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Ischaemic Heart Disease CASE A

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... was brought in to A&E complaining of chest pain, nausea and a suspected AMI. ... history of ischaemic-type chest discomfort. Changes on serially obtained ... – PowerPoint PPT presentation

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Title: Ischaemic Heart Disease CASE A


1
Ischaemic Heart DiseaseCASE A
2
CASE A
  • Mr HA, aged 60 years, was brought in to AE
    complaining of chest pain, nausea and a suspected
    AMI.

3
The Biochemical Markers
  • Creatinine Kinase Biochemical marker of
    myocardial damage.
  • CK is a ubiquitous enzyme found in nearly all
    tissues including striated muscle and the brain
    and this reduces its specificity as a biochemical
    marker for myocardial injury.
  • CK values are the first to rise after an AMI, and
    the first to return to normal if no further
    coronary damage occurs

4
CK the first to rise!
5
CK-MB
  • CK-MB An isoenzyme of CK which is more specific
    to myocardial tissue
  • Remains the most widely used enzyme marker, and
    is still the preferred marker for the diagnosis
    of AMI
  • More specific than CK for MI
  • The MB fraction is found predominantly in cardiac
    muscle. It is important to show both a rise in
    the serum concentration of CK-MB, and a rise in
    the ratio of CK-MB to total CK to diagnose MI

6
LDH
  • Lactate Dehydrogenase (LDH) Isozymes composed of
    combinations of two different subunits "H" and
    "M".
  • Subunit "H" predominates in heart muscle LDH
    which is geared for aerobic oxidation of
    pyruvate.
  • Rises acutely on initiation of an AMI. However,
    they take 2-3 days to reach maximum and thus do
    not play a major role in the diagnosis of AMI.

7
CK INDEX
  • CK-Index The ratio of CK-MB to total CK
  • In AMI the value rises 5-15 folds and takes 24hrs
    to reach maximum. A low percentage can suggest
    the CK to be from a purely skeletal source and
    therefore rule out the possibility of MI.

8
CASE A
  • Mr HA, aged 60 years, was brought in to AE
    complaining of chest pain, nausea and a suspected
    AMI.

9
CK-MB Index
  • CK-MB in ng/mL / Total CK in U/L
  • 100

10
Clinical Chemistry
11
Consistent with AMI?
  • The level of CK-MB in Mr HAs clinical chemistry
    results follows the classic pattern of rise and
    fall related to a cardiac event.
  • The usual pattern of CK-MB levels after an AMI
  • Increase 3-10hrs after the onset of infarction
  • Peak at 12-24hrs
  • Return to baseline after 36-72hrs

12
Clinical Chemistry
13
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14
Consistent with AMI?
  • Mr HAs clinical chemistry shows the CK-MB levels
    from the time of admission to A and E
  • Therefore, we can reasonably conclude that the
    results have shown that an AMI has occurred.
  • Based on this assumption, these results are
    consistent with an AMI

15
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16
CURRENT CRITERIA
  • Mr HA, aged 60 years, was brought in to AE
    complaining of chest pain, nausea and a suspected
    AMI.
  • Outline the current criteria for diagnosing
    acute myocardial infarction

17
WHO CRITERIA
  • A clinical history of ischaemic-type chest
    discomfort
  • Changes on serially obtained ECG
  • A rise and fall in serum cardiac markers

18
CASE A
  • Outline the current criteria for diagnosing acute
    myocardial infarction and the role played by the
    measurement of serum levels of the enzymes CK-MB1
    and 2 in diagnosis of myocardial infarction.
    Define the difference in measuring CK-MB activity
    compared to CK-MB mass

19
An Ideal Marker
  • Present early and in high concentration in the
    myocardium
  • Absent from non-myocardial tissue and serum
  • Rapidly released into the blood at the time of
    the myocardial injury
  • Creatinine kinase (CK) isoforms, CK-MB1 and
    CK-MB2 has long been upheld as biochemical
    standards for diagnosing AMI

20
Cardiac Markers
  • Cardiac troponin I and CK-MB12 and their ratio
    are lab tests that have improved the diagnostic
    accuracy of MI
  • Other markers compared to CK-MB

