i want to talk today about the important topic of subtle STEMI or occlusion MI i have given talks in the past related to this under my playlist myioardial infarction there are the EKG talk ST elevation talks as well as in the non- STEMI talk and STEMI part three i've described many of those patterns in today's talk I will describe some new patterns and some new examples and I will summarize as well some of the basic ideas I described in the past 20 to 30% of non- STEMI are due to acute coronary occlusion frequently left circumlex or RCA occlusion and maybe pathophysiologically STEMI equivalent or subtle STEMIS subtle ST elevation is a common finding in that 20 to 30% of non- STEMI along with other recognized subtle STEMI patterns that I will describe subtle STEMI EKGs should be recognized and taken emergently for cath and treated as a STEMI like a classic STEMI rather than a non- STEMI although many of those olusive MI are on the overlap in terms of perfusion of the infed territory they may be on the overlap between non STEMI and STEMI and they may still benefit from later perfusion however they should be taken emergently to cal and addressed initially similarly to a classic STEMI guidelines give cut points to define STEMI but as I described before those cut points are flawed in fact lesser ST elevation in the right context frequently still implies injury and qualifies for emergent reperusion usually PCI not litics when you're below those cut points and conversely SC elevation above those cut points above the millimeter or above 2 mm in the anterior precordial leads is frequently not stemming so it's much much more important to focus on the shape rather than the size of the ST elevation and there are five major causes of SC elevation particularly for STEMI early polarization pericarditis and SC elevation secondary to depolarization abnormality from LVH or left bundle branch block there are five morphological criteria that imply STEMI any of them implies STEMI sc elevation that is straight or convex upward blending with the T to form a dome such as this one this morphology suggest STEMI you have wide upright T or inverted T so two wave abnormality whether large or wide or inverted along with a subtle ST elevation or you have Q waves or you have a size of ST elevation or Q wave that almost approximate QRS height and in those patient what you frequently have you have a shrinking of the QRS along with a rising of the T-wave so QRS shrink and key rises so much so that QRS and T almost approximate or ST elevation almost approximates half of the QRS so SC elevation approximating half of the QRS or T-wave approximating the whole QRS suggest STEMI then you have reciprocal ST depression which may be seen in LVH and left bundle branch block when you have secondary reporization abnormalities you will have ST depression when QRS is upright and C elevation when QRS is down so that may mimic reciprocal ST depression and there are four major pattern of occlusive MI i will elaborate particularly on the first pattern which is the most common pattern and the most frequently missed pattern which is an ST elevation that is subtle less than 1 millm sometimes in only one or two lead unlike the paradigm that you need to have it in two contiguous leads sometimes it's only in one or two non-ontiguous lead and it's small less than a millimeter but the morphology is consistent with STEMI and you have any of the following either a glaring or subtle reciprocal acid depression or not even acid depression T inversion or you have evolving Q waves or you have that shrinking QRS that I like so much before you develop Q waves before that myioardial inferted area becomes electrically inert and becomes a Q you develop a shrinking of that QRS so the QRS shrink while you have a relatively large T and ST the T may not be large in absolute value the ST segment may not be very high in absolute value but T approximate QRS and ST approximates half of QRS a small QRS that is very suggestive of stemming another feature is upward pull of the S-wave lifting it above the baseline this is what we call terminal QRS distortion and I will show you some of those patterns so this is a patient who's having shrinking of the QRS along with a YT that T is not very wide in absolute value it's not more than 10 mm but it is approximating the QRS size and QRS is shrinking that size mismatch is indicative of STEMI then I mentioned that S being pulled up by the ST so when you have a STEMI QRS shrinks and the S wave gets pulled up by the ST segment so much that the S-wave rises above the baseline and is no longer called an S-wave but I still like to call it an S that is being pulled above the baseline this is a very suggestive of stemming this is such a case where you have ST elevation