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Chem Path > L25 Cardiac markers > Flashcards

L25 Cardiac markers Flashcards

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1
Q

Troponins are sarcomeric protein complex that regulates muscle contraction by binding to myosin.
Which troponin have cardiac-specific isoforms?

A

cTnI and cTnT

Troponin I and T

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2
Q

What is the universal definition of myocardial infarction?

A
  1. Biochemical evidence - Cardiac markers
  2. Evidence of myocardial infarction
    either 1:
    - Symptoms of ischemia/
  • ECG: new ST-T changes, LBBB, pathological Q waves
  • Imaging: evidence of new loss of viable
    myocardium/regional wall motion abnormality /
  • Intracoronary thrombus: angiography/autopsy
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3
Q

What is a significant change in cardiac markers? (what is the cutoff)

A

Rise/fall in cTn (cardiac troponin) with at least one value above 99 percentile of upper reference limit

  • Higher cut-off for those in the setting of PCI/CABG
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4
Q

How can we classify myocardial infarction?

A
  1. Type 1: MI related to atherosclerotic plaque rupture in patients with underling severe CAD = Acute coronary syndrome (ACS)
  2. Types 2-5: Non-ACS types of MI
    - Type 2: Ischemic myocardial necrosis not due to ACS. (O2 supply imbalance)
    - Type 3: Sudden cardiac death (SCD)
    - Type 4: Secondary to PCI/stent thrombosis
    - Type 5: CABG related (Coronary Artery Bypass Grafting(
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5
Q

The measurement of cardiac troponin is by the kinetics of high sensitivity cardiac troponin assays. (hsTnI/hsTnT)
What would be the onset of elevation in MI?

A
  • 30-60 mins (from onset of chest pain) and peak at 24-48 hours
  • level returns to baseline after 5-14 days
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6
Q

Give examples of analytical interference that may result in a positive troponin.

A
  1. Heterophile antibody

2. Rheumatoid factor

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7
Q

Myocardial infarction = Acute Coronary Syndrome. T/F? Explain.

A

False
- Myocardial infarction can be due to non-ACS causes

e.g.
Coronary: increased demand/hypertension/embolism…
Non-coronary: Hypoxia, Global ischemia, Hypoperfusion/CT surgery…

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8
Q

What is Acute coronary syndrome?

A

Classic Acute myocardial infarction

  • Unstable angina
  • STEMI
  • Non-STEMI
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9
Q

What are the possible reasons for positive troponin?

A
  1. Ischemic
    - Myocardial infarction due to ACS/non-ACS causes
  2. Non-ischemic
    - Not MI
    - Cardiac e.g. CHF, infection, myocarditis, pericarditis, Trauma, malignancy…
    /
    - Systemic: PE, toxicity, trauma, renal failure…
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10
Q

To approach positive troponin, we have to first exclude any analytical interference.
Then we should have a serial measurement of hsTnI/TnT with correlations risk factors and symptom onset.

What to do if:
1. Very high cTn (>5x 99%URL)

  1. High cTn >99% URL
A
  1. Very high cTn (>5x 99%URL)
    - invasive management immediately
  2. High cTn >99% URL
    - retest after 3h, if have 50% rise/fall > treatment
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11
Q

If the patient with cardiac symptoms but tested cardiac troponin -ve, what to do?

A

Retest later around 2 hours later, cannot rule out STEMI

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12
Q

When troponin is +ve, what can we rule out?

A

Unstable angina

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13
Q

When there is no ECG changes, what can we rule out?

A

STEMI, but not NSTEMI

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14
Q

If there is no ECG changes and serial troponin measurement shows no fall (persistent high troponin), what can we rule out?

A

can rule out NSTEMI (because persistent elevated)

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15
Q

If the troponin levels are persistently raised, what causes can we consider? (2)

A
  1. Chronic myocardial injury
    - CHF, myocarditis, AF
  2. Non-cardiac causes:
    - CKD, PE
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16
Q

The patient has chest discomfort that radiates to bilateral shoulders. ECG shoes ST depression over V3-6 and pathological Q waves. No consolidation or free gas unde diaphragm on CXR.
Plasma hsTnI is 10158, rr: <34.2

What is the diagnosis? Why?

A

Acute myocardial infarction because there is a rise in TnI with at least one TnI >99th percentile of upper reference limit

17
Q

The patient has chest discomfort and plasma hsTnI is <10;
rr: 15.6

After 2 hours, hsTnI is done again and it is also <10.
What can be ruled out?

A

Acute myocardial infarction

18
Q

A patient who is 8-years-old has normal development, good past health.
She has palpitation since 7pm when attending swimming class. Mild dizziness and retrosternal chest discomfort after palpitation.

ECG shows sinus rhythm, HR 90bpm, NAD, no ST changes.

Plasma TnI is 31.1; rr: <21

2nd time is taken the other morning
Plasma TnI is 35.9

What is ruled out? What can be the possible diagnosis?

A

No rise/fall pattern of cardiac troponin >99th percentile of upper reference limit.

Acute myocardial infarction is ruled out.

  • Interference is suspected.
19
Q

What other markers can be assessed if suspected myocardial ischemia? (other than cardiac troponin) (4)

A
  1. LDH
  2. AST
  3. Creatine kinase - MB (CK-MB) (muscle damage)
  4. Myoglobin
    - release early from onset of MI (~1h)
    - cannot differentiate skeletal from myocardial source
    - For Dx of rhabdomyolysis
20
Q

Name the 2 types of natriuretic peptides and their sources.

A
  1. Atrial natriuretic peptides
    - from atria and ventricles
  2. Brain natriuretic peptides
    - primarily from heart, also from brain
21
Q

What are the physiological functions of natriuretic peptides (2)?

A
  1. Inhibition of RAAS: renal excretion of water and Na, lowering BP
  2. Inhibition of endothelia: causing vasodilation
22
Q

Nesiritide is recombinant BNP. What is it used for?

A

Treatment for acute decompensated heart failure (HF)

23
Q

How to distinguish HF from other causes of dyspnea?

A

By BNP

NT-proBNP rises more (4x) than BNP in LV dysfunction

24
Q

What are the limitations of using BNP to find cause of dyspnea?

A
  1. Patient may present with more than one cause of dyspnea (other than CHF)
  2. some CHF patients have persistently high BNP despite treatment
  3. It is non specific, elevated also in
    - LVH
    - AF
    - AKI/CKD
    - Liver cirrhosis
    - Endocrine: hyperaldosteronism, Cushing’s
25
Q

What is C-reactive protein?
Site of synthesis?
Raised when?

A

An acute phase protein synthesised predominantly in liver.
Raised in infection, inflammation, major tissue injury.

**Present in unstable atherosclerotic plaques.

26
Q

What are the physiological functions of C-reactive protein? (2)

A
  1. Activate complement system

2. Enhance macrophage phagocytosis

27
Q

When is C-reactive protein assessed? (1)

How is its kinetics? (3)

A
  1. Acute illness
    - extremely sensitive but not specific.
  2. CV risk stratification
  • Rise to 10000 fold within 6h
  • Peak at 48 hours
  • Decline with a half-life of 18h
28
Q

How is C-reactive protein used in CV risk stratification?

A

High-sensitivity CRP is used as a marker of atherosclerotic process in healthy population without acute illness

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