These are the common ECG terminologies with which clinical cardiology is being practiced over the years .In this era of instant interventions the exact meaning for these terms may not matter much for many of us.Still , Ischemia could denote a more benign connotation , while injury suggests an emergency (like an accident) .Of course , this is a dangerous way of defining them. Still, there may not be an entity called “chronic injury”. while chronic ischemia is all too common.
Logistically , both could mean the same (except the perception) and related to the intensity of the index reduction in blood supply to the varying thickness of myocardium.While injury is diagnosed by ST segment elevation , ischemia is diagnosed by ST depression or T inversion.
No, its wrong , come again please ,
Shall we say . . . most injures are ST elevating while most ischemia are ST depressing , but still injuries can be ST depressing as well. We know Ischemia can be sub-endocardial , transmural or rarely sub-epicardial ,while injury can either be sub-endocardial or subepicardial (Rarely transmural ?)
Can you refine it ?
Only subepicardial ischemia(Injury) elevates ST segment while sub endocardial ischemia depress it.The leads facing the affected subendocardial and epicardial surface will determine whether its going to be ST elevation or depression .
Does the opposing sub-endocardial and sub-epicardial forces negate or cancel out ? If so what is the status of reciprocal ST depression in STEMI if remote ischemia occurs in sub-endocardial or sub-epicardial zones ? Can there be reciprocal ST elevation for primary ST depressive forces ?
If ischemia and Injury are to be defined only with reference to ST segment , which area of myocardium is linked to critical T wave ischemia (Both Tall T and dynamic Wellens type T )
Still more , If Injury is represented by ST elevation, then what represents infarct ?
ST elevation in acute MI-STEMI is actually due to transmural* injury while infarct is represented by Q waves in strict sense.In that case not all acute STEMIs are not true Infarcts.Thats why many STEMI can get totally aborted with zero LV dysfunction and negligible enzyme release. (Should we call these as Non Infarct STEMIs ?)
*Though STEMI results in transmural ischemia , it is the sub-epicardial zone of injury that elevates the ST segment. This implies any degree of subepicardial injury is suffice to elevate ST segment (eg pericarditis) and transmurality of ischemia is not mandatory.
What is reversible vs irreversible Injury ?
If irreversible injury is equivalent to infarct , reversible injury is same as ischemia ? (Whats the histopathological correlates , Cell swelling, mitochondrial / nuclear death .(We know , enzyme release are linked to cell death even in chronic stable angina )
Where is the epicardium for the IVS ?
Most ACS involve interventricular septum .In this case does septum has any defined sub-epicardium or endocardium? How does septal STEMI forces behave with reference to partial or full thickness septal infarct ?
Acute Ischemia and injury can mean “one and the same thing” or “totally different” entities depending upon the totality of obstruction within the coronaries and sparing of sub epicardial zones of myocardium. In my view , any acute ischemia can be labeled as injury.Bifurcating ACS into STEMI and NSTEMI has largely removed the embarrassment of these entities .
Forget the basic science , electro-physiological concepts can wait.Lets live in a realistic world. Get to know the underlying lesion . What can be done for it ? Go ahead , wheel your patient to cath lab . Alert the staff .Be pragmatic ,make sure your patient has sufficient insurance coverage to open up all his blocks ! That’s it !
The intention is not to confuse the readers.Only to make us realise ,the gap in basic science is “huge and wide” which I hope is filled up by the generation next !
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