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U N I T 5
Circulatory Function
Unstable Angina/Non–ST Elevation
Myocardial Infarction
Unstable angina/non–ST elevation myocardial infarc-
tion (UA/NSTEMI) is a clinical syndrome of myocardial
ischemia ranging from angina to myocardial infarc-
tion.
14–16
Typically, unstable angina and NSTEMI differ
in whether the ischemia is severe enough to cause suf-
ficient myocardial damage to release detectable quan-
tities of serum cardiac markers. Persons who have no
evidence of serum markers for myocardial damage are
considered to have unstable angina, whereas a diagnosis
of NSTEMI is indicated when there are detectable serum
markers of myocardial injury.
The pain associated with unstable angina typically
has a persistent and severe course and is characterized
by at least one of three features: (1) it occurs at rest
(or with minimal exertion), usually lasting more than
20 minutes if untreated (i.e., without nitroglycerine); (2)
it is severe and described as frank pain and of new onset
(i.e., within 1 month); and (3) it is more severe, pro-
longed, or frequent than previously experienced.
16
The risk of acute MI in an individual diagnosed with
UA/NSTEMI is classified as low, intermediate, or high
based upon the clinical history, ECG pattern, and serum
biomarkers. The ECG pattern associated with in NSTEMI
may display normal or ST-segment depression (or tran-
sient ST-segment elevation) and T-wave changes. The
degree of ST-segment deviation from baseline is an impor-
tant measure of ischemia and indicator of prognosis.
ST Elevation Myocardial Infarction
Acute ST elevation MI (STEMI) is characterized by the
necrosis of myocardial tissue and a consequence of ath-
erosclerotic disease of the coronary arteries. The specific
area of infarction is determined by the affected coronary
artery and its distribution of blood flow (Fig. 19-4).
Pathologic Changes.
The size and pattern of the
infarct depends on the location and extent of occlusion,
amount of heart tissue supplied by the vessel, duration
of the occlusion, metabolic needs of the affected tissue,
extent of collateral circulation, and other factors such
as heart rate, blood pressure, and cardiac rhythm. An
infarct may involve the endocardium, myocardium, or
epicardium, or a combination of these tissue layers.
6
Transmural infarcts involve the full thickness of the ven-
tricular wall and most commonly occur when there is
obstruction of a single artery (Fig. 19-5). Subendocardial
infarcts involve the inner one third to one half of the
ventricular wall and occur more frequently in the pres-
ence of severely narrowed but still patent arteries.
The principal biochemical consequence of MI is the con-
version from aerobic to anaerobic metabolism with inad-
equate production of energy to sustain normal myocardial
function.
18
As a result, a striking loss of contractile function
occurs within 60 seconds of onset.
6
Changes in cell struc-
ture (i.e., glycogen depletion and mitochondrial swelling)
develop within several minutes. These early changes are
reversible if blood flow is restored. Although gross tissue
changes are not apparent for hours after the onset of MI,
the ischemic area ceases to function within a matter of min-
utes, and damage to cells occurs in approximately 40 min-
utes. Irreversible myocardial cell death (necrosis) occurs
after 20 to 40 minutes of severe ischemia
6
(Fig. 19-6).
The term
reperfusion
refers to the reestablishment
of blood flow using fibrinolytic therapy or revascular-
ization procedures. Early reperfusion after onset of
occlusion can prevent necrosis and improve myocar-
dial perfusion in the infarct zone. Reperfusion after a
A
B
A
B
C
P
T
U
Q
S
R
ST elevation
ST
ST
V
5
ST
ST
V
5
Subendocardial injury:
ST depression
Transmural (epicardial) injury:
ST elevation
Almost
4 mm
1 mm
wide
FIGURE 19-3.
(Top)
(A)
Electrocardiogram tracing
showing normal P, Q, R, S,
andT waves.
(B)
ST-segment
elevation with acute ischemia.
(C)
Q wave with acute myocardial
infarction. (Bottom) Current-
of-injury patterns with acute
ischemia.
(A)
With predominant
subendocardial ischemia,
the resultant ST segment is
directed toward the inner layer
of the affected ventricle and the
ventricular cavity. Overlying leads
therefore record ST-segment
depression.
(B)
With ischemia
involving the outer ventricular
layer (transmural or epicardial
injury), the ST vector is directed
outward. Overlying leads record
ST-segment elevation. (Bottom
from Zipes DP, Bonow RO, Mann
DL, et al., eds. Heart Disease:
ATextbook of Cardiovascular
Medicine. 8th ed. Philadelphia,
PA: Saunders Elsevier; 2008:174.)
