Found in high concentrations in myocardium

Released rapidly after the onset of pain

Not to be found in other tissues in trace
amounts or under pathological conditions
Have a convenient diagnostic time window
Reflect as much as possible the evaluation of
myocardial damage
Some markers are unique to the heart.
This occurs in a fairly predictable manner for
serum cardiac markers, with a rise, peak, and
a fall over time.
Each marker tends to have a distinct kinetic
pattern in blood

Heart has a high concentration of a particular
cardiac marker in relationship to its
concentration in other organs or blood.
Following myocardial necrosis, dead cardiac
myocytes release their cellular contents into
blood after tissue reperfusion.
Elevated markers have become the
definitive diagnostic criteria for AMI

Enzymes
Total creatine kinase
Creatine Kinase from Heart (CK-MB)
Lactate Dehydrogenase Isoenzyme 1:2 ratio
(LD1:LD2)
Troponins
Myoglobin (heme protein)
catalyze the reaction of phosphocreatinine to
creatinine
important for energy utilization.
Most circulating CK is from muscle.
can be measured by one total enzyme or can
be separated into 3 isoenzymes
isoenzymes help to detect MI and muscular
diseases
Isoenzyme
CK-I(BB) CK-II (MB) CK-III
(MM)
produced by smooth
muscle, brain
tissue
heart tissue muscle
tissue
muscle 0% 2-3% 97-98%
brain 97-98% 10-15 % 85-90%
Enzymes will disappear from the
bloodstream.
CK may disappear in less than 36-48 hr after a MI.
Total CK
Female: 30-135 U/L
Male: 55-170 U/L
CK increased in the following:
Myocardial infarction
Progressive muscular dystrophy
Alcoholic myopathy
Hypothyroidism
Exercise
Intramuscular injection
Specific index of injury of myocardium and
muscle
Increased Serum CK
First enzyme to be elevated after a MI
Rise: 6-8 hrs
Peak: first 18-24 hrs
Duration: 4 days
Some patients returns to normal within 16 hrs
If CK is elevated then CK-MB taken.
CK MB
Chronic muscular dystrophies
Chronic renal failure
Lung disease exacerbation ( acute respiratory
exertion)
Protocol for Early Detection of AMI
Measure CKMB isoforms or Myoglobin
Catalyze the reversible oxidation of lactate to
pyruvate
LD activity is measured by monitoring
absorbance at = 340 nm (NADH)
Total LD activity has poor specificity
Several types of LDH isoenzymes (LDH 1-5)
Total LDH, LDH1 and LDH2 are used to detect MI.
LDH 1 and LDH 2: hemolytic and macrocytic
anemia
LDH 4 and LDH 5: liver damage
Rises: 12-14 hrs in MI
Peak: 36-48 (24) hours
Duration: 96-160 hours (10-14 days)
Serum LD: 30 IU/L

LD elevated in the following conditions:
Carcinomatosis
Severe shock
Hypoxia
myocardial infarction
Pulmonary infarction
Granulocytic leukemia
Infectious mononucleosis
Progressive muscular dystrophy
Isoenzyme Normal
serum
Heart
muscle
Liver Skeletal
muscle
LDH1 25 45 0 0
LDH2 35 40 5 0
LDH3 20 10 10 10
LDH4 15 5 15 30
LDH5 5 0 70 60
LD1/LD2, Post AMI
Increase: 8-12 hrs
LD1/LD2 1: 48-72 hrs
Return to normal: 8-14 days
Troponin is an important component of the
contractile machinery of skeletal and cardiac
muscle.
The troponin complex is located in the thin
filaments at intervals set by the length of a
tropomyosin unit.
Each troponin complex regulates the
interactions of 7 actin units.
During skeletal and cardiac muscle
contraction:
the binding of calcium to Troponin C induces a
conformational change
transmitted to other members of the troponin
complex and then to tropomyosin
resulting in shortening of the actin-myosin
complex and muscle contraction
Troponin C (18kd)
Calcium-binding subunit
No cardiac specificity
Troponin I (26.5kd)
Actinomyosin-ATP-inhibiting subunit
Cardiac-specific form
Troponin T (39kd)
Anchors troponin complex to the Tropomyosin
strand

Recommend as the gold standard, more sensitive
than CKMB
Troponin I
Increase: 4-6 hrs
Peak: 20-24 hrs
Duration: up to >144 hours
Troponin T
Increase: 3-4 hrs
Peak: 20-24 hours
Duration: >240 hours (7-10 to 14 days)
Oxygen-binding protein
After a MI, myoglobin is the earliest marker
of MI but can be elevated by many other
factors such as skeletal muscle damage
May be used to assess for reperfusion injury
of myocardium after thrombolytic therapy
Myoglobin = <90 g/L
Sensitivity 95-100% poor specificity
Serum Myoglobin Levels Increased in:
AMI
Open heart surgery
Exhaustive exercise
Skeletal muscle damage
Progressive Muscular dystrophy
Shock
Renal failure
Following IM injection
Serum Myoglobin Levels Remains Normal:
Chest pain without AMI
CHF without AMI
Cardiac catherization
Moderate exercise
First marker to appear is myoglobin and
peaks at 8 hours after infarction and return to
normal within 18-24 hours
CKMB 10-12 hours after infarction remains
elevated 24 -36 hours, troponin peaks 24
hours after infarction, falls slowly and
detectable 7-10 days.