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Disease of Major Organs > Cardiac biomarkers > Flashcards

Cardiac biomarkers Flashcards

1
Q

What is CVD?

A

Conditions that are cause by atherosclerosis, the narrowing of the artery lumen due to lipid/protein deposition in the arterial wall

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2
Q

What can CVD progress to?

A

coronary heart disease (ischaemic heart disease and coronary artery disease), where the coronary circulation can’t meet oxygen demands of the heart

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3
Q

What is a stable angina?

A

Stable angina describes the narrowing of coronary artery

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4
Q

What are acute coronary syndromes?

A

Range of disorders that are caused by sudden obstruction of coronary arteries due to plaque rupture. 3 catagories:

  • unstable angina
  • acute myocardial infarction: NSTEMI and STEMI
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5
Q

Match the following causes of ACS

  1. Unstable angina
  2. Acute myocardial infarction
  3. NSTEMI
  4. STEMI

A. Non-ST elevation MI
B. Narrowing of arteries causing myocardial ischaemia at rest
C. Blockage in coronary arteries causing cardiac ischaemia+necrosis
D. ST elevation MI

A

1B
2C
3A
4D

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6
Q

How do you differentiate between the two acute myocardial infarctions?

A

Based on ECG findings

  • STEMI; a major blockage in coronary artery causing elevated ST segment
  • NSTEMI: non complete blockage of CA/complete blockage of minor artery causing changes to ECG but no ST elevation
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7
Q

What cellular damage cause necrosis in the heart?

A

Damage to myocytes results in necoris - marker for necrosis

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8
Q

What is the current cardiac biomarker? and how does it compare to previous ones?

A

The previous were non-specific, e.g. LDH, AST/ALT, CK, CK-MB and myoglobin

Troponin is the current marker as it is more specific.

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9
Q

What is troponin and its physiological function?

A

A protein complex made up of 3 units troponin T, I and C. Control the interaction between actin and myosin to control striated muscle contraction

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10
Q

Match the following

  1. Troponin I
  2. Troponin C
  3. Troponin T

A. Bind tropomyosin
B. ATPase inhibitor of actin-myosin interaction
C. Binds calcium

A

1B
2C
3A

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11
Q

What is the detection method of troponin and how does it work?

A

Uses immunoassay, which is possible because they differ in AA composition. Thus allowing us to distinguish between them.

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12
Q

What causes variability to troponin immunoassays?

A

Assays are not standardised so they give variable results.

- Variability is due to lack of reference material and use of different antibodies + cut-offs

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13
Q

Upon admission what is the process of diagnosing ACS?

A

ECG is the first line test.

  • Persistent ST-elevation shows STEMI
  • ST/T abnormalities or normal/undeteremined ECG require cardiac marker testing

Cardiac markers
- used to determine NSTEMI or unstable angina

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14
Q

What is the clinical utility for troponin?

A

cTnT and cTnI are biomarkers of cardiac muscle necrosis

  • As oxygen availability decreases there is an increase in troponin causing arrest of muscle contraction
  • Thus myocytes cant incuce contraction for heart beat
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15
Q

What makes troponin an ideal marker?

A

High specificity for myocardial damage (cardiac tissue damage)

  • Gold standard for MI
  • Increase occurs 1hr within MI
  • Peaks at 18-24hrs
  • Elevated for 2 weeks
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16
Q

What is the definition of diagnosing MI?

A

“Detection of a rise or fall of cardiac biomarker (preferably cardiac troponin) with at least one value above 99th percentile upper reference limits…”.

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17
Q

What are some interferences of troponin release/other causes?

A
  • Any tissue damage to the heart, e.g. heart failure

Elevated in:

  • hypothyroidism
  • drug toxicity
  • pulmonary embolism
  • tachyarrythmias
  • hypertensive crisis
  • chronic or acute renal dysfunction
  • rhabdomyolysis
18
Q

What is a rise or fall in troponin?

A

99th centile

- Meaning a value +/- 3SD from mean

19
Q

What is one major flaw of cTn assays causing potentially significant rises in troponin?

A

The analytical sensitivity

- Lowest amount of troponin can be reliably quantified by standard troponin assays is higher than the 99th percentile

20
Q

What do the high sensitivity troponin assays mean?

A

Improved analytical sensitivity of assay allowing the detection of smaller but potentially more significant changes in troponin that may indicate MI

21
Q

What is NICE definition of high sensitivity troponin assays

A

high sensitivity troponin tests are those that have a coefficient of variation of 10% or less at the 99th percentile (upper limit) and able to detect cardiac troponin in at least 50% of the reference population

22
Q

How is the rise and fall detected in omitted patients?

