 So today is the day for cardiac imaging and the field of cardiac imaging is really advancing and I would like to share my experience and how imaging can be helpful. So all of us know about this MRI brain with an acute infection on the diffusion weighted images and once it shows the hemorrhage, the prognosis is different, the treatment is different, the entire concept towards the patient changes by the clinician. Similarly, the same is true even for the myocardial infection. So today I'm going to present an article about intramyocardial hemorrhage and how it happens with the reperfusion injury and how it compromises myocardial salvage. It is clinically very relevant and very important to clinician because the entire management and the prognosis is different. So this is an article which is recently published in Journal of American College of Cardiology. Dr. Ting Liu from Hong Kong is the main author along with others. The article is based about acute myocardial infarction. So as we are aware that these infarctions are treated with reperfusion therapy, whether it could be pharmacological or it could be post-trenting. This reperfusion therapy for acute MI is life-saving but the benefit of the reperfusion therapy can be paradoxically diminished by the reperfusion injury. Reperfusion injury basically means microvascular obstruction, intramyocardial hemorrhage and all this, the patient prognosis will be impaired and also the MI size will also increase. So what they've seen that they've studied the cardiac troponin markers that is biomarkers in all those patients with ST segmented elevated MI patients. Once on the ECG you have ST segment, you definitely know that it is a full thickness transmural myocardial infarction. These patients were then classified whether they developed hemorrhage or non-hemorrhage, non-hemorrhagic infarct. Same thing like how we do it for our brain cases. We will discuss about how cardiac MR can differentiate between the hemorrhagic MI and non-hemorrhagic MI. In this study basically these patients were followed up along with biomarkers along with MRI and how they improved on the treatment. So the final bottom line is that myocardial hemorrhage is determinant for size of the myocardial infarction. It drives the MI expansion after reperfusion and compromises myocardial salvage. This introduces a clinical role of intramyocardial hemorrhage in the acute care management, risk assessment and future therapeutics. So basically this is about the microvascular well-letcher of the heart. So as we are aware that apart from these epicardial arteries there is significant microvascular micro vessels which are there all throughout the heart. Once they get obstructed it deals with microvascular obstructions. Now these areas of MVOs can expand up to 48 hours following reperfusion. Also once they are destroyed they can result into intramyocardial hemorrhage. As we are see over here that you know there could be some capillary burst and some RBCs and WBCs which could be going down in the myocardium itself. Now this intramyocardial hemorrhage will increase the infarction size and it is known that it will exaggerate the microvascular compromise by causing further external compression, further vasospasm and thus by extending the zone of hypoxia. In case if there is hemolysis there will be some iron which will be released which will be further cytotoxic and this will be again increasing the edema. So this all these effects of MVO and intramyocardial hemorrhage are really deteriorating for the patient. So as once you do reperfusion whether it could be pharmacologic or post-tenting there will be some amount of cytotoxic biomarkers which are already released. There will be some high distending intramuscular pressure in the distal vessels. Because of all this there will be bursting of the hypoxic capillary endothelium and which will further lead to intramyocardial hemorrhage. So in this study they have studied around 64 patients with ST segmented elevated MI. All these patients underwent coronary angiography. They identified the culprit vessel which was either most of the cases LAD, LCX or RCA. All these patients proponent markers were studied before and during the study. Cardiac MRI was performed after five days and then this amyocardial infarction were classified as hemorrhagic and non-hemorrhagic. Apart from these patients they also had a canine model in which they also along with to look for the area at risk that is why they did the dual modality system with integrated positon emission tomography system as well. From the cardiac MRI all the patients underwent a routine dedicated cardiac MRI with sine images, late gallulium enhancement images. For intramyocardial hemorrhage T2 star mapping is the modality is the sequence of choice. Basically it is the same sequence it is a multi-echo sequence what we use it for the thelaemia for the ion overload. So T2 star is very sensitive to ion so it would be very important sequence to do in intramyocardial hemorrhage. All CMR image analysis was performed on a dedicated cardiac MR software processing software. They all the MIs were identified based on the late gallulium enhancement images and they were quantified that anything above five standard deviation to the remote as to the mean signal