21
Identifying Risk Factors In ACS
  • Troponin IT are both important establishing
    risk stratification of patients with acute
    coronary syndrome
  • Also CK-MB isoforms have a superior role

22
CASE A
  • Outline the current criteria for diagnosing acute
    myocardial infarction and the role played by the
    measurement of serum levels of the enzymes CK-MB1
    and 2 in diagnosis of myocardial infarction.
    Define the difference in measuring CK-MB activity
    compared to CK-MB mass

23
CK-MB mass Vs CK-MB activity
  • CK-MB activity measurements only measure enzyme
    catalytic activity
  • CK-MB mass measurements only measure the amount
    of CK-MB released regardless of its activity
  • Compare and contrast both these terms

24
CK-MB mass Vs CK-MB activity
  • CK-MB activity
  • Activity is detected using electrophoresis and
    immunoinhibition, it has limited reliability due
    to interferences
  • CK-MB mass
  • Not subject to interferences mentioned in
    immunoinhibition
  • Measure of CK-MB mass by immunoassay involving
    monoclonal antibodies is much reliable, sensitive
    and specific under 1µg/L

25
CK-MB mass Vs CK-MB activity
  • CK-MB activity increases in MI in a greater
    extent (6) than in skeletal muscle trauma (
  • Specific for late diagnosis but not sensitive
    enough for early use ie relatively non-specific
    and requires longer time
  • CK-MB mass is increased in both skeletal muscle
    trauma and myocardial infarction
  • Specific diagnosis marker at 6 hours of onset

26
Cardiac Troponins
  • Troponins are complex regulatory proteins that
    are tightly complexed to the contractile
    apparatus of muscle cells. Different Troponins
    isoforms appear in different muscle cells.
  • Troponin T (cardiac selective)
  • Troponin I (cardiac selective)
  • Troponin C (non-cardiac selective)
  • Circulating levels are normally low, but they
    rise rapidly after an AMI

27
Advantages of Cardiac Troponins as Biomarkers of
MI
  • Cardiac troponins cTnT and cTnI
  • High Sensitivity
  • High Specificity
  • Remain elevated in serum for a number of days
    giving it a long diagnostic window
  • Reference interval effectively zero giving very
    little background noise

28
Disadvantages of Cardiac Troponins as Biomarkers
of MI
  • cTnT and cTnI measured in different laboratories
    show different results
  • Non diagnostic marker due to cardiac trauma other
    than an MI.
  • Ischaemic heart disease can exist even in the
    absence of a raised cardiac troponin level.
  • Cannot be used as an early marker (appear 3-6 hrs
    after MI)
  • Prolonged troponin levels do allow detection of
    re-infarction

29
Monitoring Following Thrombolytic Therapy With
Streptokinase.
  • Trials clearly show that hospital and 30-40 day
    mortality are statistically related to the level
    of reperfusion at 90 minutes following
    thrombolytic therapy.
  • Kinetics of myocardial protein appearance in
    circulation, namely CK-MB, myoglobin, cTnI and
    cTnT, following their release from the injured
    myocardium, depend on infarct perfusion and can
    be used to assess coronary reperfusion early
    after administration of thrombolytic therapy.

30
Reperfusion Monitoring The Use of Myoglobin
  • Compared to total CK activity, cTnI and cTnT
    release, myoglobin can be used very early (within
    90 minutes of thrombolytic therapy) to detect
    reperfusion.
  • A myoglobin to total CK activity ratio of 5.0
    obtained from a single sample taken at the time
    of admission predicts spontaneous reperfusion 90
    minutes following thrombolytic therapy.
  • A single myoglobin measurement at 90 min after
    the start of therapy combined with clinical
    variables improve prediction of reperfusion.

31
Reperfusion Monitoring The Use of Cardiac
Troponins
  • Guidelines to assess reperfusion
  • An increase of cTnT levels to 0.5 µg/mL at 60
    minutes following therapy.
  • A relative increase in cTnT levels at 90 minutes
    following therapy of 6.8.
  • A 90 minute concentration/baseline concentration
    following therapy of
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