Expansion
overcome :
lumen narrows
Diabetes Infection?
Atherothrosclerotic
American Heart Association. Heart and Stroke Facts: 1997 Statistical Supplement; Wolf. Stroke 1990;21(suppl 2):
II-4–II-6; Laurila et al. Arterioscler Thromb Vasc Biol 1997;17:2910-2913; Grau et al. Stroke 1997;28:1724-1729;
9 Graham et al. JAMA 1997;277:1775-1781; Brigden. Postgrad Med 1997;101(5):249-262.
Atherosclerosis Timeline
Foam Fatty Intermediate Atheroma Fibrous Complicated
cells streaks lesion plaque lesion rupture
Endothelial Dysfunction
From First Decade From 3rd decade From 4th decade
• Angina klasik
Rasa tidak enak di daerah substernal, sifatnya tumpul,
seperti ditekan / diperas, menjalar ke lengan kiri / leher,
dapat disertai kesulitan bernapas, berdebar-debar, keringat,
mual atau muntah
• Angina Equivalent
Tidak ada nyeri / rasa tidak enak
di dada yang khas,
namun pasien menunjukkan
gejala gagal jantung mendadak
(sesak napas),
atau aritmia ventrikular
(palpitasi, presinkop, sinkop)
Atherothrombosis: Thrombus Superimposed
on Atherosclerotic Plaque
Adapted with permission from Falk E, et al. Circulation. 1998;92:657-671. Slide reproduced with permission
from Cannon CP. Atherothrombosis slide compendium. Available at: www.theheart.org.
Atherothrombosis:
a Generalized and Progressive Process
Plaque Unstable
Athero-
Normal
Fatty
streak
Fibrous
plaque
sclerotic
plaque
rupture/
fissure &
thrombosis
angina
MI
}ACS
Ischemic
stroke/TIA
Critical leg
Clinically silent
ischemia
Stable angina
Intermittent claudication Cardiovascular
death
Increasing age
ACS, acute coronary syndrome; TIA, transient ischemic attack
Characteristics of Unstable and
Stable Plaque
Unstable Stable
Lack of
Inflammatory inflammatory
cells cells
Thin Thick
Few fibrous cap More fibrous cap
SMCs SMCs
Intact
Eroded endothelium
endothelium
Activated
macrophages Foam cells
Adapted with permission from Libby P. Circulation. 1995;91:2844-2850. Slide reproduced with permission from
Cannon CP. Atherothrombosis slide compendium. Available at: www.theheart.org.
Correlation between frequency of plaques, degree of
stenosis, and risk of complication per plaque as a
function of plaque progression
Although the average absolute risk of severely stenotic plaques may be higher than the average absolute risk of
mildly stenotic plaques, there are more plaques with mild stenoses than plaques with severe stenoses.
Thrombus Formation and ACS
Plaque Disruption/Fissure/Erosion
Thrombus Formation
Old
Terminology: UA NQMI STE-MI
20
Timing of Release of Various Biomarkers
After Acute Myocardial Infarction
Shapiro BP, Jaffe AS. Cardiac biomarkers. In: Murphy JG, Lloyd MA, editors. Mayo Clinic Cardiology: Concise Textbook. 3 rd ed. Rochester, MN:
Mayo Clinic Scientific Press and New York: Informa Healthcare USA, 2007:773–80. 22
Anderson JL, et al. J Am Coll Cardiol 2007;50:e1–e157, Figure 5.
Sequence of Events in Ischemic
Heart Disease
• Arrythmias
• Lost of muscle
• Angina MI
• Silent Ischemia
Remodeling
CAD
Progresif dilatation
Endothelial dysfunction
Heart Failure
Death
Risk Factor
Terimakasih
27