College Answer

Key features

•    Troponin I, T and C form a 3 unit complex with tropomyosin in cardiac actin filament, CTnI and cTnT used as cardiac specific markers, small amount in cytoplasm but a large actin pool, slowly released, and slowly degraded with small elevation in renal failure

•    Greater sensitivity to cardiac damage than CK-MB which can also be found in skeletal muscle (increased in myopathies), gut, uterus, and IgG complexes CK-MB, rises 4-6 h after onset symptoms for myocardial infarction, useful prognostic marker in acute coronary syndromes (higher level = worse prognosis)

•    Elevated level also seen with PE, sepsis, myocarditis, pericarditis, cardiac trauma, drug- induced myocardial injury, cardioversion

Discussion

This question is almost identical to Question 10 from the second paper of 2011.

To simplify revision and wreck some SEO, the answer for Question 10 is reproduced below.

Rationale for the use of troponin in the critically ill:

• Troponin is an enzyme involved in the excitation-contraction coupling of the myocardium.
• Troponin T serves to attach the troponin complex to actin and tropomyosin.
• Myocardiac damage (for example infarction) causes the release of troponin.
• There is a cytosolic pool (which is released early in the infarct) and a structural pool (which is slowly released over days as the damaged myocardium decomposes).

Advantages of using troponin in critically ill patients

• Its a sensitive and specific marker of myocardial ischaemia.
• It is more sensitive and specific than AST, CK and CK-MB (which are also found is skeletal muscle)
• It is an independent predictor of 30-day mortality in STEMI 
• It is associated with a poorer outcome in the critically ill patients.
• Troponin levels can be used to monitor for myocardial ischaemia in critically ill patients when history and examination are unreliable.

Advantages of using troponin in acute coronary syndromes

• Troponin forms a part of the ECS and AHA universal definition of acute coronary syndrome (it consists of a troponin rise as well as a demonstration of ischaemic symptoms,  echocardiographic evidence, or ECG changes.)
• The troponin levels are not diagnostic, but are a risk stratification tool to be used together with echocardiography, ECG, history and examination.
• Troponin levels can be used for the late diagnosis of MI and to monitor for reinfarction
•  The use of troponin as a part of a risk stratification strategy is important in selecting patients for anticoagulation and anti-platelet therapy, so as to prevent the exposure of patients to unnecessary bleeding risk.

Disadvantages for the use of troponin in critical illness

• A reliance on biomarkers may become unhealthy if it takes focus off clinical examination and history.
• It is not quantitatively validated outside the setting of ACS / AMI, but only qualitatively: i.e. a "positive" troponin is associated with worse outcomes in noncardiac critical illness, but we don't know whether a higher troponin is associated with a proportionally higher mortality.
• As with all biomarkers, inappropriately low threshold levels or testing out of appropriate clinical context could give rise to unnecessary treatments (eg. loading doses of antiplatelet drugs) or investigations (eg. angiography, with needless contrast exposure)
• Troponin levels can be raised for a variety of non-cardiac reasons.In their 2006 article, Korff et aloffer an excellent table of things which cause troponin elevation, together with the mechanism of troponin release or assay confusion. Their Table 1 is reinterpreted here. 
  • Myocarditis 
  • Renal failure - its cleared renally
  • Sepsis
  • Atrial fibrillation
  • Post-cardioversion 
  • Cardiac trauma 
  • Pulmonary embolism 
  • Acute stroke
  • Intracranial haemorrhage
  • Severe burns
  • Rhabdomyolysis (particularly during recovery)
  • Skeletal muscle damage in glycogen storage disease
  • Defective assay (cross-reactivity with skeletal troponin isoforms)