intensity of remote myocardium then there was a delineated whether there is myocardial infarction with MVO and those patients with MVO who had this T2 star values which were at least two standard above the normal values then they were classified as intramyocardial hemorrhage. One other parameter what can help is at least two standard above the T2 star values or basically taking that anything below 20 milliseconds then you know that T2 star below 20 milliseconds is definitely IMH. So the images were classified whether hemorrhagic or non-hemorrhagic MI. So all these patients with ST segmented elevated MI underwent an angiogram. Post PCI they were classified as infarction with so what you see over here this dark areas are the areas of microvascular obstruction. So this is an area of infar and the MVO's were calculated and within this MVO in case if the patient had anything T2 star values with less than 20 milliseconds they were classified as hemorrhagic myocardial infarction. Again base mid and apical that is why try to taking the entire left ventricle in the short axis views is important. Non-hemorrhagic MI again from taking the short axis views basal mid and apical assessing the late cadmium enhancement images taking an area of infarction and calculating in case if there is any T2 star values. So T2 star values less than 20 milliseconds were classified as hemorrhagic MI while non-hemorrhagic MI when T2 star values were more than 20 milliseconds. So those patients who developed intramiocardial hemorrhage as it is seen over here. So these are the short axis images and you see an area of hyper enhancement delayed hyper enhancement images within this bright areas there is this dark areas. So these are the areas of microvascular obstruction as you see over here. So in case if this within this MVO if the patient had any values of T2 star values of less than 20 milliseconds this quantifies intramiocardial hemorrhage and then serially these patients were studied over less than 1 hour 24 hours, 2 days, 5 days, 7 days and 8 days. So these patients were serially followed up for the in fact size amount of IMH amount of LV function and all other myocardial salvage parameters. Again this is the T2 star value T2 star mapping is obtained as base mid and apex and within this we can classify and quantify the amount of intramiocardial hemorrhage. These are the patients who developed who did not have intramiocardial hemorrhage and as you can see over here that within this these are the areas of late gallulium enhancement late gallulium enhancement is seen over here and these areas they did not show any T2 star values of less than below 20 milliseconds and there was no evidence of any altered signal attenuation signal density in these areas. So these were classified as the patients who did not have intramiocardial hemorrhage. So all these patients 64 patients were studied and followed up and these were the few main conclusion or main results what they found. They found that all those reperfused semi patients with intramiocardial hemorrhage had larger myocardial infarctions. So the in fact size was significantly higher in this group and we can see it on these images as well. Just look at this bright scar. So this is an area and even after 8 weeks the amount of infarction which was present while comparatively in those patients who did not have intramiocardial hemorrhage definitely had a reduced MI size. MI size the larger the size worst is the prognosis more is the arrhythmia risk more is the morbidity. So the entire management and complications will be increased in this group of patients. Troponin markers. Cardiac troponin markers were also significantly high in intra with the patients with IMH as you see over here they have a rapid rise and they were still persistently higher even after day 5 or day 7. So all those patients with IMH they had significant rise of cardiac troponin markers. Cardiac troponin that is tropi is basically one of the parameter for myocardial necrosis. More is the necrosis the higher will be the values. Timelapse non-invasive imaging shows that the MI size post reperfusion depends on the IMH status. So even after 8 weeks as we had seen in the diagram the scar size which was persistent was significantly higher in those patients who had IMH present in the myocardium. So again more is the scar more is the chance of arrhythmia worst will be the clinical outcome. So all this is very important for the patient's follow-up. Patients who had myocardial hemorrhage they had an infarction which was expanding transparently in wavefront fashion. So basically this is the how the reperfusion injury ischemia and reperfusion will again go and this will be like a time dependent phenomenon and this will be like a wavefront. While those patients who did not have IMH will have a prognosis like this but here there will be spikes of increase of the ischemia and reperfusion. Again because of myocardial hemorrhage there will be compression, vasospasm and again the ischemia it will be like a vicious cycle. More importantly even there is a therapeutic window for reperfusion. Now what you see over here that once the patient's develops and myocardial infarction it is important that the reperfusion is performed within 12 hours. If this is the therapeutic