PATOFISIOLOGI

SINDROMA KORONER
AKUT
Mampu membedakan secara patofisiologi:
Spektrum penyakit jantung koroner
nyeri dada non kardiak
angina pektoris stabil
angina pektoris tidak stabil
angina pektoris khas infark miokard
Patofisiologi thrombus jalur agregasi platelets dan
koagulasi
Perjalanan Aterosklerosis
Sel Fatty Lesi Fibrous Ruptur Lesi
Busa streaks Intermediate Atheroma plaque kompleks

Disfungsi Endotel
Dekade ke 1 Dekade ke 3 Dekade ke 4

Progresifitas tu. akumulasi lipid Sel otot Thrombosis

polos & hematoma
Kolagen
Perjalanan Penyakit Kardiovaskular

Victor J. Dzau et al. Circulation. 2006;114:2850-2870

Patofisiologi SKA of ACS
Evolusi Thrombosis koroner
Pathofisiologi of Angina stabil dan SKA

Patofisiologi SKA

Penurunan Pasokan O2
stenosis yang menggangu aliran

Asimptomatik
Anemia
Plaque rupture/clot

Angina
Peningktan kebutuhan O2

O2 pasokan/kebutuhan tidak seimbang

Ischemia

Myocardial ischemianecrosis
Rhee JW, Sabatine MS, Lilly LS: Ischemic heart disease. In Lilly LS. Pathophysiology of heart disease, 5th ed. Philadelphia, Lippincott Williams & Wilkins,
Wolters Kluwer, 2011, pp 137.
 Morrow, David A.,
Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 54, 1182-1244
Dampak dari Iskemia

Morrow, David A.,

Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 54, 1182-1244
Angina Pektoris Tidak stabil

Morrow, David A.,

Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 54, 1182-1244
Sindrom koroner Akut
Masalah Pasokan
c

Morrow, David A.,

Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 54, 1182-1244
 Normal
Lumen paten
Fungsi endotel normal
Agregasi platelet (-)

Angina
stabil Diameter lumen sempit
karena plak
Vasokonstriksi yang tidak
normal

Angina
Tidak Plak pecah
Stabil Agregasi platelet
Pembentukan trombus
Vasokonstriksi

Angina
variant Plak (-)
Vasospasme

Rhee JW, Sabatine MS, Lilly LS: Ischemic heart disease. In Lilly LS. Pathophysiology of heart disease, 5th ed. Philadelphia, Lippincott Williams & Wilkins,
Wolters Kluwer, 2011, pp 145.
Efek Nitrat

Morrow, David A.,

Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 54, 1182-1244
Nyeri dada non Kardiak
Dengan peningkatan kebutuhan oksigen keluhan tidak
bertamabah atau bahkan hilang
.
ENZIM JANTUNG SEBAGAI
PENANDA IMA
Creatine Kinase-Myocardial band (CK-MB)
Troponin I dan Troponin T
Creatine Kinase (CK)
Aspartate amino transferase (AST)
Lactate dehydrogenase (LDH)
Myoglobin
Cardiac troponin
Penanda kerusakan/nekrosis otot jantung
Troponin lebih spesifik daripada CKMB
Troponin mulai meningkat jam ke-4 pasca onset dan
bertahan sampai 2 minggu di dalam darah
High sensitive troponin sudah mulai banyak digunakan,
yang mampu mendeteksi kadar sangat rendah sehingga
dapat mendiagnosis IMA lebih awal
ESC
2007
 Thrombus
formation
Pathway

Roffi M, et.al.Task Force for the Management of ACS

in Patients Presenting without Persistent ST-Segment Elevation of
the European Society of Cardiology (ESC). 2016;37:267-315.
Unstable
NSTEMI STEMI
Angina
Non-occlusive
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
SKA dengan elevasi SKA tanpa elevasi
segmen ST persisten segmen ST persisten
STEMI N- STEMI
1. REPERFUSION 1. Anti - Ischemia

2. Anti - Thrombotic 2. Anti - Thrombotic

3. Anti - Ischemia 3. Revascularization

Fungsi ventrikel kiri - lemah Fungsi Ventrikel Kiri - Normal
Gagal jantung
Jalur pembentukan Thrombus
Pilihan Reperfusi untuk Total Oklusi
Pharmacotherapy
Medical/ fibrinolysis
Streptokinase
alteplase
Mechanical Therapy
Primary PCI

Facilitated PCI
fibrinolysis + GPIIb IIIa + immediate PCI
Full fibrinolysis + immediate PCI
Full GPIIb IIIa + immediate PCI
Pharmacoinvasive
Full fibrinolysis + PCI 3-24 hr
Rescue
 Time = Muscle
The goal of reperfusion is to salvage as much myocardium as possible, as quickly as possible.

100
As reperfusion is delayed,
additional myocardium is damaged
Mortality Reduction, %

80
With increasing myocardial
60 damage, patient outcomes worsen

40

20
Extent of
Myocardial Salvage
0
0 4 8 12 16 20 24
Time From Symptom Onset to Reperfusion Therapy, Hours
Critical time-dependent period Time-independent period
Goal: myocardial salvage Goal: open infarct-related artery

27
Animation. Gibson. 2002.
Adapted from Gersh BJ, et al. JAMA. 2005;293:979.
 Saat Nyeri
datang dada

Diagnosa Sindroma koroner akut

Kerja

Persistent abnormalitas EKG Normal

ECG ST-elevasi ST/T Atau tidak jelas

Diagnosa STEMI NSTEMI/ UAP

Troponin Troponin
Bio-kimia
naik /turun normal

Unstable
Diagnosis STEMI NSTEMI
Angina