2. The clinical biochemistry laboratory often plays a
central role in the diagnosis and management of acute
myocardial infarction
3. Myocardial infarction (MI) (ie, heart
attack) is the irreversible death
(necrosis) of heart muscle secondary to
prolonged lack of oxygen supply
(ischemia).
Acute myocardial infarction (MI) is a clinical
syndrome that results from occlusion of a coronary
artery, with resultant death of cardiac myocytes in
the region supplied by that artery.
5. These cause narrowing of the arterial
lumen, resulting in reduced coronary
perfusion, the clinical manifestation of
which is chest pain (angina pectoris ذبحة
صدرية
6. If an unstable plaque
ruptures, the released
contents precipitate the
formation of a clot.
This process, known as thrombosis,
may result in sudden complete
occlusion of the affected artery and
infarction of the area of myocardium it
supplies.
7. Contraction of atria
االذين
Ventricular depolarization
Ventricular repolarization
depolarization
causing
contraction
(activation)
repolarization
corresponds with
relaxation of the
myocardial muscle
8. Acute coronary syndrome
refers to chest pain and other related
symptoms attributed to impaired
blood supply to the heart.
STsegment elevation
myocardial infarction
(STEMI),
Non-STsegment
elevation myocardial
infarction (NSTEMI),
unstable angina.
9.
10.
11. Biochemical Markers for Diagnosis of
Myocardial Infarction
Cardiac enzymes
(isoenzymes):
Total CK ,
CK-MB activity
LDH,
AST
2Cardiac proteins:
Myoglobin
Troponins
12. CK-MB
Creatine kinase (CK) is a cytosolic enzyme
CK is a dimer composed of two subunits B (brain type) and M (muscle type),
resulting in three isoenzyme:
CK-BB (CK1) : is of brain origin, found in blood only when BBB is damaged.
CK-MB (CK2) : it is relatively specific for myocardial origin
CK-MM (CK3) : it is found primarily in skeletal muscle
M B
13. CK-MB :
it is a valuable tool for the diagnosis of MI because of
its relative high specificity for myocardial damage.
Rise : 4-6 hrs after onset of symptoms
Peak : 12 hrs
Return to normal : 24-36 hrs
Can be used to indicate early re-
infarction if level normalizes and then
increases again.
14. LDH
An intracellular enzyme present in nearly all metabolizing cells
in the body. The highest concentration of enzyme is located in
the heart, skeletal muscle, liver, kidney, brain, and
erythrocytes. There are 5 isoenzymes of LDH.
LD1 LD2 LD3 LD4 LD5
heart, red blood cells and kidneys. lungs liver, skin, and the skeletal muscles.
15. Total LDH: 70-200 IU/L
Newborn: 300-1500IU/L
Child: 50-150 IU/L
LDH elevates in 24-48 hours
and peaks in 48-72 hours
16. AST
AST, (Aspartate Aminotransferase) Normal Values: 5-40 U/ml
This enzyme shows an
elevation 8-12 hours after
infarction. Peak levels are
reached 24-48 hours after the
MI.
High levels of SGOT may be
obtained with trauma to the
skeletal muscles, in liver
disease, pancreatitis and
others.
17. Troponins
Troponins are contractile
proteins found within
muscle fibers that help
regulate contractions.
troponin C
troponin I
troponin T
calcium-binding component
inhibitory component
tropomyosin-binding component
18. During the process of muscle necrosis, troponins I and T are
released from the dying muscle fibers into the bloodstream.
19. Small-size heme protein found in all tissues mainly assists in oxygen transport
It is released from all damaged tissues
Released from damaged tissue within 1 hour
Normal value: 17.4-105.7 ng/ml
Timing:
Myoglobin
Earliest Rise:1-4 hrs
Peak: 6-9 hrs
Return to normal:12 hrs
useful for the early diagnosis of acute
myocardial infarction
20. Lipids and lipoproteins
•Lipids are carried
in the bloodstream
by complexes
known as
lipoproteins. This
is because these
lipids are not
soluble in the
plasma water.
21. • High levels of LDL-cholesterol in
blood are a primary cause of heart
attacks. LDL can be found in the wall
of heart arteries.
Low levels of HDL-cholesterol also
increase the risk of heart attack. Some
scientists believe that HDLs help
remove cholesterol from tissues
22. D-Dimers And Deep Vein Thrombosis
• D-dimers are released into the
plasma upon thrombosis formation
when fibrinogen is converted to
fibrin. Raised plasma D-dimer
concentration is, therefore, a useful
marker of the presence of a
thrombus and a useful tool in the
diagnosis of a DVT.
deep vein
thrombosis
(DVT),
24. A 46-year-old man was admitted late at night (23.30 h) to casualty by ambulance
because of a tight central chest pain that had started at 03.00 h that morning. He had
delayed calling for medical assistance because he thought it was only indigestion. In the
ambulance, the paramedicsالمسعفين gave him an intramuscular injection of diamorphine
for pain relief. The ECG was normal.
Plasma
Creatine kinase (CK) 565 U/L (< 250)
Troponin T 1.0 ng/L (< 10)
25. The normal plasma troponin T makes a diagnosis of
acute myocardial infarction unlikely, as this would be
expected to be elevated in view of when the chest pain
started.
The elevated plasma CK concentration is not specific
for cardiac damage and may have been raised as a
result of muscle damage secondary to the
intramuscular injection: beware of interpreting
elevated plasma CK concentrations in the presence
of intramuscular injections.