Help Doctor, I have Troponinitis!

Every speciality has its bugbear. Emergency departments have D-dimers (always positive if you spend more than 2 mins in a hospital, seemingly). Gastroenterologists have “melaena” (often just dark brown stool or even frank PR bleeding). Rheumatologists, chronic back pain (the worst thing you can do is admit them to hospital).

And cardiologists have troponins.

Good ol’ troponin. Touted as “the” test for myocardial infarction (heart attacks to the layman), troponin has gone from being the wunderkind of cardiology to a much maligned villain due to its (sometimes) excessive sensitivity. “Why did they order a troponin?” I hear you cry. “Don’t bother with it, it’s just troponinitis.”

What is troponinitis? What is this entity which like “acopia” appears to have entered the everyday parlance of the hospitalist? It is, quite simply, a troponin higher than the 3 times the reference range which for whatever reason is not felt to be due to a myocardial infarct.

Troponin is an enzyme that only occurs in cardiac muscle, and thus is only released during death or damage to cardiac myocytes. There is obviously a small baseline amount of damage that is normal wear and tear. The main worry with a very high troponin, then, is a large amount of cell death secondary to a clot or stenosis completely obliterating arterial supply to cardiac muscle – an acute myocardial infarction. Rises in troponin can also occur secondary to sepsis, uncontrolled tachycardia, pulmonary embolus, cardiomyopathy and other causes for cardiac strain. Additionally a troponin can be mildly elevated when it isn’t been excreted by the kidneys- in renal impairment.

So should we worry about a high troponin in the setting of sepsis, tachycardia or other causes?

The key issues here are as follows. Is this:

1. A real myocardial infarction, and if so:
   1. Is this caused by thrombus (clot) post plaque rupture (type I MI)?
   2. Is this caused by cardiac failure/hypotension in the setting of fixed coronary artery disease (type II MI)?
2. Is this another condition causing a raised troponin, and if so:
   1. Does the raised troponin mean there is cardiac damage?
   2. If not, does the raised troponin have any significance?
3. Is there coexisting cardiac as well as other pathology?

Obviously the above must be evaluated in every patient. Additionally any test – including a troponin – should be ordered at an appropriate time when you have a high pre-test probability of an acute coronary syndrome. Thus, underlying risk factors (especially diabetes), clinical features- history and examination, an appropriate acute deterioration, etc.

Now, for the controversial bits:

• It is possible to have a watershed infarct in the setting of fixed coronary artery disease where hypotension, tachycardia or cardiac failure is present (eg sepsis or arrhythmia)
• It is also possible to have clinically significant cardiac damage in those settings even without true infarction secondary to strain
• Raised troponin has been shown to be associated with a significantly worse prognosis in acutely unwell patients where another pathology is shown to be the cause

Which leads to my next conclusion:

A raised troponin in an acutely unwell patient, especially one with risk factors and evidence of haemodynamic compromise and/or heart failure should never be ignored.

“But what are you going to do about it?!” you say, incredulously. Watershed infarct without a thrombus? “Troponinitis” due to sepsis? What the heck are you going to do about that? Shouldn’t we just stop checking the damned thing?

Given that these patients have in fact had the possibility of thrombosis, fixed coronary atherosclerosis, severe cardiac strain/hypoxia or just very bad underlying disease the following should be done:

1. Follow up troponins to monitor trend – MI less likely if troponin persistently raised
2. Aspirin (if not contraindicated) and prn anginine
3. Optimisation of fluid status, strict fluid balance and daily urea, electrolytes and creatinine
4. A transthoracic echocardiogram to assess heart function and see if there is in fact evidence of either infarction or heart failure
5. Cardiologist review in all patients
6. Referral for percutaneous coronary intervention/angiogram:
   1. In patients with ST elevation and likely infarction and who are well enough for the procedure and do not have sepsis (risk of septicaemia and endocarditis)
   2. In patients who will benefit and are well enough for the procedure in whom there is high pre-test probability- as an elective procedure when well.
7. Therapeutic anticoagulation for 48-72 hours in patients with high pre-test probability of infarct with no ST elevation and no contraindication to anticoagulation
8. Addition of cardiac risk factor modifying agents and optimisation of cardiac failure medications
9. Treatment of acute illness, underlying problems and optimisation of chronic conditions
10. Discussion with the patient and family regarding diagnosis and prognosis

Of course, unfortunately the one thing that everyone will groan about is the fact that I have listed 10 things that need to be done for sick patients with “troponinitis”. It is much easier to ignore it and do nothing- but that is a grave disservice to our patients and very contradictory to the actual evidence on the matter.