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MSC: Disease of major orgns > Cardiac Biomarkers > Flashcards

Cardiac Biomarkers Flashcards

1
Q

What is Cardiovascular Disease?

A
  • Caused by atherosclerosis = deposition of lipid/protein in the arterial wall
  • Causes Coronary Heart Disease and strokes
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2
Q

What is Coronary Heart Disease?

A
  • UK’s biggest killer (1 in 4 men, 1 in 6 women)
  • AKA Ischaemic Heart Disease (IHD) and Coronary Artery Disease (CAD)
  • Commonest cause = atherosclerosis in coronary arteries. Coronary circulation can’t meet oxygen demands of the heart. Lack of oxygen causes ischaemia
  • Can lead to Stable angina and Acute coronary syndrome
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3
Q

What is Acute Coronary Syndrome?

A
  • Range of disorders most commonly caused by sudden obstruction of coronary arteries due to plaque rupture
  • Medical emergency that commonly presents as chest pain which severe, persistent and not alleviated by rest

–

700,000 ED presentations and ~250,000 admissions pa in England and Wales

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4
Q

What are major categories of disease in ACS?

A
  • Unstable angina (UA): Arteries narrowed (but not completely blocked). This causes myocardial ischaemia at rest, but not necrosis
  • ST elevation MI (STEMI): Blockage in coronary arteries resulting in cardiac ischaemia and necrosis
  • Non-ST elevation MI (NSTEMI): Blockage in coronary arteries resulting in cardiac ischaemia and necrosis
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5
Q

What causes a STEMI?

A
  • Major blockage in coronary artery
  • Elevated ST segment on ECG
  • Poorer short-term prognosis
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6
Q

What causes a NSTEMI?

A

More common

  • Non complete blockage in coronary artery/complete blockage of a minor artery
  • May see changes on ECG, but no ST elevation
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7
Q

How is Biochemistry useful in ACS?

A
  • Damage to myocytes results in necrosis which release biochemical markers of necrosis
  • Can differentiat between NSTEMI and Unstable Angina
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8
Q

What are characteristics of an Ideal Acute Myocardial Infarction biomarker?

A
  • Sensitive - increased in all patients with disease
  • Specific - increased only in patients with disease
  • Detectable/increased early in disease
  • Provides prognostic information/responds to treatment
  • Analytically accurate/precise/convenient/stable
  • Cost-effective
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9
Q

What are old cardiac biomarkers?

A

Lactate Dehydrogenase (LDH)

  • Present in cardiac tissue, skeletal muscle, RBCs, platelets

Aspartate/Alanine Aminotransferase (AST/ALT)

  • Present in cardiac tissue, skeletal muscle, pancreas, kidney

Creatine Kinase (CK) and CK-MB

  • Present in SKM (50,000x plasma) and myocardium (10,000x plasma). Subject to physiological variations
  • CK comprises 2x subunits – M and B. Hence can exist in 3x forms - MM (SKM), BB (Brain), MB (myocardium)

Myoglobin

  • Haem protein is released from damaged muscle
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10
Q

What is the speed at which the cardiac biomarkers are released?

A
  • AST: Increased 6-8 hours, Peaks 18-25 hours, Lasts 4-5 days
  • LDH: Increased 6-12 hours, Peaks 24-48 hours, Lasts 5-10 days
  • Myoglobin: Increased in 1-4 hours, Peaks6-7 hours, Lasts 24 hours
  • CK/CK-MB: Increased 3-12hours, Peaks 18-24 hours, Lasts 36-48 hours
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11
Q

What is Troponin?

A
  • Protein complex that controls the interaction of actin and myosin
  • Regulates the contraction of striated muscle (i.e. SKM and cardiac muscle)
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12
Q

What is Troponin composed of?

A
  • Troponin T: Binds troponin to tropomyosin
  • Troponin I: Modulate interaction of actin-myosin. ATPase inhibitor
  • Troponin C: Binds Calcium
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13
Q

What are Isoforms of Cardiac Troponins?

A
  • Troponins exist in both heart and skeletal muscle, but ~40% sequence heterogeneity with cardiac troponins (cTn) for I and T
  • Amino acid sequences of cTnT, cTnI, and cTnC differ
  • Can therefore distinguish specific cardiac troponin isoforms by immunoassays (ie, cTnI, cTnT). Usually serum samples. Haemolysis is an issue
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14
Q

How can Troponin be used clinically?

A
  • cTnT and cTnI are biomarkers of cardiac muscle necrosis
  • Release of troponins from myocytes indicates severe and likely irreversible cardiac damage
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15
Q

What are the benefits of using cardiac troponins for cardiac damage?

A
  • Specificity of cardiac troponin for myocardial tissue: Makes it an ideal biomarker for cardiac damage. Some evidence that cTnT assays may not be specific in certain neuromuscular diseases
  • Highly Sensitive for cardiac tissue damage
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16
Q

Why is Cardiac Troponin the gold standard biochemical marker?

