Troponins as cardiac markers

Cardiac conditions

Certain subtypes of troponin (cardiac troponin I and T) are very sensitive and specific indicators of damage to the heart muscle (myocardium). They are measured in the blood to differentiate between unstable angina and myocardial infarction (heart attack) in patients with chest pain or acute coronary syndrome. A patient who had suffered from a myocardial infarction would have an area of damaged heart muscle and so would have elevated cardiac troponin levels in the blood. This can also occur in patients with coronary vasospasm.

It is important to note that cardiac troponins are a marker of all heart muscle damage, not just myocardial infarction. Other conditions that directly or indirectly lead to heart muscle damage can also increase troponin levels. Severe tachycardia (for example due to supraventricular tachycardia) in an individual with normal coronary arteries can also lead to increased troponins for example, presumably due to increased oxygen demand and inadequate supply to the heart muscle.

Troponins are also increased in patients with heart failure, where they also predict mortality and ventricular rhythm abnormalities. They can rise in inflammatory conditions such as myocarditis and pericarditis with heart muscle involvement (which is then termed myopericarditis). Troponins can also indicate several forms of cardiomyopathy, such as dilated cardiomyopathy, hypertrophic cardiomyopathy or (left) ventricular hypertrophy, peripartum cardiomyopathy, Takotsubo cardiomyopathy or infiltrative disorders such as cardiac amyloidosis.

Heart injury with increased troponins also occurs in cardiac contusion, defibrillation and internal or external cardioversion. Increased troponins are commonly increased in several procedures such as cardiac surgery and heart transplantation, closure of atrial septal defects, percutaneous coronary intervention or radiofrequency ablation.

Non-cardiac conditions

The distinction between cardiac and non-cardiac conditions is somewhat artificial; the conditions listed below are not primary heart diseases, but they exert indirect effects on the heart muscle.

Troponins are increased in around 40% of patients with critical illnesses such as sepsis. There is an increased risk of mortality and length of stay in the intensive care unit in these patients. In severe gastrointestinal bleeding there can also be a mismatch between oxygen demand and supply of the myocardium.

Chemotherapy agents can exert toxic effects on the heart (examples include anthracycline, cyclophosphamide, 5-fluorouracil and cisplatin). Several toxins and venoms can also lead to heart muscle injury (scorpion venom, snake venom, venom from jellyfish or centipedes). Carbon monoxide poisoning or cyanide poisoning can also be accompanied by release of troponins due to hypoxic cardiotoxic effects. Cardiac injury occurs in about one third of severe CO poisoning cases, and troponin screening is appropriate in these patients.

Some patients with dissection of the ascending aorta have elevated troponins, and increased hemodynamic stress has been suggested as a mechanism.

In both primary pulmonary hypertension, pulmonary embolism and acute exacerbations of chronic obstructive pulmonary disease (COPD), right ventricular strain with increased wall tension and ischemia. Of course, patients with COPD exacerbations might also have concurrent myocardial infarction or pulmonary embolism, so care has to be taken to attribute increased troponin levels to COPD.

Central nervous system disorders can lead to increased sympathetic tone and/or catecholamine release which lead to cardiac overstimulation. This is seen in subarachnoid hemorrhage, stroke, intracranial hemorrhage and (generalized) seizures (in patients with epilepsy or eclampsia, for example).

Patients with end-stage renal disease can have chronically elevated troponin T levels, which are linked to a poorer prognosis. Troponin I is less likely to be falsely elevated.[8] This is why why troponin I cardiac markers are reliable.

Strenuous endurance exercise such as marathons or triathlons can lead to increased troponin levels in up to one third of subjects, but it is not linked to adverse health effects in these competitors. High troponin T levels have also been reported in patients with inflammatory muscle diseases such as polymyositis or dermatomyositis. Troponins are also increased in rhabdomyolysis.

In hypertensive disorders of pregnancy such as preeclampsia, elevated troponin levels indicate some degree of myofibrillary damage.

Cardiac troponin T and I can be used to monitor drug and toxin induced cardiomyocyte toxicity.

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