window for reperfusion anything below 12 to 24 hours you can see that the salvaged myocardium will be significantly reduced. So in case whenever the patient develops an infarction the reperfusion therapy should be obtained in this initial few hours. More than 24 hours there is no scope for pharmacological or interventional reperfusion and this is how even the mean MI size with normalized to area at risk it is different for the intra myocardial hemorrhage with or without IMH. Now this is another article how it shows that how reperfusion images. So for example that after occlusion this is the area at risk and there is a hypothetical benefit that you know following reperfusion maybe you can you know salvageable myocardium and only this will be the infarction size but actually the real benefit after infarction therapy is only this much because there will be definitely some amount of muscle loss due to reperfusion injury. So it is always like a double edged sword where you can actually without reperfusion injury sometimes the benefit is more rather than along with reperfusion because it will definitely compromise some amount of myocardial salvage. This is the central illustration of this article that how it shows that once the patient gets a myocardial infarction if the infarction is hemorrhagic which we can very well see it on cardiac MR using T2 star mapping values after there will be in case those hemorrhagic MI will have a rapid infarction expansion and then along with that there will be a stable infarction size but you can see the amount of myocardial scar which will be there which is over here while those non-hemorrhagic will have only minimal infarction expansion and they also will have a stable infarct infarct size but the amount of infarct size what you can see is significantly different. So hemorrhagic MI's post reperfusion the cardiac troponin peak is earlier as we had seen they expand following a wave front pattern and they are more transmural as it is seen over here hemorrhagic myocardial infarctions are twofold larger in size and they have a threefold progressive loss of salvageable myocardium. So this is the difference between the hemorrhagic myocardial infarction and non-hemorrhagic myocardial infarction which is clinically so important. The bottom line of this that once there is a non-hemorrhagic infarct there will be some amount of necrosis edema but in the chronic stage it will stabilize to a scar pattern. Once the patient has a scar which is significantly higher in cases of hemorrhagic myocardium along with some amount of necrosis edema the scar size will be more iron again will be cytotoxic which would be persistent and the edema also will persist for a longer time. So the entire prognosis the scar size edema pattern all this will be different from the hemorrhagic and non-hemorrhagic myocardial infarction. So it is important that we identify these cases of intra myocardial hemorrhage tell the clinicians because depending on that the pharmacotherapy will be different depending on that patient prognosis will be different. Also important that reperfusion therapy is like a double edged sword it has to be performed within that crucial window similarly like how we do it for the cerebral infarction and everything. So similarly the field is we have to be competent enough and tell our clinicians the and explain the prognosis. Yeah so now I'll move over to the case so basically here I'm going to show two different cases of cardiac MR. So in cardiac MR whenever you have this viability imaging especially in acute coronary syndrome it is important that we evaluate also for intra myocardial hemorrhage. Yeah so okay so this was a 54 year old male non-diabetic non-hypertensive early morning five o'clock he had resting angina by the time he reached to this nursing home it was 1 p.m. and there he was thrombolyzed pharmacological thrombolysis was done clinically he improved ECG showed less than 50% of resolution but however since it was a tertiary he was shifted to a better hospital. Hospital he reached around 1230 and again he had an ECG re-elevation so because of this there was no angina no LVF troponin levels were elevated but this ECG re-elevation and anyway he required a catheter angiography so they went ahead with the catheter angiography. This is an ECG where you can see that from V1 to V6 this is an ST segment elevated MI so once you have this much ST segment elevation you know that this is a transmural scar these are the 2D echo images and you can see over here this part the apical part is not moving so there is a kinesia partly of the septum and all apical segment so this fits into LAD territory in fact so this is how the catheter angiography was performed and you can see over here there is a tight stenosis in the proximal left anterior descending artery again if you can see over here there is almost 80 to 90 percent stenosis in the proximal LAD right coronary artery no significant narrowing so since this was a short segment tight stenosis they went ahead with the and he was still in that window period of 24 hours they went ahead with the plastic and stenting you can see the guide wire which is going inside inflating the bulb and putting the coronary stench so this is how a good result definitely the interventional