Myocardial Infarction

Unstable Angina
Pericarditis
Pathogenesis of Chest Pain

Normal coronary arteries mediate changes in

coronary blood flow in response to changes in
myocardial oxygen demand (MV0 2 ).
When the demands of the heart increases (during
exercise)

the coronary arteries dilate to allow

increased blood flow to meet these
demands
Pathogenesis of Chest Pain

When a coronary artery

becomes narrowed by greater
than 70%, its blood flow is
by approximately 90%.
Pathogenesis of Chest Pain

In this setting, maximal coronary vasodilation

occurs and allows for enough blood flow to
meet the metabolic demands of the resting
heart

However, during periods of increased myocardial

demand (exercise), the artery is unable to dilate further,
resulting in inadequate coronary blood
flow and ischemia
Pathogenesis of Chest Pain
caused by
Reduction in oxygen supply
Increase in myocardial oxygen demand
superimposed on an atherosclerotic
coronary plaque, with varying degrees
of obstruction
Four pathophysiologic processes
1. Plaque rupture or erosion with
superimposed nonocclusive
thrombus
the most common cause
2. Dynamic obstruction
Coronary spasm
(Prinzmetal's variant angina)
3. Progressive mechanical
obstruction
Rapidly advancing coronary
atherosclerosis or restenosis
following percutaneous coronary
intervention
4. Secondary UA related to
increased myocardial oxygen
demand and/or decreased supply
Tachycardia, anemia
 Fissue or
ruptures Tissue factor
plaque is released
Coronary exposure of with the
atheroscleros Crack or sub- arterial injury
is an essential fissure in the endothelial ext Occlusive
part of the diseased matrix coagulation thrombus
process in arterial wall elements cascade and
most patients platelet promotes
activation and formation of
thrombus fibrin
formation
 , the 2 layers of the
pericardium are separated by a pericardial
space that contains 50 mL of clear fluid
The fluid lubricates the pericardium and
prevents friction between the two layers
during caridiac contraction
Pericarditis is marked by
infiltration of the
pericardium by
polymorphonuclear
leukocytes with eventual The inflamed pericardial layers
deposition of fibrin in the rub against each other during
pericardial space each cardiac contraction, often
resulting in pain and an audible
friction rub