along with a wide and relatively large T that approximates the QRS size in lead V2 and even more so in lead V3 and in V3 you have that terminal QRS distortion that S wave that is getting pulled above the baseline and as it is always important in those subtle STEMI always repeat the EKG five to 15 minutes later multiple times potentially and see the progression a STEMI will progress somehow the QRS will further shrink you may have evolving QAS you may have a more glaring white tea or you may start having T-wave inversion or you may start having more pronounced uh reciprocal ST depression or T inversion so again repeat the EKG and look for those evolving signs and this patient EKG is repeated and you have now a full-blown Qwave in lead V3 and you have further shrinkage of QRS in lead V2 and further rise of that T-wave which becomes larger than the QRS along with that you have that S-wave being pulled above the VA baseline in lead V4 and you have reciprocal inferior ST depression subtle but in context significant this is an EKG of a 61year-old woman presenting with chest pain and diaphoresis that started 1 hour previously this EKG may be read as normal in an asymptomatic patient if you're reading just a stack of EKG but with her ongoing distress you have to seek those mild features of subtle STEMI and in this case we have subtile Q waves in leads V1 and V2 you have subtle SC depression in the inferior leads you see it here in 2 three and AVF and you have a wide T-wave in V4 and relatively tall T that approximates the size of a shrinking QRS also in lead V4 you have that S wave being pulled above the baseline by the ST so all this is suggestive of a stem this patient was taken to the cath lab and indeed she had 100% occlusion of the LED just before a large first septile and she had CC2 and grade three collateral from a large first diagonal branch as well as from the RCA as you may see here and those collaterals and the fact that it probably was chronically severely stenosed before it fully occluded explains why SC elevation is so subtle in this patient there is some flow to that infarted territory that may be why some of those subtle STEMI are on the overlap between non STEMI and STEMI they have some perfusion to the infared territory but they need to be cath and recanalyzed immediately this is another case a 34 yearear-old female obese presents with chest pain for 3 hours worse with supine position even though she's only 34 years old this EKG has many subtle STEMI features you have subtle anterior ST elevation with a shrinking QRS and T-wave that approximate the QRS size especially in lead V2 and V3 you have an ST that is only about 1 mm elevated in lead V3 but that exceeds 50% of that small shrinking QRS so ST that exceed 50% of a shrinking QRS is very concerning for STEMI you also have subtle inferior ST depression you also have that terminal QRS distortion that Swave that's being pulled above the baseline in leads V3 and especially in lead V4 and indeed the patient had an acute thrombotic occlusion of the mid LED just after a large diagonal branch you can see here the heavy thrombus of the occlusion this is another case 63 year old female smoker with severe hypertension and no prior cardiac history she had chest pain for 3 hours before presentation you can see on the CKG there is mild SC elevation in all of the precorial leads from V1 through V6 especially in leads V4 V5 where it is approximately a 2 mm and where it's particularly discrepant to the QRS size you have a T-wave here and before V5 that almost approximates or exceeds the QRS size and you have an ST morphology that is convex or straight upward that looks almost like a dome in leads V4 through V6 occasionally you may see a T-wave that is large compared to the QRS at the transition zone when QRS moves between negative to positive but when you have it outside the transition zone or when you have it in multiple leads that becomes even more concern you also have in the reciprocal leads some T-wave abnormality some bifphasic T-wave in the inferior leads which in another patient would not be worrisome but in conjunction with those findings is concerning for reciprocal abnormality from an anterior MI another thing why would she have a C elevation she does not have LVH and early reporization is unusual in a woman her age earlier reporization is more common in men young or middleage men and indeed this patient had complete middle acute occlusion this is another case where we have a glaring ST elevation in most of the leads and despite that ST elevation being glaring this is actually not a STEMI this is acute pericarditis because this patient had none of the five features of STEMI you have SE elevation that is concave you do not have a shrinking QRS or Q waves