C h a p t e r 1 9
Disorders of Cardiac Function
447
of the lipid core, smooth muscle cells, macrophages, and
collagen. The lipid core provides a stimulus for plate-
let aggregation and thrombus formation.
6
Both smooth
muscle and foam cells in the lipid core contribute to the
expression of tissue factor in unstable plaques. Once
exposed to blood, tissue factor initiates the extrinsic
coagulation pathway, resulting in the local generation
of thrombin and deposition of fibrin (see Chapter 12).
Platelets are critical to the events following plaque
disruption in acute CAD. Platelets adhere to the endo-
thelium and release substances (i.e., adenosine diphos-
phate [ADP], thromboxane A
2
, and thrombin) that
promote further aggregation of platelets and thrombus
formation. Glycoprotein receptors expressed on the
platelet surface bind fibrinogen and cross-link platelets,
contributing to thrombus formation. Platelet adhesion
and aggregation occurs in several steps. First, release
of ADP, thromboxane A
2
, and thrombin initiates the
aggregation process. Second, activation of glycoprotein
IIb/IIIa receptors on the platelet surface occurs. Third,
fibrinogen binds to the activated glycoprotein receptors,
forming bridges between adjacent platelets.
Acute Coronary Syndrome
Acute coronary syndrome (ACS) represents a spectrum
of acute ischemic heart diseases ranging from unstable
ischemia to acute MI based on the presence or absence of
an ST-segment elevation or depression on the ECG.
11,12
This criterion allows for immediate classification of
risk and guides whether a person should be considered
for acute reperfusion therapy. The evaluation of serum
biomarkers (e.g., troponin I) is then used to determine
whether an acute MI has occurred.
Electrocardiographic Changes
The classic ECG changes that occur with ACS include
ST-segment elevation, T-wave inversion, and development
of an abnormal Q wave
11,12
(Fig. 19-3). These changes
may not be present immediately after the onset of symp-
toms and vary considerably depending on the duration of
the ischemic event (acute versus evolving), its extent (sub-
endocardial versus transmural), and its location (anterior
versus inferior posterior). Because these changes usually
occur over time and are seen on the ECG leads that view
the involved area of the myocardium, provision for con-
tinuous and serial 12-lead ECG monitoring is indicated.
The T wave and ST segment, which represent the
ventricular repolarization phase of the cardiac action
potential on the ECG, are usually the first to be involved
during myocardial ischemia and injury.
13
During myo-
cardial ischemia, repolarization is altered as the involved
area becomes ischemic. This leads to T wave abnormali-
ties, such as T-wave inversion. ST-segment changes also
occur with acute ischemic myocardial injury. Normally,
the ST segment of the ECG is nearly isoelectric (i.e., does
not deviate from the baseline) because healthy myocar-
dial cells attain the same resting membrane potential
during early repolarization. Acute ischemia reduces the
resting membrane potential and shortens the duration of
the action potential of the cells within the ischemic area.
The voltage difference in the cell membranes between
the normal and ischemic areas of the myocardium
leads to a “current of injury” between these regions.
FIGURE 19-2.
Atherosclerotic
plaque.
(A)
Stable fixed
atherosclerotic plaque in stable
angina and
(B)
unstable plaque
with plaque disruption and
platelet aggregation in the acute
coronary syndromes.
Adventitia
Media
Intima
Lumen
Stable angina
Asymptomatic
atherosclerotic
plaque
Stable fixed
atherosclerotic
plaque
A
Plaque disruption
and platelet aggregation
Unstable angina
Non–ST-segment
elevation MI
ST-segment
elevation MI
Unstable
plaque
Thrombus
Acute coronary syndromes
B
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