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UG Biochemistry > 9. Acute Coronary Syndrome > Flashcards

9. Acute Coronary Syndrome Flashcards

1
Q

Define acute coronary syndrome

A

Set of signs + symptoms/conditions brought on by decreased blood flow in coronary arteries to heart muscle

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2
Q

Describe the hearts blood supply

A

Heart requires blood to supply O2

Coronary arteries supply blood to heart muscle

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3
Q

Describe the pathophysiology + complications of coronary artery disease

A

Build up of cholesterol + calcium on walls of blood vessel forms plaques (atheroma)
- process = atherosclerosis

The plaques narrow the lumen + reduce blood supply to the heart muscle = ischemia

Plaques can rupture leading to formation of clots (thrombus) which block the vessel
- complete lack of blood supply to heart = infarction leading to muscle death

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4
Q

How is an MI classified?

A

MI is currently classified according to WHO criteria

2/3 of;

  • ischemic symptoms
  • ECG changes
  • increased serum biomarkers
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5
Q

What is the typical patient work up in ED for ACS?

A

ACS symptoms lead to an initial ECG;

  • ST elevation/new left bundle branch block = start immediate treatment
  • no ST elevation = still undifferentiated from unstable angina

Cardiac markers are used to differentiate MI and unstable angina but take longer

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6
Q

What are the clinical features of ACS?

A 
Chest pain is most common;
 - radiating to left should/left angle of jaw
 - crushing/central
Nausea + vomiting
Breathlessness (dyspnea)
Dyspepsia
Others; atypical presentation (no pain)
 - common in women, elderly, DM
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7
Q

What proportions of chest pain patients are diagnosed with MI?

A 
Only a small proportion;
STEMI 10%
NSTEMI 10%
Unstable angina 14%
Other/non-AMI 66%
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8
Q

What are the 3 clinical manifestations commonly associated with ACS?

A
  1. STEMI
  2. NSTEMI
  3. Unstable angina

Classified by ECG appearance + cardiac markers

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9
Q

What is the difference between ischemia +infarction? How does this relate to cardiac biomarkers?

A 
Ischemia = only symptoms + reversible muscle damage
Infarction = muscle death, irreversible damage

Cardiac enzymes + macromolecules used as markers are only released on cell death = markers of myocardial injury

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10
Q

What are ideal characteristics of a cardiac biomarker?

A

Diagnostically;

  • high sensitivity (detect MI)
  • high specificity (absent in non-cardiac injury)
  • rapid release to detectable concentration
  • long t1/2
  • correlates efficiently with extent of MI

Analytically;

  • high sensitivity (lower detect limit)
  • high specificity (less interference)
  • easy
  • inexpensive
  • rapid
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11
Q

List the types of cardiac markers used

A

Diagnostic markers;
ENZYME;
- creatine kinase (CK) + subforms
- lactic dehydrogenase

PROTEIN;

  • troponin
  • myoglobin
  • fatty acid binding protein

Prognostic + risk stratification markers;

  • CRP (acute phase protein - inflamm)
  • MPO (myeloperoxidase - coronary art disease)
  • homocysteine (risk of future CVD)
  • troponin
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12
Q

Describe troponin + its relevance as a cardiac biomarker

A

Tpn is a complex of 3 regulatory proteins;

  • TpnC
  • TpnI
  • TpnT

It is integral to muscle contraction in skeletal + cardiac muscle (not smooth);

  • different types in each
  • skeletal TnC subunit = 4x Ca+ binding sites
  • cardiac TnC subunit = 3x Ca+ binding sites

Tpn subunits are used as cardiac biomarkers;

  • TpnI + T used
  • TpnI is more specific as some TpnT in skeletal muscle
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13
Q

How does troponin level change during cardiac injury?