and the ST and T while large in absolute value they are small relatively to the QRS in all these they are nowhere near approximating the QRS size you do not have T-wave abnormality whether large T or inverted T and you do not have reciprocal ST depression except for the ST depression that is expected in pericarditis in AVR and a little bit in V1 the leads that look away from the axis of the heart the axis of the diffuse ST elevation so this patient has acute pericarditis also ST elevation while prominent never exceeds 5 mm sc elevation in pericarditis should never exceed 5 mm sc elevation in earlier reporization should never exceed 2 and a half to 3 mm this patient has also PR depression in leads to V5 and V6 however PR depression can be seen in acute MI pr depression does not imply pericarditis if MI features are present also PR depression that is mild less than a millimeter may be seen in early reporization this is another patient cancer patient with dismia she has diffused ST elevation in all the leads with ST depression in AVR like this prior patient so this may initially suggest malignant pericarditis you also have PR depression in leads to AVF and V5 V6 however having pericarditis feature does not necessarily rule out STEMI one should search for the five STEMI features and make sure none of them is present in in this patient the ST elevation has a dome morphology with an upwardly convex shape and a wide and high T fus with the ST segment very typical of STEMI also the size of the ST elevation over 5 mm in V2 through V4 and larger than the QRS the shrinking QRS in V4 is definitely suggestive of stem and keep in mind that 30% of antapical MI cause diffuse ST elevation without reciprocal ST depression like pericarditis this is because the apex is seen by all the EKG leads the anterior leads but also the inferior leads which see the inferior apex supplied by a wraparound LED this is another EKG shared with me by one of my fellows Nasim i love this EKG this is a 66 year old man diabetic with ongoing chest pain at first look it may seem that the EKG is normal but look more carefully for subtle signs and the most important finding to me is here in leads V5 and V6 you have that shrunk tiny QRS in those leads along with a T-wave that seems small but that is actually relatively large compared to the QRS and that matches the size of that tiny QRS so this shrinking QRS with a relatively large T that is equal or nearly equal in size to the QRS strongly suggests occlusion MI and I get asked what do you mean by shrunk QRS if you have serial EKG you will see QRS progressively shrinking in size and eventually evolving into a QA if you are looking at only one EKG in time QRS shrinking usually means to me a QRS that is small less than 5 to 10 mm along with a T that is large in relative terms meaning it approximates the height of QRS not necessarily exact height of the QRS but close to it also you may have a sea elevation that is mild in absolute term but it is concerning when it is over 50% of the size of a tiny shrinking QRS this is not published in those exact proportion but that fits with the standard STEMI EKG progression there are more subtle features on that EKG you have a Q wave in V5 V6 that is small but that is actually significant and pathologic because it's wider than one box it's wide and an abnormal Q wave is mainly defined by its width more than one box this is the case here also you have mild ST depression in lead V2 normally you should not have any ST depression in V2 if anything you normally have a little bit of ST elevation in lead V2 subtle ST depression in V2 suggests posterior STEMI and if you do in this patient record leads V7 through V9 you may find more pronounced ST elevation anyway the constellation of findings in that patient suggests low lateral and posterior occlusion mi likely from a low OM it's unlikely to be diagonal because diagonal you will have typically ST elevation in ABL and indeed on coronary angography this patient had an acutely oluded OM4 which was acutely recanalyzed and now I want to move on and describe three particular morphological features that are talked about in the literature one is that terminal QRS distortion which strongly indicates STEMI simply because it is not seen in early reporization and it consists of lifting that S-wave above the baseline so it's no longer really an S-wave and in those patient it's not just lifting the S-wave above the baseline there is also no Jwave there is a sharp J there is no Jwave so compare this to the earlier polarization here where you still have an S below the baseline and where you may have a J wave not just a J point so this is a case I had where I had ST elevation along with an S-wave that is being pulled clearly above the baseline V3 V4 V5 