C h a p t e r 1 9
Disorders of Cardiac Function
449
Vessel Compression.
The large
coronary arteries lie on the epicar-
dial surface of the heart, with the
smaller intramyocardial vessels
branching off and moving through
the myocardium before merging
with a plexus of vessels that sup-
ply the subendocardial muscle with
blood. During systole, the contract-
ing cardiac muscle has a squeezing
effect on the intramyocardial ves-
sels while at the same time produc-
ing an increase in intraventricular
pressure that pushes against and
compresses the subendocardial ves-
sels. As a result, blood flow to the
subendocardial muscle is greatest
during diastole. Because the time
spent in diastole becomes shortened
as the heart rate increases, myo-
cardial blood flow can be greatly
reduced during sustained periods of
tachycardia.
3
Coronary artery
Epicardium
Endocardium
Intramyocardial
coronary vessels
Intramyocardial
coronary vessels
Subendocardial
plexus
Subendocardial
plexus
Muscle
contraction
Muscle
relaxation
Systole
Diastole
Flow
These currents of injury are represented as a deviation
of the ST segment on the ECG. When the acute injury is
transmural, the overall ST vector is shifted in the direc-
tion of the outer epicardium, resulting in an elevation of
the ST segment (see Fig. 19-3). When the injury is con-
fined primarily to the subendocardium, the ST vector is
shifted toward the inner ventricular layer, resulting in an
overall depression of the ST segment. Additional ven-
tricular depolarization (QRS) changes may follow the
T-wave and ST-segment abnormalities.
11,13
With actual
infarction, depolarization (QRS) changes often follow
the T-wave and ST-segment abnormalities.
Serum Biomarkers
Serum biomarkers for ACS, referred to as a cardiac panel,
include cardiac-specific troponin I (TnI) and troponin T
(TnT), creatine kinase MB (CK-MB), and myoglobin.
12,14
As myocardial cells become necrotic, their intracellular
contents diffuse into the surrounding interstitium and
into the blood. The rate at which the enzymes appear in
the blood depends on their intracellular location, molec-
ular weight, and local blood flow. For example, they
may appear at an earlier-than-predicted time in patients
who have undergone successful reperfusion therapy.
The
troponin assays
have high specificity for myo-
cardial tissue and are the primary biomarker tests for
the diagnosis of MI. The troponin complex, which is
part of the actin filament, consists of three subunits
(i.e., TnC, TnT, and TnI) that regulate the calcium-
mediated actin–myosin contractile process in striated
muscle (see Chapter 1, Fig. 1-19). Troponin I and tro-
ponin T, which are present in cardiac muscle, begin to
rise within 3 hours after the onset of myocardial infarc-
tion and may remain elevated for 7 to 10 days after the
event. This is especially useful in the late diagnosis of
MI.
12
Creatine kinase
is an intracellular enzyme found
in muscle cells. There are three isoenzymes of CK, with
the MB isoenzyme being highly specific for injury to
myocardial tissue. Serum levels of CK-MB exceed nor-
mal ranges within 4 to 8 hours of myocardial injury
and decline to normal within 2 to 3 days.
12
Myoglobin
is an oxygen-carrying protein, similar to hemoglobin,
expressed in cardiac and skeletal muscle. This small
molecule is released quickly from infarcted myocardial
tissue, and elevated levels can be detected in the blood
within 1 hour after myocardial cell death with peak lev-
els reached within 4 to 8 hours.
12
Because myoglobin is
present in both cardiac and skeletal muscle, this mol-
ecule is not specific to cardiac injury.
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