A

1st sample upon admission (0hrs) followed by sampling at various times
- Hs-cTn have recorded earlier detection of increased troponin, and thus, may require less frequent time intervals

23
Q

How can change in troponin be measured?

A
  • Delta changes of 20-100% used to define a change
  • Delta changes will depend on troponin conc of 1st sample
  • Some suggest the use of absolute change as a better discriminator
24
Q

What are the NICE guidelines for troponin measurements intervals?

A
  • Roche hs-TnT and abbotts hs-TnI for early rule out of NSTEMI in suspected ACS
  • Sample at 0hrs and 3hrs
  • ESC guidelines also recommend to test at 0hrs and 3hrs
25
Comment on the current NICE guidelines for testing patients?
- several hs-Tn assays as options to rule out NSTEMI - Use gender specific 99th centiles - A single sample on presentation using threshold near limit of detection. If positive does not rule in NSTEMI - Multiple sampling strategies using second sample at 30min ->3hrs and use 99th percentile threshold High risk - Hs-Tn Low risk - If first troponin test is + then use hs-Tn to to rule out NSTEMI
26
What are some newer cardiac markers?
Ischaemia modified albumin (IMA) - Marker of cardiac ischaemia - Role in MI diagnosis Heart type fatty acid binding protein - Early AMI/ACS biomarker used in conjunction with troponin - combined with troponin for rapid MI exclusion Copeptin - role as early rule out marker for AMI - data show that troponin and copeptin can be used as early ACS exclusion
27
What is heart failure?
Failure of the heart ot provide sufficient cardiac output to meet needs of tissue
28
Symptoms of HF
Non-specific: dysnopea, peripheral oedema, fatigu
29
What causes HF?
Structural/functional cardiac disease, e.g. ischaemic heart disease, coronary artery disease, previous MU, arrythmias, cardiomyopathy, valve defects
30
What is the pathogenesis of HF?
RAAS forms a worsening cycle. 1. HF causes reduced BP/cardiac output 2. RAAS activation causing fluid retention and vasoconstriction causing fluid overload (increases burden on heart)
31
What is the problem with non-cardiac biomarker based diagnosisi of HF?
using a transthoracic 2D echocardiography to identify valve abnormalities and left ventricular ejection fraction (LVEF) is very expensive
32
What is a good cardiac marker for HF?
``` Natriuretic peptides (vasoactive hormones) - Three in the produced in the heart: ANP (atria), BNP (ventricles), CNP (vasculature, paracrine vasodilator effects) ```
33
What receptors do natriuretic peptides act on?
Natriuretic peptide receptors (NPRs) - NPRA: mediates action of ANP/BNP - NPRB: mediates action of CNP - NPRC: clears NPs from circulatio
34
Where are the different natriuretic peptides secreted?
ANP+BNP- synthesised and secreted from storage granules in the heart in response to cardiac stretch
35
What are the actions of ANP and BNP?
- Oppose those of RAAS - Net increase of GFR - dilate afferent arteriole and constricts efferent arterioles - inhibits Na resorption in CD - inhibits aldosterone secretion - suppress salt appetite and ADH secretion - suppress sympathetic catceholamine release
36
How is natriuretic peptides used in HF?
Plasma conc of natriuretic peptides increase in HF. Can be used to rule out/in HF in primary care
37
What assays are available to measure natriuretic peptides?
BNP and N-terminal proBNP assays
38
What is the difference between BNP and NT-proBNP?
BNP is the active form, which occurs at a higher concentration than NT-proBNP. But NT-proBNP has a longer half life and correlate better to GFR. - BNP: EDTA plasma (labile) - NT-proBNP: serum/plasma (stable)
39
What constitutes a raised BNP?
BNP: 100-400ng/L | NT-proBNP: 400-2000ng/L
40
What are some positive interferences of BNP measurements?
- ischaemia/tachycardia - left ventricular hypertrophy - ACS - ventricular overload - Hypoxaemia - renal dysfunction - sepsis - old age - exercise - cirrhosis
41
What are some negative interferences of BNP measurements?
- obesity - diuretics - ACEi - angiotensin receptor blockers - aldosterone antagonist
42
What are the NICE BNP/NT-proBNP guidelines?
Recommend the measurement of BNP or NT-pro BNP if acute heart failure is suspected, which if positive can be followed by an echocardiography.

Disease of Major Organs (14 decks)

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