V6 however unlike this here there is a Jwave it's not just a sharp J there is a J wave so this tells me this may very well be earlier polarization if you have an S pulled above the baseline with a sharp J pawn this is not early parization but when you have it with a Jwave it may be early parization and indeed in this patient this is his full EKG this was early reporization and this was based on the fact that he had the same EKG a couple of years ago he also had negative serial troponin and note that with early reporization SC elevation is usually not that high but it can be up to 3 mm particularly in younger men or men who are athletes or Africanameans in the STEMI case I showed earlier look at this S lifted above the baseline and you have a sharp J point you don't have a Jwave here sharp J point s lifted with a sharp J point and this is from the paper by Dr smith that fairly standardized that feature and here you can see S lifted above the baseline with a sharp J point in that paper they did not define how many patient with lifted S-wave and sharp J point are STEMI they just showed that nobody with early reporization had that pattern now there is a second pattern that is being talked about that I want you to recognize it's called the South African flag pattern and in that case you have an ST elevation in two non-ontiguous leads in lead AVL and lead V2 along with inferior reciprocal SC depression so SC elevation in AVL and V2 sometimes in lead one this is very suggestive of acute diagonal occlusion and this is why it's called South African flag because it can fit within the colors of a South African flag so you have ST elevation in AVL and V2 and ST depression in lead three and in the inferior leads and sometimes ST elevation in lead one so again suggestive of diagonal occlusion now this is a third pattern that's being talked about this is what we call the aslanger pattern so in this case you have diffused ST depression particularly in the lateral leads 1 AVL and V4 through V6 sometimes pronounced ST depression along with ST elevation in one lead only usually lead three sometimes also in V1 and AVR but mainly in lead three this pattern is suggestive of an inferior occlusive MI or MI along with critical conccommittant non-ulprit disease so what happens the critical non-culpritate eskeeia will cause diffuse profound ST depression while the occlusion in the inferior territory will cause ST elevation this ST elevation in one territory and conccommittant ST depression from the anterior eskeeia will attenuate the inferior ST elevation except in lead three which is furthest away from the anterior wall and from the anterior wall ST depression axis so it's basically negation of the inferior ST elevation by the ST depression caused by anterior eskeeia however this is the pattern that to me is the weakest in terms of suggesting occlusive MI because the concern is that many of these patients rather have acute subindocardial eskeemia from left main or le disease along with CTO of the RCA or left circumflex not acute occlusion the CTO of the RCA receives collaterals from the L so when the LED gets eskeemic the CTO territory gets even more severely eskeemic and develop subtle ST elevation along with a diffuse ST depression attributed to the left main and L eskeia so it's a subtle ST elevation from diffused subendocar eskeeia that is more pronounced in the territory of a CTO so we need to take those patients urgently to the kath lab but don't feel compelled to intervene analyze your inj carefully and if you believe there are grade three or CC2 collaterals to an occluded RCA it may be CTO of the RCA with eskeema because of acute non-totally occlusive LED disease you may stop and consult for cabbage don't feel compelled to intervene again aser pattern out of all those patterns is the one that is least strongly suggestive of OMI in my experience And not just my experience based also on the asinger paper where patient with asinger pattern had a troponin that is way lower than the stem troponin 2.3 versus 34.8 a troponin although their tropponin was higher than the classic non- STEMI and also the aser patients only 25% had an acute occlusion here and 25% had a chronic total occlusion with which fits with my concern that many of those patient have just diffused subendocardial eskemia and a CTO in one territory that makes a still a little elevated in that particular territory this is another such case that illustrates my idea this is a 71-year-old man who's presenting with acute chest pain he has diffused pronounced SC depression along with ST elevation in V1 and AVR and ST elevation in lead three this patient actually has left main or three vessel diffused subendocardial eskeeia with CTO of the RCA so the eskeeia is more pronounced in