T waves attract less attention in STEMI ,except for the fact tall T waves implies hyper acute phase of STEMI.
What is the duration of hyper acute phase ?
Any of the above
No one exactly knows .It can be highly variable . So , 5 could be the correct answer .
* Most importantly hyper acute phase need not occur in all patients with STEMI as suggested in experimental models.
Some observations in T wave behavior in STEMI
Mechanism of hyper acute T waves
It is the pottsium channel dynamics.Transient intracellular hyperkalemia is thought to be responsible.
T wave as marker of reperfusion
Inverted T wave in precordial leads are a good marker of IRA patency especially in LAD
Slowly evolving STEMI
This is relatively new concept . STEMI with a prolonged hyper acute phase , ie , T waves “ dilly dallying” for hours or even few days have been recognised. (This was refered to pre-infarction angina in the past )
This sort of T wave behavior makes it difficult to diagnose STEMI.Enzymes will help , still thrombolytic guidelines demand us to wait till ST elevation to occur. This is unfortunate .But as physicians we are justified to thrombolyse tall T waves with a clinical ACS .The other simple solution is to shift the patient to cath lab to find what exactly is happening in the LAD !
Now , what is new about T waves in STEMI ?
It is the localizing value in LAD infarct
A tall persistent hyper acute T wave helps us to localise a LAD lesion .This paper from Netherlands , clearly confirms this observation. The study was done from a primary PCI cohort, a perfect setting to assess the T wave behavior in the early minutes /hours of STEMI .
Other mysteries about T waves in STEMI
Does hyperacute T waves occur in infero-posterior STEMI ?
I would believe it is very rare .Our CCU has not seen any tall T waves in inferior lead. Further analysis of the data from the above study could answer this question .
How often a hyperacute T waves transform into NSTEMI ?
This again is not clear.Most of the hyper acute T will evolve as STEMI .But , nothing prevents it to evolve as NSTEMI a well . After all , a hyper acute T MI can spontaneously lyse in a lucky few , ( Who has that critical mass of natural circulating TPA ) .If these natural lytic forces are only partially successful , it may evolve into de nova NSTEMI.
Bi-phasic T waves in ACS.
A benign looking T waves with terminal negativity in precordial leads can some times be a deadly marker of critical LAD disease.This has been notorious to cause deaths in young men which often correlates with the widow maker lesion in LAD.
What is a slowly evolving STEMI ?
Prolonged tall T wave phase possibly indicate , the myocardium is relatively resistant to hypoxic damage .
The most bizarre aspect in our understanding about ACS pathophysiology is the concept of time window , based on which , all our ACS therapeutics revolve !
Does all myocardial cells have a same ischemic shelf life ? Can some patients be blessed with resistant myocardial cells when confronted with hypoxia or ischemia ?
It is well-known , in some hearts , the muscles go for necrosis within 30 minutes of ischemia, while some hearts can not be infarcted even after 24 hours of occlusion .So , slowly evolving STEMI is a feature of myocardial ischemic resistance .This is not a new phenomenon as we have extensively studied about the concept ischemic preconditioning .
We wonder there is something more to it . . . the quantum of preconditioning can be inherited .Further , we are grossly ignorant about the molecular secrets of non ischemic metabolic preconditioning .
T waves attract less attention in STEMI . Cardiologists are often tuned to look only the ST segment , after all , ACS itself is classified based on the behavior of this segment.(STEMI/NSTEMI) . We need to recognise ,there is a significant subset of ACS affecting exclusively T waves. Shall we call T elevation MI ? ( TEMI )
Do not ignore T waves in STEMI. It has more hidden electrophysiological treasures that is waiting to be explored .