Accumulation of excess LDL beneath the endothelium Oxidized and produces

free radicals

Migration of macrophages in response to cytokine produced by endothelial cells

Trigger local inflammation
Macrophages engulf and accumulates with fat droplets called foam cells
Forms fatty streak beneath the vascular lining

Later migration and proliferation of smooth muscles from tunica media around
the accumulated lipid Atheroma

Area around the plaque degenerate and triggers the fibroblasts to produce
excessive CT over the plaque Scelrosis

Angina

Shortness of breath.
Palpitations (irregular heart beats,
skipped beats, or a "flip-flop" feeling
in your chest)
A faster heartbeat.
Weakness or dizziness.
Nausea.

Age
Sex
Family history
Smoking
High blood pressure
High blood cholesterol levels
Diabetes
Obesity
Physical inactivity
High stress

Sometimes coronary artery disease

develops without any classic risk
factors. Researchers are studying
other possible factors, including:

Sleep apnea.
High triglycerides
Lipoprotein

Source: Peter Libby and Pierre Theroux, Pathophysiology of Coronary Artery Disease 2005

Asymptomatic Phase (compensatory enlargement)

- Preventative therapy
1). Aspirin: Inhibit platelet aggregation
2). Statin: Reduce cholesterol synthesis
3). ACE inhibitor: Vasodilation (decrease BP and oxygen demand of heart)

Stable Angina with stenotic lesion (no positive remodeling)

- Anti-ischemia therapy
Nitroglycerin: Relaxes vascular smooth muscle
(Vasodilation)
Beta blocker & Calcium channel blocker: Reducing HR,
contractility and so will the oxygen requirement
- Reperfusion therapy: Aim to restore blood flow
Coronary bypass graft: Surgical procedure in which
artery or vein is grafted to provide alternative blood supply
Percutaneous coronary intervention: Non-surgical
procedure in which the narrow artery is enlarge

Involves non-stenotic lesion susceptible to rupture and

thrombosis Unstable Angina or MI
- Anti-platelet and Anti-thrombotic therapy: To prevent
thrombus propagation and stabilize vulnerable plaque
Aspirin & Glycoprotein IIb/IIIa inhibitors: Inhibit platelet
aggregation
Unfractionated heparin & Clopidogrel: Inhibit blood clot

- Blood test: Test for specific protein

> Myoglobin : Heme protein in cardiac muscle (early
marker), Elevated 1 hrs after infarction, return to baseline in
24 hrs
> Creatine Kinase/Creatine kinase-MB (CK/CKMB):
Comprises about 40 % of CK activity in cardiac muscles,
Elevated 2-4 hrs after infarction, return to baseline in 2-3
days
> Cardiac troponin (I or C): Proteins of thin filament
useful after 48 hrs onset, cardiospecific , Elevated 4-9 hrs
after infarction, return to baseline in 7-14 days
- Cardiac stress test: Measure heart respond to stress
(induced by exercise or drug), used for detection of
ischemia or prognosis of MI

- Stages in Myocardial Infarction: Blood supply is cut off

Reduce perfusion to tissues (ischemia) Injury to affect area
and necrosis Recovery with the formation of scarred tissue
(fibrosis)
Ischemia: Symmetrical T wave inversion or elevation and ST
segment elevation or depression
Injury: ST segment elevation or depression
Necrosis: Abnormal Q waves
Fibrosis: Persistent Q wave with normal ST segment and T
wave

http://www.surgeryencyclopedia.com/A-Ce/Cardiac-MarkerTests.html
http://www.nhlbi.nih.gov/health/healthtopics/topics/cad/diagnosis.html
Pathophysiology of Coronary Artery Disease, Author: Peter Libby
and Pierre Theroux, Journal of American Heart Association,
2005;111:3481-3488
Human Physiology From Cells to Systems 7 edition, Lauralee
Sherwood, Pg 333-335