Positive Troponin? Can you not think?

This is a frequently annoying issue. However, I do not condone people looking for ‘excuses’ of justifying missing a diasnosis of MI in a patient with positive troponin. Any positive troponin, should be investigated. But a knee-jerk reaction of pronouncing every positive troponin as ‘NSTEMI’ is a thoughtless action, in many situation, this is done even without referring at ECG and clinical context!

Let me illustrate the potential danger and waste of this blind, knee-jerk reaction:

Waste of resources – transferring a patient to an acute unit, when in fact, even if it was a real ACS, already too late! Diagnosis should have been made earlier, based on clinical presentation and skilful reading of ECG with appropriate consultation with Cardiologist

Potential bleeding – I have seen a number of patients bled, to death or near death, from ‘empirical’ prescribing of clexane, plavix, aspirin in a positive troponin situation. This particularly applies to elderly and CKD patients. So beware.

‘No brainer’ syndrome – come on, let us our brain and the long years of training in clinical medicine! Suspicion is one thing, but to treat something based on suspicion alone, may be disastrous. One more things, patient’s medical notes may be littered with incorrect or unverified diagnosis.

One thing to remember, patients who develop positive troponin, from whatever condition, may actually have worse prognosis compared to the same group who don’t. Therefore it is imperative that they be appropriately investigated. What I am annoyed is, the thoughtless, sudden pronounciation of ‘NSTEMI’ without connecting to clinical suspicion, and ECG interpretation. Do keep in mind, on the other hand there are still a number of patients, who were not suspected, have either negative troponin or troponin NOT DONE, actually are suffering from ACS!

CAUSES OF CARDIAC TROPONINS APART FROM MI

Demand ischemia

Sepsis/systemic inflammatory response syndrome

Hypotension

Hypovolemia

Supraventricular tachycardia/atrial fibrillation

Left ventricular hypertrophy

 

Myocardial ischemia

Coronary vasospasm

Intracranial hemorrhage or stroke

Ingestion of sympathomimetic agents

 

Direct myocardial damage

Cardiac contusion

Direct current cardioversion

Cardiac infiltrative disorders

Chemotherapy

Myocarditis

Pericarditis

Cardiac transplantation

 

Myocardial strain

Congestive heart failure

Pulmonary embolism

Pulmonary hypertension or emphysema

Strenuous exercise

 

Chronic renal insufficiency

(from Allen Jeremias, MD, and C. Michael Gibson, MS, MD Ann Intern Med. 2005;142:786-791)

Other causes related to biochemical states:

Heterophile antibodies
Human anti-mouse antibodies
Autoantibodies
Fibrin clots
Rheumatoid factor
Microparticles in specimen
Interference by endogenous components in blood (bilirubin, hemoglobin, lipemia)
High concentration of alkaline phosphatase
Immunocomplex formation
Analyzer malfunction