I want to talk today about non stemy Cath and PCI tips and I want to focus on those three ideas how to manage non stemi after cath according to the severity of stenosis particularly mild or intermediate stenosis number two if you have multivessel disease how do you decide which one is the culprit and if you have multivessel disease how to manage what you consider non-c corate lesions first in non stemi if cath shows a major coronary artery with hazy stenosis less than 50% do not stent it but strongly consider ivis of this Legion if the diameter stenosis is truly less than 50% do not stent it even if there is a thrombus or plaque rupture this is what we call minoa mi with nonobstructive coronary arteries which is treated medically if the stenosis is over 70% in a major coronary territory then perform PCI as per the early invasive Trials of non stemi if cath shows a stenosis of 50 to 70% this is where the decision making is tricky what do you do next you can do IFR or ffr R but conceptually ffr does not make much sense for the culprit Legion or what is considered to be culprit leion particularly in the setting of single vessel disease as the microcirculation is impaired in the first 24 hours of ACS so we cannot get microvascular hyperemia and that microcirculation remains impaired for up to 5 days so IFR ffr is much validated and much less conceptually valid in mi than in CAD setting especially for what is suspected to be culprit stenosis yet there is some data that suggests it's acceptable in mi you have the famous non stemi trial where PCI versus ffr guided PCI of all lesions in non stemi culprit or not culprit uh led to the same M at one here so ffr was not harmful and it reduced the number of stance then you have the prime ffr registry where systematic ffr measurement in the setting of non stemi led to a change in management strategy in 38% of patient from medical therapy to revascularization or vice versa without an adverse impact on mace death Mii or engina at one year you also have have a trials using ffr and IFR for non-culprit stenosis in stemi and non stemi particularly for 50 to 70% stenosis which indirectly May validate the use of ffr IFR for non-culprit stenosis in ACS setting and those are the fire trial and biov vasque trial as well as frame Ami and less so flower Ami so I or ffr may be used but it's questionable in the setting of Mi some data support it's used but the better option in those intermediate leion in non stemi setting is to do IIs and in mi context stent if IIs shows a diameter stenosis more than 50% with a plaque disruption or thrombus or if it shows diameter stenosis more than 70% and here for those ivis features I'm extrapolating from The Landmark early invasive trials which used diameter stenosis to decide about stenting and that would be diameter stenosis at the leion site in comparison to the distal reference Lumen or the average proximal and distal reference lumens however since by I and OC we usually go by area minimal Lumin area rather than diameter you may rather use more traditional Imaging criteria to decide about stenting as for example the criteria used in the flavor trial of ivis versus ffr or the prevent trial and that will be a minimal Lumen area at delion sites Less Than 3 mm squar or 3 to 4 mm squared with a plaque disruption or a plaque burden More than 70% plaque burden meaning this plaque at the legion site More than 70% of the whole vessel area at the leion side this is a recently published metaanalysis of PCI of non-ul stenosis after Mi and it showed that in mi setting for non culprit PCI there was no significant differences in all cause or cardiovascular mortality or mace between angiography and Physiology guidance therefore ffr is less validated in mi setting than in stable CAD but it may remain useful for 50 to 70% lesions especially when those lesions are deemed non-culprit and is not harmful compared to neographic guidance and and ffr IFR guidance is given a class 2B for non- culprate lesion in the setting of non stemi by ACS guidelines it's not given a recommendation for culprit lesions in non stemi now aside from those intermediate Legions if you find a plaque disruption by occt or ivis and the diameter stenosis is less than 50% what what is the next step should you stent it finding a plaque rupture or erosion with stenosis L 50% does not imply stenting this is what we call minoa again but it is relevant to make the diagnosis of plaque rupture or erosion for secondary Mi prevention for example you should use DAP in those patient aggressive Statin and LDL lowering and aggressive blood pressure management and why do I say that those patients should not receive stenting this is based on the landmark studies of early invasive strategy in non stemi those big three taac stei Frisk 2 and R 3 trials and based on the landmark studies of primary PCI in stemi and pharmaco invasive trials in stemi all recommended revascularization for culprit stenosis more than 50% in geographically or even 70% in half of the studies PCI for Mi with luminal stenosis Le less than 50% and highrisk IIs features has not been studied on a large