Cardiac Enzyme Studies

Lactic Acid Dehydrogenase (LDH), CK (Creatine Kinase), CPK (Creatine

Phosphokinase), Creatine Kinase (CK), Creatine Phosphokinase (CPK), Creatine
Phosphokinase!" #soenzyme (CPK!"), Heart Attack Enzymes, LDH$ (Lactate
Dehydrogenase #soenzymes)
Test Overview
Cardiac enzyme studies measure the %e&e%s o' the enzyme creatine phosphokinase (CPK, CK) and
the protein troponin ((n#, (n() in the )%ood* Lo+ %e&e%s o' these enzymes and proteins are norma%%y
'ound in your )%ood, )ut i' your heart musc%e is in,ured, such as 'rom a heart attack, the enzymes and
proteins %eak out o' damaged heart musc%e ce%%s, and their %e&e%s in the )%oodstream rise*
"ecause some o' these enzymes and proteins are a%so 'ound in other )ody tissues, their %e&e%s in the
)%ood may rise +hen those other tissues are damaged* Cardiac enzyme studies must a%+ays )e
compared +ith your symptoms, your physica% e-amination 'indings, and e%ectrocardiogram (EK.,
EC.) resu%ts*
Troponin (TnI and TnT)
/orma%0 TnI0 Less than 1*2 micrograms per %iter (mcg3L)
TnT0 Less than 1*$ mcg3L
A)norma%0 E%e&ated troponin may )e present +hen you ha&e heart musc%e in,ury* "%ood
%e&e%s o' troponin typica%%y rise +ithin 4 to 5 hours a'ter a heart attack, reach
their highest %e&e%s +ithin $1 to 64 hours, and 'a%% to norma% %e&e%s +ithin $1
days*
Total CPK (creatine phosphokinase)
/orma%0 !en0 778$91 internationa% units per %iter (#:3L)
;omen0 218$27 #:3L
A)norma%0 CPK %e&e%s genera%%y rise +ithin 4 to < hours a'ter a heart attack, reach their
highest %e&e%s +ithin $6 to 64 hours, then return to norma% +ithin 2 to 4 days*
CPK-MB
/orma%0 Less than 2*1 nanograms per mi%%i%iter (ng3mL) (1= o' tota% CPK)
A)norma%0 CPK!" is 'ound in %arge amounts in the heart musc%e* A CPK!" greater than
2*1 ng3mL may )e present +hen you ha&e musc%e damage caused )y a heart
attack* "%ood %e&e%s o' CPK!" typica%%y rise +ithin 6 to 5 hours a'ter a heart
attack, reach their highest %e&e%s +ithin $6 to 64 hours, and 'a%% to norma% %e&e%s
+ithin 2 days*
An ongoing high %e&e% o' CPK!" %e&e%s a'ter 2 days may mean that a heart
attack is progressing and more heart musc%e is )eing damaged*
What Affects the Test
1
>easons you may not )e a)%e to ha&e the test or +hy the resu%ts may not )e he%p'u% inc%ude0
?ther diseases, such as muscu%ar dystrophy, certain autoimmune diseases, and >eye@s
syndrome*
?ther heart conditions, such as myocarditis and some 'orms o' cardiomyopathy*
Emergency measures to treat heart pro)%ems, such as CP>, cardio&ersion, or de'i)ri%%ation*
!edicines, especia%%y in,ections into musc%es (#! in,ections)*
Cho%estero%%o+ering medicines (statins)*
Hea&y a%coho% use*
>ecent strenuous e-ercise*
Kidney 'ai%ure*
>ecent surgery or serious in,ury*
Tests for cardiac enzymes and protein
Name of test How soon does the test
show evidence of a
heart attack?
How long after a
heart attack are
results reliable?
How useful is the test
in diagnosing a heart
attack?
Troponin (T or I) 46 hours after the heart
attack begins
1014 days Very useful
Creatine kinase !"
fraction (C#$!)