cardiologist will be very happy to see this kind of result post stenting follow-up and it can be seen that there is good amount of all the distal vessels are also filling up and the complete opacification of mid and distal LAD is seen yeah so with angiography anyone will say it is a very good positive result patient's clinical outcome should be very good this is the post stenting angio but let us see what happened on cardiac MR so again this as compared to this similar study the cardiac MRI was performed on day five after the catheter angiography or stenting was done before the discharge just to prognosticate the patient so these are two chamber four chamber and three chamber sine images what you can see over here as was seen on the 2d echocardiography there is a kinesia involving all the apical segments and interventricular septum the lateral wall inferior wall is moving well so it is important that you compare all the long axis images this is again the anterior wall and apical segments are really a kinetic and this is the three chamber images so this is the short axis sine stack images and since it is an acute MI there is no loss of myocardium so hence there is no thinning what you see in chronic myocardial infarction but there is definitely a kinesia of the anterior wall interventicular septum and all apical segments ejection fraction was significantly reduced around 27 to 30 percent this is a normal perfusion scan not an adenosine stress perfusion this is a rest perfusion scan and as you can see over here there is a perfusion defect in the interventricular septum all the basal mid and apical lv segments show perfusion defect and this is fitting into l ad territory this is the strain mapping images for all the novices in cardiac imaging basic this is a cmr strain with feature tracking images basically it is a definitely a better parameter for lv systolic function because on the ef you are just explaining the short axis views but it is important that we understand about the longitudinal deformation as well and hence all the new prognostic markers are based on the global longitudinal strain so this is a gls parameter that will be again helpful for the clinician parametric mapping it is important that you do t1 and t2 mapping t1 mapping is for the fibrosis t2 mapping is for the edema so especially in interesting cases like in this cases of acute coronary syndrome or cardiomyopathy it is important that we perform this and again taking base mid apical three short axis views and as you see over here this is a 16 segment mullsi model where each and every segment whatever is the value we can quantify and here what you see over here that on the native t1 mapping there is definitely some amount of fibrosis which is set in in the septum and as well as the apical segments post t1 for the calculation of this extra corpuscular volume it is important that we take t1 mapping values pre and post contrast now wherever the contrast is gone the gadolinium that part will actually show gadolinium uptake and then it will be reduced signal intensity but as you can see over here this part in the interventricular septum is showing increased signal because the gadolinium has not reached there and which means that there is some amount of microvascular obstruction t2 mapping values are important especially for the myocardial edema and as you can see there is increased value in the septum so whenever there is an acute mi t2 mapping values will be elevated and the most crucial set of images in any cardiac MR is late gadolinium enhancement images and as you can see over here there is a transmutals scar involving the anterior wall interventricular septum and all the apical segments so this is a transmutals scar but within this scar there are this dark areas so these are the dark areas which are called as microvascular obstruction so as we had seen in the article whenever there is a significant disease and the microvascular microvascular of the myocardium gets destroyed you will have this kind of it is termed as no reflow phenomenon so here basically there will not be any gadolinium which will be going there and hence this will be a microvascular destruction MVOs areas of MVOs and within you can as you can see over here you can see the entire anterior wall all apical segments all the territory is completely scarred with large areas of microvascular obstruction and destruction these are LG images again should be obtained in all the planes all the short axis four chamber two chamber and three chamber and they have to be seen together along with long axis and short axis view as well as with the sine images so as we can see over here even with the delayed images there is a persistent area of MVO which are seen in the septum and apical segments T1 pre-contrast and post-contrast images but as you can see over here this area is relatively does not take up gadolinium and hence this was suspicious for intramiocardial hemorrhage and hence we evaluated these are the T2 star images the gradient echo images basically taken in basal mid and apical segments and here when we take an ROI in that involved area the T2 star values are below 20 milliseconds 9 milliseconds so this is a definite area of intramiocardial hemorrhage which has occurred post reperfusion this is