Many of us use Troponin T as an enzymatic marker for unstable coronary artery disease, thinking that these trop T elevation is due to enzymatic leakages from death of myocardial cells. In fact, this is one of the WHO criteria for diagnosis of AMI. Now, is this true all the time?
In an article published in the 13th August issue of New England Journal of Medicine, Dr Brendan Everett and investigators looked into the BARI-2D data, and found that in 2,285 patients with diabetes mellitus and stable coronary artery disease, 40% had elevation of Troponin T without chest pains. Trop T levels > 14ng/L was the cut off. 27.1% of those with Trop T had a clinical event, defined as CV death, MI or strokes in 5 years. While 12.9% of those with normal Trop T had any clinical events in 5 years.. This was statistically significant at
The other surprising thing is that, those with Trop T elevation who were revascularised, did not normalise their Trop T, neither did it improve the outcome. Now this is puzzling.
It then bags the question, where is this Trop T coming from, and what is the cause of its elevation?
What then shall we do wit diabetics who present to ER with chest pains that are like that of acute myocardial infarction? Shall we treat them all as AMI? knowing that it may not alter prognosis? or shall we repeat serial Trop T in an attempt to better define this group.
Is Trop T a reliable indicator of myocardial necrosis? Or are there other reasons for Trop T elevation like poor glucose control? presence of metabolic syndrome and high TG levels?, Or is it hypertension with myocardial over-stretch?
I suppose as always, there is so much that we do not yet know. Obviously more studies need be done, to look nto this.