41% hours after the
heart attack begins
1& days Very useful
yoglobin %4 hours after the heart
attack begins
%& days 'o(e)hat useful
*actate dehydrogenase
(*+,)
%4%4 hours after the
heart attack begins
-10 days .ot /ery useful
0spartate
a(inotransferase (0'T)
1%%4 hours after the
heart attack begins
&- days .ot /ery useful
Cardiac Troponins
Troponins are protein components of striated muscle. There are three different troponins:
troponin C, troponin T and troponin I. Troponins T and I are only found in cardiac muscle
o Troponin T (1)
84% sensitivity for myocardial infarction 8 hours after onset of symptoms
(1) 81% specificity (1)
lo! specificity " ##% for unsta$le an%ina
advanta%es
hi%hly sensitive for detectin% myocardial ischaemia
levels may help to stratify ris& after!ard
o Troponin I
'(% sensitivity for myocardial infarction 8 hours after onset of symptoms
(1) ')% specificity (1)
lo! specificity for unsta$le an%ina " *+% " note ho!ever that there is
evidence that (#)
2
troponin I elevation is useful for predicting in-hospital risk for unstable
angina patients admitted to a community hospital. The association of
ECG changes and high troponin I identifies a population at very high
risk ho!ever" the absence of both variables in patients !ith a
diagnosis of unstable angina does not preclude the development of
events
rises after *"+ hours (1)
pea&s at a$out #( hours (1)
%eneral advanta%es (*)
o troponin T (cTnT) and troponin I (cTnI) are released only follo!in% cardiac dama%e
C, and C,"-. are found in s&eletal muscle as !ell as cardiac muscle "
therefore if there is dama%e to s&eletal muscle, elevations of C, and C,"
-. !ill occur and can ma&e the dia%nosis of myocardial infarction difficult.
In such a situation levels of cTnT and/or cTnI !ill not rise unless
myocardial infarction has occurred
o troponin T and I are present for, and remain elevated, a lon% time
unli&e C, and C,"-., cTnT and cTnI are released for much lon%er !ith
cTnI detecta$le in the $lood for up to ) days and cTnT for 0"1( days
follo!in% -I. This allo!s an -I to $e detected if the patient presents late.
1or e2ample, if a patient comes to the sur%ery !ith a history of chest pain
#"* days a%o, measurement of cTnT or cTnI !ill allo! the dia%nosis or
e2clusion of -I as a cause of the chest pain
o troponin T and I are very sensitive
there is al!ays a lo! level release of C, and C,"-. from s&eletal muscle
at a lo! level all the time so there is al!ays a $ac&%round value. This is
not the case for the cardiac structural proteins such as cTnT and cTnI and
therefore, they are very sensitive. 3tudies have revealed that a$out one
third of patients admitted !ith unsta$le an%ina, in !hom -I !as
apparently e2cluded $y C, and C,"-. measurement, have raised levels of
cTnT and cTnI. 1ollo! up studies have revealed that these patients are at
si%nificantly %reater ris& of death, su$se4uent -I or readmission !ith
unsta$le an%ina than patients !ho did not have detecta$le levels cTnT or
cTnI
%eneral disadvanta%es (*)
o elevation of cTnT or TnI is a$solutely indicative of cardiac dama%e, $ut this can
occur as a result of causes other than -I e.%. myocarditis, coronary artery spasm
from cocaine, severe cardiac failure,cardiac trauma from sur%ery or road traffic
accident, and pulmonary em$olus can cause cardiac dama%e !ith an
accompanyin% elevation of cardiac troponin(s)
o failure to sho! a rise in cTnT or cTnI does not e2clude the dia%nosis of ischaemic
heart disease
o $oth cTnT and cTnI may $e elevated in patients !ith chronic renal failure and
indicate a hi%her lon%"term ris& of death. They can $e distin%uished from chan%es
due to myocardial infarction $y repeatin% the tests. -yocardial infarction causes a
rise and fall in cTnT or cTnI, $ut in renal failure the elevated levels are sustained
o reference ran%es may vary $et!een la$oratories and are dependent on methods of
measurement used
#eference$
1. 5$ell -6 et al (#(((). 7 systematic revie! of troponin T and I for dia%nosin% acute
myocardial infarction. 8 1am 9ract, 4', ))("+.
2. :ev 5sp Cardiol #((# 1e$))(#):1(("1(+ ;Is Troponin I <seful for 9redictin% In"6ospital
:is& for <nsta$le 7n%ina 9atients in a Community 6ospital= :esults of a 9rospective 3tudy.
.odi > >, 3anchis 8, ?lacer 7, @raells -?, ?lorca ?, Chorro 18, Insa ?A, Bavarro 7, 9lancha
5, Cortes 18, 9once Ae ?eon 8C, >alls 7
%
.ritish 6eart 1oundation (1actfile (8/#((*). Chat are cardiac troponins=
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