the inferior wall when the left main gets eskeemic the RCA which is being fed by collaterals from the left gets more eskeemic than anything else and gets so eskeemic that you develop some degree of ST elevation injury in the inferior wall this is not primary RCA stemi you need to take this patient to the lab preferably urgently and if this patient's having active massive pulmonary edema you have the time probably to stabilize him diaries him before rushing him to the lab and decompensating his heart failure furthermore try to stabilize him if he's not stable yet and as I will describe in a little bit diffuse ST depression with ST elevation in V1 and or AVR is not a STEMI equivalent it is suggestive of profound eskeemia potentially in the left main but it's not a STEMI equivalent so we don't need to rush those patients to the Kath lab unless ST abnormality is profound and persistent which was the case of this patient that is why we took him urgently to the kath lab and found severe left main and led disease along with RCA CTO as we expected this is another asinger case from the literature and in this case with that ST elevation in three and ST depression in the lateral leads and somewhat diffusely as well as ST elevation in AVR this patient did not have an acute occlusion he had a critical left main lane led disease and not a full occlusion and that caused something similar to the asinger pattern so again beware of that pattern it's not always OMI now I described the first and most important group of OMI which is a subtle estation with morphological accompanying feature suggesting stem i will describe the three other ones number two is what we call hyperacute large and wide T- waves which also fit to some degree with the features I described under one the T-wave is not necessarily tall in absolute value most importantly it is wide and almost fused with the ST segment in one convex dome or it is tall in relative term it's almost the size of the shrinking QRS especially if associated with a shrinking QRS or subtle ST elevation or subtle reciprocal ST depression one subtype the dwinter hyperaccute T-wave is characterized by an ups sloping ST depression in less v1 through V6 followed by a tall upright T-wave unlike the classic typical hyperaccute T-wave that the winter pattern somehow never progresses to ST elevation so those patient are stuck in the phase of hyperaccute T-wave even as their MI evolves it doesn't have to be the dwinter hyperaccute wave any of those wide and or relatively tall T-wave are concerning for STEMI then the third pattern is STD depression that is maximal in leads V1 through V4 and which indicates posterior OMI typically it's SD pressure in V1 V4 along with an upright T-wave in those leads and frequently prominent Rwave in at least one of the leads V1 or V2 could be prominent in height or in width and it's reciprocal to a posterior Qwave then you have the fourth pattern which is left bounded branch block or LVH or ventricular pacing with a discordant ST elevation more than 25% or concurrent ST elevation so this is the posterior MI where you have a C depression in leads V2 through V4 along with an upright T and frequently a wide and or tall Rwave in leads V1 or V2 reflective of a posterior Q wave this is the winter hyperacute T-wave here in the anterior precordial leads you have that tall T-wave exceeding the height of QRS in leads V2 and almost in lead V3 along here with Q waves in leads V2 V3 and along with reciprocal ST depression in the inferior and lateral leads and along with ST elevation in AVR which indicates basil septile injury as in left main or proximal LED and in this particular case it was a proximal LED and be careful distinguish the winter T-waves from wellins T-wave the winter T- waves are anterior STEMI whereas well T-wave are non STEMI wellins T- waves are those bifphasic positive negative T- waves in le V2 through V4 with a sharp downs slope of the T almost 90° between the upright and the negative portion or deeply inverted T-wave in those precordial leads preceded by a straight or convex ST segment those well T-wave indicate L critical stenosis unstable stenosis but not STEMI and this is not an indication for emergent C this is a post eskeemic finding in a patient who at some point likely had ST depression or ST elevation but now is having the post eskeemic T abnormality now I will move on to the fourth group of OMI which is left bundle branch block with ST elevation i've given talks about that in the past keep in mind that acute new left bundle branch block is rarely seen with acute MI it was seen in 1% of acute in the gusto trial simply because the left bundle is supplied by the LED and the RCA it has dual supply so it's difficult to infark the left bundle and a new left bundle