scale and is not recommended and actually PCI of lesions with luminous stenosis less than 50% and high-risk ivis features have been questioned by several small scale studies such as those ones IIs o is still highly valuable in mi with less than 50% angiographic culprit stenosis one to assess luminal stenosis and confirm it's truly less than 50% and when you assess the luminal stenosis by ivis you're comparing it to the reference Lumen whether the distal reference Lumen or the average proximal and distal reference lumens the second value of ivis occt in this setting is to establish the diagnosis of plaque disruption versus other causes of what seems to be minoa such as myopericarditis or coronary vasospasm and when you establish diagnosis you dictate aggressive medical therapy so the bottom line of all I'm talking about is if you have a plaque rupture with luminal stenosis truly less than 50% do not stand if you have a plaque rupture with luminal stenosis over 50% definitely stand as I indicated here and if you have luminal stenosis in non stemi over 70% regardless of other ivis feature in the setting of non stemi you should definitely stand so those are three case scenarios where the luminal stenosis is less than 50% in geographically but the legion looks hazy and indeed it's it's much more severe by ivis Imaging this is an Ecentric leion and Lumen is indicated by the white most in Geographic views as indicated by the blue arrows will make that leion appear mild as the whole vessel may seem to be filled with contrast only this angle here will show you the true severity of the Legion but you may not perform that angle look at this Legion here this Legion is tight but looks mild angiographically from all angles it's a serpiginous legion with mild contrast filling in all directions this is the third type of deceiving lesions angiographically this is a legion that is tight with an ulcer a crater here the ulcer is not a functional Lumen but it fills with contrast and may make the angiographic stenosis look mild in most views those Legions may not look tight in geographically but may look hazy and that's your hint in non stemi to a potentially more severe unstable leion now the second big topic of this talk if you have a non stemi and you find multivessel disease how do you define which one is the culprit these are important ideas to recognize culprit leion is unclear or misidentified in 40% of non- stemi patient and this has been confirmed in an MRI study published in 2019 this study here and the culprit lesion is misidentified especially that multiple obstructive more than 50% stenosis with complex angiographic features are seen angiographically in up to 40% of Mi patients this has been demonstrated in stemi based on the Goldstein Landmark trial published in 2000 and by extrapolation in non stemi and in fact based on the Vanquish analysis multiple Legions have been considered culprit in 10% of non stemi so it's not only that you have multiple complex obstructive plaques in up to 40% of patients you have impossibility to discern the culprit in 10% of non-stemi patients and what do you use to the side the culprit you can use the geographic lesion features EKG echal motion abnormality and ivis OCT and I will explain some of those MRI is the best but it's not cost effective and by MRI you go by the erasion of late gadolinium enhancement or acute edema on tt2 Imaging to define the infar area and this is from the ESC guidelines they recommend going by some geographic features I will explain but they mainly recommend IIs or preferably OC in those patients looking for plaque erosion or plaque rupture or what we call erosive calcified nodule as well as a scad features as I've explained under my OCT talk of complex coronary lesions and this is how we defined a complex Legion in geographically the legion has to be over 50% obstructive along with one of those three morphological features number one thrombus and thrombus is defined as around intraluminal filling defect or as D stain that hangs around after contrast clear from the remainder of the vessel and in case you have an acute occlusion if that occlusion abruptly ends with a squared off or convex morphology that suggests an acute occlusion the second morphological feature is an ulcerated plaque and an ulceration is defined as contrast seeping beyond the Lumen into the vessel wall and number three complex feature is what we call an Ecentric lesion with irregular edges or an Ecentric lesion with overhanging edges this is what we call here overhang now regarding EKG can you define in non stemi the culprit by EKG the answer is frequently no and the reason for that is that ST depression unlike St elevation does not localize eskee the extent and the the magnitude of SC depression correlate with the extent and the severity of esia but not with the location of eskia however if you have extensive and deep ST depression you're more likely to have left man or LED or multivessel esea such as in the case scenario of diffuse ST depression in more than six leads with st elevation in AVR and V1 however the location of the SD depression does not