Coronary Artery Disease

Arief Santoso, S.farm., Apt.

Introduction
• CAD is the collective name for a number
of condition in which obstructive lession
of the coronary arteries restrict
myocardial blood flow
• It is also called “ischaemic heart disease”
• Ischaemia  “to hold back blood”
• The main clinical manifestasions are
angina pectoris and myocardial infarction
Epidemiology
• CAD is the greatest single cause of death,
especially premature death, in
industrialized society
• There were wide geoghraphic, ethnic,
and national variations in prevalence
Aetiology
• The etiology, pathology, and treatment
of CAD can best be understood in the
general context of vascular obstruction
(partial block) and occlusion (complete
block)
• The main chronic processes responsible
for chronic arterial obstruction are
arteriosclerosis and aterosclerosis
Clinical manifestasions of atherosclerosis
Risk factors

Atheroma

Atherosclerosis

Renal Peripheral Cerebral Coronary

Renovascular Peripheral rupture

disease vascular disease

Renal failure Claudication, Stroke

gangrene
Clinical manifestasions of atherosclerosis
Risk factors

Atheroma

Atherosclerosis

Cerebral Coronary
Dementia
CAD
rupture
Occlusion
Partial obstruction
(thrombosis)

Stroke Myocardial
Angina pectoris
infarction
 Risk factors
• Lipid hypothesis…???
Aetiology of atherosclerosis
• Vascular endothelial damage
• Abnormal flow
Pathophysiology of atherosclerosis
 Progression of Atherosclerosis

Alteration of endothelial function due to risk factors

Deposition and oxidation of LDL; fatty streak formation

Thickening of arterial wall; “remodeling” of artery

Formation of fibrous cap over lipid core

Stable plaque Unstable plaque

Increased growth Plaque rupture

Stenosis Thrombus/MI
The Healthy Endothelium
 The Dysfunctional Endothelium

Endothelial Leukocyt Endothelial Leukocyte

permeability e adhesion adhesion
migration
Ross R. N Engl J Med. 1999;340:115-126.
 Compensatory Enlargement of a Coronary
Artery

Progressio
n
Expansion
Compensatory overcome:
expansion lumen narrows
maintains constant
lumen

Normal Minimal Moderate Severe

vessel CAD CAD CAD

Glagov S et al. N Engl J Med. 1987;316:1371-1375.

 Vulnerable Plaque Is Prone to Rupture
Fibrous cap
Media
Lipi
d
Lumen core
area of
detail

“Vulnerable” plaque

Lumen – T lymphocyte
Lipi
d
– Macrophage
core foam cell (tissue factor+)
– “Activated” intimal SMC (HLA-DR+)
– Normal medial SMC

“Stable” plaque
Libby P. Am J Cardiol. 2000;86(suppl):3J-9J.
 Plaque Rupture Leads to Thrombus
Formation

Yeghiazarians Y et al. N Engl J Med. 2000;342:101-114.

Myocardial ischaemia
• Why the heart …???
– The myocardium has a high O2 demand
– The heart work continously
– There are relatively few coronary collateral
vessels
Angina pectoris
• Angina is both defined and diagnosed by
clinical criteria
• Typical ischaemic cardial pain is
retrosternal, intense, diffuse rather than
sharp, and griffing
• In classical angina pain comes on acutely
following exertion and is relieved within
a few minutes by resting or taking buccal
or sublingual GTN
Management
• There are 3 objevtives :
– To abolish the symptoms of an acute attack
– To prevent or minimize the frequency of
symptomatic or silent MI
– To reduce the progression of the underlying
atherosclerosis
Management
• Strategies
– Reducing O2 demand
– Improving O2 supply
– Prevent further obstruction
Management
• Reducing O2 demand
– Reduce cardiac workload
• Reduce perfusion demand  rest, avoid stress
• Reduce preload  venodilator
• Reduce afterload  arteriadilator
– Reduce rate / contractility  (-) inotrope
– Improve cardiac efficiency  improve fitness
Management
• Improve O2 supply
– Increase coronary flow
• Arteriadilator
• Surgery
Management
• Prevent further obstruction
– ↓ risk factors  diet, stop smoking
– Antiplatelets
– Lipid lowering agents
Management
• Acute attack
– GTN
– CCB
Management
• Prophylaxis
– Beta blockers
– CCB
– Nitrates
Myocardial infarction
• It occurs when a coronary vessel become
occlused for more than 6 hours whether
or not the occlusion is subsequently
relieved
• It is not simply an intensification of
angina
Diagnosis
• The diagnosis depends on significant
findings in at least 2 of 3 main areas
– Clinical presentation and history
– Progressive ECG changes
– Progressive serum enzyme changes
Management
• The aims in managing MI are :
– To act promptly to save life and reduce
complication
– To treat acute symptoms
– To minimize subsequent infacrt size
– To treat complications
Management
• Strategies
– Cardiac workload reduction
– Metabolic support
– Reperfusoin thrombolysis
Pertanyaan
• Aspirin
• Aspirin vs heparin
• Angina post infark Vs angina stabil
• Penggunaan verapamil …???
• Penggunaan aspirin vs HCT
 Pertanyaan
• Exercise ringan …???
• Clopidogrel ….???
• Atherosclerosis pada DM…???