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