localize ischemia and I will explain why in any esia transmural or nontransmural esia you get voltage gradient during the ST segment between the normal area and the es schic area which causes St deviation now in transmural esia this gradient will be looking toward the injured area hence you get St elevation in that area you have all those vectors looking to the esic area which causes St elevation in the leads corresponding to that area in subendocardial esia on the other hand the gradient will be from all normal areas but also from the normal areas within the same wall between the sub epicardium and the subendocardium since the LV and Apex have the largest myocardial mass and repolarize earlier than the rest of the LV like the base of the LV the current will often originate from this apical area leading to a c depression in V4 V6 even if you have inferior esia so even if you have inferior esia you'll get the biggest ST depression in V4 V6 more than the inferior leads so that's why I C depression doesn't localize esia now other ideas that help you localize esia on the EK G in non stamy is wellin Wellen T abnormality in the precordial leaves indicates LED disease this by phasic T abnormality or that deep T inversion preceded by an UPS sloping convex or straight ST segment that localizes esia to the LED subtle St elevation also localizes esia to the area of subtle s elevation now those patients are on the overlap between stemy and non stemi they are not really truly a non stemi and Echo wall motion abnormality helps localize ischemia the problem is that frequently you don't have W motion abnormality you must either have ongoing esia or you must have had extensive esea so that a degree of stunning or necrosis persist after esia resolves I'll move on to the third big topic of this talk if you have non stemi with multivessel disease over 50% on Cal and you've been able to define the culprit using some of those prior feature whether intravascular Imaging or inogram or some of the EKG or Echo features in those cases should you do multivessel PCI or culprit only and What's the timing of non-culprit PCI so the answer answer to number one is yes perform complete multivessel PCI rather than culprit only PCI as we do in stemi this is based on extrapolation of stemi trial and are there any trials in non stemi there is really only one trial that addresses that question directly in non stemi that you should perform multivessel PCI in non stemi it's the fire trial which showed that in L patient more than 75 with stemi or mostly non stemi PCI of non-culprit stenosis more than 50% Guided by IFR or ffr immediately after culprit PCI in the same setting or before discharge reduces Mi and even death at one year compared to culprit only PCI so yes we should perform multivessel PCI whether in the same setting or soon afterward then the question is what's the exact timing of non-culprit PCI well it's probably even more important in non stemi to perform multivessel PCI in the same setting because the culprate artery may not be clearly identified in non stemi and therefore multivessel intervention is further justified in non stemi and as I mentioned according to MRI analysis the culprit artery is misidentified by catheterization in 3 5 to 40% of patients and to further prove this point you have the biov vasque trial which compared immediate multivessel PCI of culprit and non-culprit in the same setting versus treating the culprit then treating the non-culprit PCI later on within six weeks and it showed the biov vas that immediate non- culprate PCI was as safe as later PCI in non stemi and in stemi but specifically in the non stemi subgroup immediate non-culprit PCI was associated with 3% significantly less recurrent Mi mainly because the culprit may be misidentified and this is particularly the case if you think the non-culprit is simple and quick the Ral function is preserved you haven't used a lot of contrast and especially if the patient is not too sick to tolerate a more prolonged multivessel procedure bias suggests a significant early risk of non-culprit Ami during the waiting period particularly because in nonsi you may misidentify the culprit and that non-culprit may actually be your culprit Legion hence the importance of limiting the delay before non- culprate PCI so even if you don't do multivessel PCI on the same setting try to do it before discharge or maybe within 2 weeks don't wait 6 weeks so the bottom line of that talk is the following in non stemi perform PCI of culprit and non-culprit lesions that are in geographically More than 70% this is based on early invasive trial and biov vasque trial and try to perform multivessel PCI in the same setting or before discharge or probably at the latest within two weeks perform PCI of all lesions that are 50 to 70% stenotic if they have unstable features by IIs occt or potentially if they are deemed significant by IFR ffr as in the fire and biov vasque trials which use IFR ffr for those intermediate lesions keeping in mind that IFR ffr is less validated in the Mi setting than stable CAD setting particularly for what seems to be a culprit Legion