definitely a poor prognostic science and the clinician should be aware this patient should require more follow-up and more aggressive medical treatment so it is imperative that you know the entire prognosis morbidity all this will be different for this group of patients as we have seen in our article moving on to another case this was another patient who presented with chest pain and who developed again the similar infarction in the septum and the anterior wall these are the long axis images two chamber four chamber and again the anterior wall is a kinetic apical segments LV apex anterior wall is relatively a kinetic as compared to lateral wall and this is an area of transpural scar with a large scar of micro vestibular obstruction as it can be seen over here but again the same LED territory in fact with late gradient enhancement images but as we see over here when we took this T2 star values and in T2 star values taking the ROI putting the ROI in the septum area the T2 star values are definitely about 20 milliseconds which confirms that there is no intra myocardial hemorrhage so this patient will have better prognosis as compared to the first one but however still he has a large LED territory in fact but the entire pharmacotherapy the entire management the entire prognosis is different something about the area at risk and myocardial infarction as we can see over here that whenever there is an increased duration of ischemia so normally acute MI develops when there is myocardial ischemia which is lasting for more than 20 to 40 minutes but once the ischemia goes for a longer time then the infarctoid myocardium will actually start from the end of subendocardium and that will be progressing like a wave front to the epicardial layer once you have a complete transpural necrosis ischemia has already lasted for four to six hours so if this ischemic myocardium is repurposed early that is within 24 hours the degree of myocardial salvage exceeds the necrosis mvo or im mesh basically they go hand in hand they are closely linked and they often coexist so it is important that those areas of mpo we also do 32 star values and assess for imh by this mvo occur that whenever there is an ischemia there will be some amount of inflammation some amount of myocyte death edema will be there in the adjoining tissues because of this there will lead to endotere dysfunction some micro thrombi can also go and again which will result into a reperfusion injury and with stenting there will be some embolic emboli which will go into the microvascular microvascular all this patient who lead more myocyte death and leading to myocardial stunning and arrhythmia and this will be definitely causing worsening of the ischemic cardiac injury mvo can happen whenever there is a prolonged ischemic injury as we have seen like more than 4 to 6 hours it can also occur because of reperfusion injury as it could be pharmacological or post intervention sometimes because of the distal embolization as we have seen that the thrombus itself can go into microvascular and cause the mvo or when the injury is so much prolonged and extensive that there is an injury to micro circulation so all these are the causes which leads to microvascular obstruction and it is basically an independent risk factor and there is definitely increased cases of all cos mortality and heart failure it will lead to adverse left ventricular remodeling and poor prognosis cardiac mr basically with multiple sequences using late gallium enhancement images sometimes early gallium enhancement can be done for the mvo perfusion scan parametric mapping all this sequence is probably we can actually calculate the amount of area it is the amount of infection microvascular obstruction hemorrhage and thrombus so this is a value of cardiac mr in cases of acute coronary syndrome lastly what we have studied today is about the intramiocardial hemorrhage it is a subset of severe microvascular damage and it is a its presence of IMH is a malicious sign because it will lead to severe ischemic injury not in the acute setting but even in the healing phase here this amount of necrotic tissue will be replaced by scar which will be much more in the size and will have a poor outcome simple microvascular obstruction will reduce in size so what you can see over here whenever you have a doubt whether there is a thrombus or a wall ladder and thrombus or a microvascular obstruction it is better that you take a delayed images the area of mvo's will fill up so there will be some amount of temporal evaluation that you can differentiate whether it is an presence within the mvo apart from that the microvascular obstruction will be within the areas of lge so you have to have a classical lge scar all throughout and within this bright areas you identify this dark areas which will be termed as microvascular obstruction most importantly that how we modify our protocol for whether it is like it's a cartilage assessment we tell the radiographer to do accordingly whenever there's a tumor we do our tumor protocol so similarly even in cardiac MR every clinical indication has to be studied what is the clinical question and depending on that your planning and sequences should be done and it is important that we understand everything about the physiology thank you