brush block is much more commonly a progression of a cardiammyopathy whether eskeemic or non-eskeemic chronic cardiammyopathy rather than an acute MI that said left boundary branch block is problematic in terms of STEMI diagnosis simply because left boundary branch block causes discordant ST changes so when the QRS is down in those precordial leads V1 through V4 ST will be elevated when the QRS is up in those leads one and AVL and V5 V6 ST will be depressed so imagine somebody has left bundle branch block and anterior ST elevation MI he inherently has ST elevation from the left boundary branch block how to know whether within that ST elevation there is also hidden STEMI type of ST elevation if you have concordant ST changes meaning ST depression in leads V1 through V3 or ST elevation in one or AVL that is a STEMI now the issue is that anterior STEMI from proximal LED occlusion may only have ST elevation in less V1 through V4 which would be discordant to the QRS without any concordant ST abnormality even inferior STEMI may only have discordant ST elevation with a downlooking EQRS how to tell if that isolated discordant ST elevation is a true STEMI the way you can tell is by looking at the ratio of that discordance what is that discordant ST elevation to QRS ratio if the ST elevation is large even more than 5 mm but the ST elevation to QRS is less than 25% this is just an ST elevation from left bond branch block this is not a STEMI on the other hand if you have ST elevation that is more than 25% even if it's not marked in absolute as in this patient this SC elevation here is about 2 and a half mm but it's way more than 25% % of the S or the QRS this is a STEMI here too you have an ST elevation that is about 3 mm but it is more than 25% of that QRS so this is a STEMI so the old scarosa criteria use 5 mm discordance to suggest STEMI that turned out to be insensitive and non-specific for STEMI so use the relative discordance as I've described in one paper as described by other authors such as Dr smith also in my paper a T-wave discordance meaning a discordant T that is over 50% of the QRS was also suggestive of STEMI so ST that is more than 25% of QRS and T that is more than 50% of QRS this is such an EKG of left boundary branch block with a STEMI you can see here the QRS is down there is discurrent SC elevation but that SC elevation is clearly more than 25% of the QRS in fact it's almost the size of the QRS here it's more than 25% of the QRS as well in V1 and in lead one and AVL you have concordant ST elevation and in the inferior lead you have concordant SD pressure so concordant acid depression or concordant acid elevation are suggestive of stemming in the setting of left branch block even the acid depression by itself if this concordant suggests stemming i want to explain why is ST elevation so mild in those olusive OMI or subtle stemming there are various explanation the most common explanation in my experience is that you have some flow to that infared territory you have either some spontaneous reconalization so the artery is not 100% occluded it's 99% or you have a subtotal rather than total occlusion or or you have subacute occlusion with good collateral flow and eskeemic preconditioning like the case I showed before where the patient had LED occlusion but CC2 collaterals from the diagonal and from the RCA this explains why the SE elevation is more subtle and why the troponin may not rise to STEMI level albeit it rises more than non- STEMI levels but not quite to STEMI levels and it may benefit from late PCI so those subtle STEMI even if you ended up cing them late they would still benefit from late PCI hypothetically more than STEMI these patients are on the overlap between STEMI and non- STEMI although again you should recognize those patterns and perform urgent cath and reconalization if you happen to not recognize it they would still benefit from a late cath hypothetically more than STEMI because there is some perfusion to that inferted territory another explanation why AC elevation is mild is late stemi in which case the EKG pattern would be like this you will have deep Q-wave with minimal residual Rwave so that's another case of subtle STEMI this is such a case where you have mild ST elevation but with deep anterior Qwave and you have reciprocal ST depression you have also mild acidic elevation with a shrinking QRS in leads one and AVL that also suggests STEMI now this EKG with deep Q and mild residual ST and R suggests late STEMI presentation more than 24 hours but it may be an earlier presentation with a spontaneous reconization so I would not exclude a benefit from revascularization in this patient based purely on the EKG if this patient has a history of presenting more than 24 hours ago with no ongoing