRINOLYTIC THERAPY

COMPLICATION

Thank You

TUJUAN
TERAPI
Mengatasi
&
mencegah
serangan
akut

Pencegahan
jangka
panjang
serangan
angina
Meningkatkan
toleransi pasien
terhadap latihan

ANTI ANGINA
Nitrat
organik
NO
menstimula
si
guanilat
siklase

Kadar C
GMP
Defosforilasi
Isosorbid dinitrat
miosin
Nitrogliserin

Relaksasi
otot polos

Bloker

frekuensi,kontraktili
tas
dan
tekanan
darah

tegangan dinding
Cardioselective

ventrikel

Bisoprolol,
Mengurangi
suplai
Antagonis
kalsium
Metoprolol
oksigen miokard
Hambat
ion
masuk ke sel

Ca

Kronotropik
dan
inotropic negative

Verapamil,

Prioritas kardiologi
preventif

Pasien penyakit jantung koroner / penyakit ater

Individu sehat yang beresiko tinggi PJK karena k

faktor resiko : merokok, tekanan darah tinggi, k
peningkatan kadar glukosa darah,
riwayat keluarga PJK,
hipertensi atau DM
Keluarga dekat pasien PJK /
penyakit aterosklerosis
pada usia muda
Individu lain yang ditemukan
pada praktek sehari-hari
46

Referensi
Rhee JW, Sabatine MR, Lily LS. Et al. Atherosclerosis,
Ischemic Heart Disease, Acute Coronary Syndrome in
Pathophysiology of Heart Disease.. 2011
Nabel EG, Braundwald E. A tale of Coronary Artery
Disease and Myocardial Infarction in New England
Journal of Medicine. 2012
O Connor RE, Brady W, Brooks SC, et al. Acute
Coronary Syndrome: 2010 American Heart Association
Guidelines for Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care. Circulation. 2010
2013 ACCF/AHA Guideline for the Management of STElevation Myocardial Infarction.
ESC Guidelines for the management of acute coronary
syndromes in patients presenting without persistent
ST-segment elevation. European Heart Journal. 2011
Myrtha R. Patofisiologi Sindrom Koroner Akut. CDK-192/
vol.39 no 4 th 2012

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And now what?

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