A

Damage to cardiac muscle releases Tpn;

  • levels raise 3-12hrs after onset of chest pain
  • levels peak 12-24hr

Elevations in TpnI + T can persist for up to 10 days post-MI
- good for retrospective diagnosis of AMI

Detectable levels indicate chronic disease even if not an AMI

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14
Q

Describe the use of TpnI as a cardiac biomarker

A

TpnI has only 1 isoform - cardiac isoform found only in cardiac muscle

Highly bound to tropomyosin complex in sarcomere
<5% in cytosol

N, C terminus + central portion;

  • different Abs measure different terminus (6 assays)
  • strong binding to TpnC subunit may affect measurement
  • also affected by other protein kinases + fibrinogen levels
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15
Q

Describe the use of TpnT as a cardiac biomarker

A

TpnT has 4 isoforms: fetal skeletal tissue + cardiac tpn isoform is used

Muscle injury, myopathy + renal failure cause reexpression of cTnT in muscles
- possible false positive with 1st gen assay in renal failure

Patent regulations mean only 1 manufacturer for assays
- Roche Boeringer

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16
Q

List the different generations of Tpn assays used for cardiac biomarker testing

A 
ASSAYS;
1st gen;
 - 1 step ELISA
 - 2% cross reactivity to skTnT
 - detection limit: 0.04ug/L

2nd gen;

  • no cross reactivity to skTnT
  • linearity problems
  • detection limit: 0.0123ug/L

3rd gen;

  • higher level of precision at lower end
  • detection limit: <0.01ug/L

4th gen;
- detection limit: 0.028ug/L (10%CV)

5th gen;
- high sensitivity assays

17
Q

Describe the 2 big turning points in Tpn assay use for cardiac assessment

A

In 2000: 1st Tpn assays replaced cardiac marker panels (CK, CKMB, myoglobin) for routine use

  • specific for myocardial injury measured >=12h after onset of chest pain
  • limitation: poor sensitivity in 1st few hours after onset

In 2007: worldwide task force recommended use of high sensitivity Tpn assay for cardiac assessment
- requires assay to detect hs-Tn at the 99th %ile of an apparently healthy reference population with 10% variability

This led to a change in the definition of MI to hs-Tn >99th %ile (hsTnT >14ng/L) with clinical features
- LOD was lowered vs the previous TnI std

18
Q

Describe the hsTnT assay now in use

A

Allows detection of cTnT at 99th %ile of ref pop with 10% CV
- LOD: 0.002ug/L or 2ng/L

Advantages;

  • no significant interference with skTnT/I
  • earlier detection for newly admitted patients
  • earlier rule in/rule out of MI
  • identifies more AMI patients
  • improved risk stratification in AMI
  • prediction of long term prognosis in non-ACS

Disadvantages;
- reduced clinical specificity

19
Q

How has hs-Tpn changed treatment for NSTEMI patients?

A

NSTEMI guidelines 2011 by European Society of Cardiology (ESC) for acute chest pain;
- use hs-Tn upper limit of normal in combo with symptoms to determine if discharge, retest, ddx or invasive management required

2015 ESC released new guidelines for NSTEMI patients;

  • advocate use of hs-Tpn assays in evaluating suspected ACS
  • supports use of 1hr algorithm on basis of several multicentre prospective validation studies leading on from initial single centre pilot study
20
Q

List the other causes of increased Tpn in absence of overt IHD

A

Congestive heart failure (acute + chronic)
Pulmonary embolism
Severe pulmonary hypertension
Rhabdomyolysis with cardiac injury
Inflammatory diseases e.g. myocarditis
Critically ill patients - esp respiratory failure, sepsis
Renal failure
Cardiac contusion or other trauma inc surgery, ablation, pacing, etc
Aortic dissection
Aortic valve disease
Hypertrophic cardiomyopathy
Tachy/bradyarrhythmias or heart block
Acute neuro disease inc stroke, subarachnoid hemorrhage
Drug toxicity/toxins

21
Q

What other preanalytical factors affect a Tpn result?

A 
Fibrin clots
HAMA Abs
Rheumatoid factor
Macroimmune complexes
Elevated ALP
Hemolysis, lipemia, icterus
Heparin
22
Q

Describe CK + its use as a cardiac biomarker

A

Creatine Kinase = muscle enzyme present in different tissues + cells

Mainly in 3 isoforms (other than mitochondrial form);

  • CKMM = sk muscle
  • CKMB = cardiac
  • CKBB = brain
Measured by lab photometry
Total CK = CKMM + CKMB (BB not normally detected)
 - CKMB normally <10% of total
 - 10-30% = diagnostic of MI
 - >30% = macroenzymes + CKBB

CKMB raises 4-6 hours post infarct + reaches baseline again in 48 hours

  • short time means useful in diag re-infarction (common in AMI pts)
  • Tpn levels will not have dropped in time

UG Biochemistry (14 decks)

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