chest pain and this EKG I would call this mild estivation because it's a late STEMI however an earlier presentation should be considered if symptom onset is described less than 24 hours ago or if the patient is still having ongoing chest pain in which case you need to take that patient emerently to the kath lab and recanalyze the occlusion eme now moving on the third explanation for the mild ST elevation in those subtle STEMI OMI cases again the first one is the most important one in my opinion but the third explanation is that the MI area is not well seen by 12 EKG such as posterior and lateral MI but again we have that SC depression in the anterior lead that will hint to those or you have a small MI territory that is not well seen by the EKG or you have a conccommatant STEMI in one territory example the ina territory and diffuse ST depression from eskeeia of another territory which attenuates the ST elevation as in the aser pattern and in that third subgroup such as the as a aser pattern as I explained many of the patients have diffused non- STEMI eskemia along with CTO of the RCA or left circumflex which makes the inferior wall have subtle ST elevation so we need to take those patients urgently for cal but don't always feel compelled to intervene analyze your indog carefully and if you believe there are grade three or CC2 collateral to an occluded right or left circumflex it may be CTO with eskeemia because of acute non-totally occlusive LED disease that supply collaterals to that CTO you may stop and consult for cabbage also in a patient with severe acute decompensated pulmonary edema and a pattern of mostly diffused pronounced ST depression and subtle ST elevation in one or two leads like that aser pattern consider stabilizing the patient and diarizing him before calf and seeing if EKG improves with heart failure and oxygenation improvement do not feel even compelled to take him super eagly one last note on ST elevation in AVR diffuse SC depression in more than six lead with ST elevation in AVR and V1 is not stemming it frequently indicates a high-risk non- STEMI with suggestion of diffuse extensive subendocardial eskeema from left main and or three vessel CAD that ST elevation in AVR must be accompanied by ST depression and other leads it's not just ST elevation in AVR this is not a STEMI or OMI now the explanation for that pattern is when you have diffused subendocardial eskeema in all leads you have an SC depression vector that is in this direction and you get reciprocal ST elevation in the northern leads in the leads looking away from the heart such as V1 and AVR and sometimes in lead AVL the so-called northern leads so you get that northern ST elevation in addition injury at the base of the heart from critical left main or proximal LED will cause acivvation in those northern leads V1 and AVR now that this fuse subendocara esma whether from free vessel or left main disease will cause elevation in both V1 and AVR however in the case of left main you will have more pronounce elevation in AVR than in V1 whereas in three vessel disease or in critical proximal L you will have ST elevation in V1 that is equal or more pronounced than AVR this is because left main critical disease and eskeeia cause a counterbalanced eskeemia of the proximal LED and the left circumflex the posterior wall so that you do not get as much SC elevation in V1 the SE elevation one gets attenuated by that posterior wall injury whereas SC elevation ABR remains very pronounced so elevation in AVR that is more than V1 or more than 1.5 mm is more suggestive of left main than L or three vessel eskemia so again that diffuse sta depression with SC elevation in AVR and or V1 is not STEMI and is not even always left men or three vessel disease it may be a global eskeeia from profound demand supply mismatch such as severe anemia severe prolonged hypoxmia profound hypotension or shock from any source even without any CAD and it's commonly seen it transiently postcardiac arrest even cardiac arrest with no CAD it may also be seen with severe hypocalemia so secondary eskeemia without extensive CAD is at least as commonly the cause of this EKG versus primary eskeemia and in this paper in American Journal of Medicine 10% of patient with diffused ST depression and ST elevation AVR had acute occlusion and 40% had no CAD they had that secondary eskeeia I told you about 60% overall had severe CAD so around half the time this pattern may reflect secondary eskeeia not primary CAD eskeemia now do we need to cath these patients urgently not necessarily urgent cath is needed only in case of deep and persistent ST abnormality for example persistent over 30 minutes or so in the absence of a context of demand supply mismatch like severe anemia or non-cardiogenic shock