Creatine Phosphokinase

The creatine phosphokinase (CPK) is unhelpful to make the initial diagnosis. It

takes at least 6 hours for there to be an enzyme “leak,” which denotes
myocardial cell
necrosis. Enzymes should be assessed every 8 hours for the first 24 hours, and
longer if the peak is not firmly established. The peak CPK occurs earlier when
there
has been successful reperfusion (eFig. 18.1.3) (39). This enzyme is much more
helpful in gauging the size of the MI than in making the diagnosis.

eFIGURE 18.1.3 Distribution of time to peak plasma creatine kinase (CK) activity
from onset of symptoms according to angiographic perfusion status for each of
the
three groups. (From Gore JM, Roberts R, Ball SP, et al. Peak creatine kinase as
a measure of effectiveness of thrombolytic therapy in acute myocardial infarction.
Am
J Cardiol 1987;59:1234–1238, with permission.)
Troponin T and I
More sensitive measures of myocardial necrosis have become available, which
have a similar obligatory lag in appearing in the blood (as CPK) but appear to
detect
cell damage more readily (40,41,42,43 and 44). The troponins are part of the
tropomyosin-binding protein of the contractile apparatus of cardiac myocytes and
therefore
are highly specific for cardiac origin. A rapid, bedside assay for troponin is
available and is a practical, rapid way to assess patients with ischemic symptoms
and
non–ST-segment elevation. The off-line quantitative assays of both troponin T
and I have been particularly helpful in differentiating risk, better than CPK, in
patients
with unstable angina and non–ST-elevation MI (Fig. 18.2). Both are extremely
promising for offering a more sensitive means of not only diagnosing whether
infarction
has occurred, but also discriminating the risk. However, the real utility of tests
such as troponin goes beyond the determination of risk level to favorably alter the
prognosis of the patient by knowledge of whether the test result is abnormal or
not. Indeed, responses of patients to either IIb/IIIa inhibitors or low-molecular-
weight
heparins are predicted by abnormal troponin. These sensitive markers should be
applied routinely for patients without ST-segment elevation. Troponins offer little
incremental value in classic ST-elevation MI.

FIGURE 18.2 A: Probability of death within 30 days according to the troponin T

level at hospital admission. Smoothed nonparametric estimates are shown. The
troponin T levels are plotted on a cube-root scale. The density of the data is
indicated at the top, with each mark representing one patient. The dots represent
simple
estimates of mortality derived from ranges of the troponin T level that contained
at least 70 patients. (From Ohman EM, Armstrong PW, Christenson RH, et al. for
the
GUSTO-IIa Investigators. Risk stratification with admission cardiac troponin T
levels in acute myocardial ischemia. N Engl J Med 1996;335:1333–1341, with
permission.) B: Sensitivity of troponin compared with creatine kinase-myocardial
band (CK-MB). Even in patients with a low CK-MB (less than 7.0 ng per mL), the
troponin T–positive patients (greater than 0.1 ng per mL) had a worse outcome
with respect to mortality. (Data from Ohman EM, Armstrong PW, Christenson RH,
et al.
for the GUSTO-IIa Investigators. Risk stratification with admission cardiac
troponin T levels in acute myocardial ischemia. N Engl J Med 1996;335:1333–
1341.)