A
  • Increases can be detected within 1 hour post MI
  • Peaks at 18-24 hours
  • Elevated for up to 2 weeks post-MI
17
Q

How is measurement of troponin used to define Acute Myocardial Ischaemia?

A

Detection of rise and/or fall of cardiac biomarker value (preferable cardiac troponin) with at least one value above the 99th percentile upper reference limits and with at least one of the following:

  • Symptoms of ischaemia
  • New or presumed significant ST-segment-T wave (ST-T) changes or new left bunddle branch block (LBBB)
  • Development of pathological Q waves in the ECG
  • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
  • Identification of an intracoronary thrombus by angiography or autopsy
18
Q

What are causes of raised troponin?

A
  • Chronic or acute renal dysfunction
  • Severe congestive heart failure - acute and chroninc
  • Hypertensive crisis
  • Tachy- or bradyarrhythmias
  • Pulmonary Embolism, severe pulmonary hypertension
  • Inflammatory disease e.g myocarditis
  • Acute neurological disease including stroke or subarachnoid haemorrhage
  • Aortic dissection, aortic valve disease or hypertrophic cardiomyopathy
  • Cardiac contusion, ablation, pacing, cardiovversion or endomyocardial biopsy
  • Hypothyroidism
  • Apical ballooning syndrome (Tako-tsubo cardiomyopathy)
  • Infiltrative disease e.g amyloidosis, haemachromatosis, sarcoidosis, sclerodermia
  • Drug Toxicity e.g adriamycin, 5-fluorouracil, herceptin, snake venoms
  • Burns if affecting >30% of body surface area
  • Rhabdomyolysis
  • Critically ill patients especially with respiratory failure or sepsis
19
Q

What are challenges for the laboratory measurements of Troponin?

A
  • Definition of what a raised troponin is
  • Definition of what a rise/fall in troponin is
20
Q

What is the problem with 99th Centile for cTn?

A
  • The level that 99% of a reference population are below. Universally agreed as the upper limit of normal for cTnassays. The cutoff will depend on the ‘reference’ population used. Assays should be able to measure at 99th centile with CV<10%.
  • Problem is analytical sensitivity of cTn assays. The lowest amount of troponin that can be reliably quantified by ‘standard’ troponin assays is higher than the 99th percentile. Potential to miss small but potentially significant increases in troponin
21
Q

What are benefits of using High-Sensitivity Troponin?

A
  • Does relate to the improved analytical sensitivity of newer troponin assays
  • Does not relate to the measurement of a different form of troponin
  • Aim is to detect more of the smaller but potentially significant changes in troponin that may indicate MI.
  • Improved analytical sensitivity leads to improved clinical sensitivity
22
Q

What is the definition of High Sensitivity Troponin Assay?

A

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

23
Q

Changes in troponin

A

Slide 35-41

24
Q

What is Heart failure?

A

Failure of the heart to provide sufficient cardiac output to meet the needs of tissues.

25
Q

What are symptoms of Heart Failure?

A
  • –Dyspnoea (shortness of breath). SOB
  • –Peripheral oedema (esp. ankle swelling)
  • –Fatigue
26
Q

What are causes of Heart Failure?

A

Can be the result of any structural/functional cardiac disease

  • –Ischaemic heart disease
  • –Coronary artery disease
  • –Previous MI
  • –Arrhythmias
  • –Obligatory high output (thyrotoxicosis/anaemia)
  • –Cardiomyopathy
  • –Valve defects
27
Q

What are changes in Heart Failure that worsens heart failure?

A
  • Heart Failure
  • Reduced Blood Pressure/Cardiac Output
  • Activation of RAAS
  • Vasoconstriction/Fluid retention
  • Fluid overload

RAAS activation becomes ‘maladaptive’, forms a cycle of worsening HF

28
Q

How is Heart failure diagnosed?

A

Transthoracic 2D echocardiography (“Echo”)

  • Gold-standard for heart failure diagnosis
  • Identifies valve abnormalities and left ventricular ejection fraction (LVEF).
  • LVEF ≤40% often used to define HF (normally 55-75%) = (LVSD). Can also have HF with preserved ejection fraction = (HFPEF)
29
Q

What are Natriuretic Peptides?

A

Vasoactive hormones, discovered 1981

  • Atrial natriuretic peptide (ANP)
  • B-type natriuretic peptide (BNP)
  • C-type natriuretic peptide (CNP)
  • D-type natriuretic peptide (DNP)

Characteristic 17aa ring structure, highly conserved sequence

30
Q

Where are Natriuretic Peptides secreted?

A
  • ANP = Synthesised & secreted by atria – hormone
  • BNP = Synthesised and secreted by ventricles – hormone
  • CNP = Secreted by vasculature, paracrine vasodilator effects
31
Q

Which receptors do Natriuretic Peptides act through?

A

Act on target tissues via natriuretic peptide receptors (NPRs)

  • NPR-A = mediates actions of ANP/BNP
  • NPR-B = mediates actions of CNP
  • NPR-C = clears NPs from circulation

MSC: Disease of major orgns (23 decks)

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