PATOFISIOLOGI DAN MEKANISME

SINDROM KORONER AKUT

Bambang Rahadi
 Cardiac Function

• Size of a fist
• Beats : 100.000 times/day
• Pumsp 7500L of blood/day
• Requires Oxygenated blood
( provided through coronary
arteries)
 Faktor-faktor utama suplai dan demand
oksigen miokard
Suplai Oksigen Miokard Kebutuhan Oksigen
Miokard

Kandungan Oksigen Beban

VKi
Aliran Darah Koroner
• Tekanan perfusi koroner
• Resistensi vaskular koroner Laju Nadi
• Regulasi intrinsik
• Metabolit lokal
• Faktor endotel
• Persyarafan Kontraktilitas

Rhee JW, Sabatine MS, Lilly LS: Ischemic heart disease. In Lilly LS. Pathophysiology of heart disease, 5 th ed.
Philadelphia, Lippincott Williams & Wilkins, Wolters Kluwer, 2011, pp 137.
 Supply and demand coronary reperfussion
missmatch due to CAD

Within 10 seconds myocardial cells

experience ischemia

Ischemic cells cannot get enough oxygen or glucose

Decreased electrical & muscular function

Anaerobic metabolism and produce lactic acid as waste

Pain develops from lactic acid accumulation

ANGINA SYMPTOM
Mechanism of Cell death in MI
The Cause of ACS
 ENDOTHELIUM

• Barrier between blood and arterial wall

• Prevents toxic, blood-born substances from
penetrating the artery wall
• Dilatation, constriction
 Endothelial Dysfunction

• Promotes and worsens atherosclerosis

• Aggravated by risk factors for heart disease
 Endothelial Damage

• Triggered by :
– High cholesterol
– High BPSmoking
– Immune Injury
– Obesity
– Diabetes
Evolution of Atherosclerosis Plaque
Different Stage of Atherosclerosis Development
Vulnerable Plaque
Mechanisms of coronary thrombus formation
Consequences of Coronary Thrombosis
 Atherosclerosis –Atherothrombosis A Generalized
And Progressive Disease
Atherothrombosis

Unstable
angina ACS
NSTEMI
Atherosclerosis Thrombosis STEMI

CV death

Stable angina
Adapted from Libby P. Circulation. 2001;104:365-372
Plaque Rupture with thrombosis
Jalur Trombosis
Terima Kasih