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Posted By lauren small, Thursday, June 11, 2020
Updated: Thursday, June 11, 2020

This webinar recording can be found here:


Questions & Answers


Q: Is balanced ischemia/perfusion defect a concern give the severe 3 vessel CAD?           

A: Not in the case shown because there was a clear inferior defect. We discussed the concept of balanced ischemia more in the webinar. In summary, though possible, it is less likely due to the superior resolution of CMR vs nuclear.


Q: Do you ever pay attention to myocardial thickening in vasodilator stress, or it is not worth to proceed with cine images?        

A: No - I would not use wall thickening in that way but getting an accurate assessment of global and regional LV function is one of the great advantages of CMR so would always do this as part of the protocol


Q: What’s the value PCI done for diagnosis and treatment?   

A: PCI would not have much value in diagnosis as the diagnosis was 3 vessel coronary artery disease based on the angiogram. The CMR would indicate previous coronary artery disease with an inferior infarction and superimposed inferior ischemia. I would agree that the final strategy was to stent the LAD and LCx and not the RCA even though that is where the ischemia was. However, the PCI to the LAD and LCx were easy, the RCA PCI would be either an anterograde or retrograde CTO and the huge number of collaterals on the angiogram would suggest that this would be challenging if possible. I think that the interventional cardiologist has relied on the concept of total ischemic burden to try to improve the circulation to the LAD and LCx territories and thereby improve the ability for the collaterals to increase flow to the mid to distal RCA beyond the CTO. It is not the best argument or the best use of the CMR but that is what was done, and it is not the first time I have seen these sorts of strategies (even though it seems 100% counter intuitive to the CMR). Certainly, in graft cases I have seen where performing PCI the LAD will relieve inferior ischemia due to this concept so I think in attributing ischemia to a specific artery one needs to be careful, particularly with collaterals etc. That said I would agree the CMR would have suggested treat the RCA.


Q: How do you achieve that the diaphragm does not move in the perfusion sequence?    

A: Well spotted! So, we do 2 things - the first is we get the patients to hold their breath during the first pass and usually we try to do it so that they are most still at the critical 5-7 frames when then first pass happens. We also have a motion corrected sequence (MOCO) so that will stabilize the myocardium to the centre of the image and partly deform the myocardium so that it appears the same shape (so a circle) on each image. It makes it much easier to read the results of the scan quickly!


Q:How do you explain the presence of LGE with 50% transmurality if stress perfusion was present only at stress?

A: Clarify what is telling you which piece of information. 1) Stress perfusion is to demonstrate areas of ischemia. 2) Then use the late gadolinium enhancement to assess areas of infarction 3) I rarely look at rest perfusion unless there has been a technical arterfact with the stress scan to try to see if I can then use the rest perfusion to understand that artefact and interpret the stress scan. Do not get fooled - infarction can often be present where you get a defect only during stress and the reasons why this occurs are complex and not well understood (though as rest is usually acquired after stress it is thought to relate to the fact that the infarct then has a high concentration of contrast within it). Late Gad has a much better spatial resolution and signal to noise ratio than first pass perfusion so use that for the assessment of infarction to subtract from perfusion defects.


Q: Can you give an account on tips to make the defect clearest? 

A: Window properly - I like it fairly dark and make sure the contrast enhanced areas are not too bright.


Q: Was there inferior infarct? Not super convincing on LGE or rest perfusion.

A: Yes, there was a small subendocardial infarct in the inferior wall. Not the easiest to see but was present.


Q: Isn’t the perfusion defect mainly corresponding to the RCA territory?

A: Yes.


Q: You had delayed enhancement 50%. Won’t that be non-viable?            

A: Agreed. LGE was <50% hence viable.


Q: I struggle to interpret perfusion studies in children with dilated coronaries in Kawasaki disease. I find that there is variable perfusion in areas of LGE, with minimal wall motion defects. How to interpret these?      

A: Same method as usual. I have little experience in Kawasaki disease to be honest and care should be taken as the contrast will get delayed in the coronary aneurysms. If there is some viable myocardium around dead myocardium then it may well still contract and we see this often.


Q: How did perfusion help in first case?

A: Good question…Based on CMR, there were defects in the RCA (not stented), LAD (stented), but not in the LCx (stented). This was an old case, but I think that nowadays our interventionalists would have either performed FFR to LCx or believed the CMR (post MR-INFROM study) and wouldn't have stented the LCX in the first place. PCI to RCA CTO is a different story and the patient was not very keen to proceed, given the higher risk of the procedure.


Q: How do you report or suspect CTO on CTCA? 

A: It is difficult to report a CTO, as there may be distal opacification of the lumen due to the collaterals. The problem with the CT is that you do not see the blood flow, but only the contrast and therefore they are often under diagnosed.


Q: PCI of TO LAD for young patient is better

A: In our institution, all complex cases are being discussed at the JCC and the results off the discussions are being communicated with the patients, who are being involved in the decision-making process. According to the 2018 ESC/EACTS guidelines on revascularization patients with stable CAD and prox LAD have class Ia indication for both PCI and CABG if the coronary anatomy s suitable. In that specific case, the patient had very low surgical risk and rather unfavorable anatomy for PCI, so we concluded that CABG would be the best option for him (off-pump, low mortality, better future prognosis).


Q: What if there was no perfusion defect? Should we consider collaterals have taken care of narrowing?         

A: Could be, but in that case,  you wouldn't expect the patient to have any symptoms.


Q: Any utility for MR coronary angiography?

A: Unfortunately, the spatial resolution is not that great now to look for plaques and obstructive CAD. You can assess for abnormal origins and course of coronary arteries in young patients though.


Q: What resolution do you usually use during your routine CMR perfusion sequences?     

A: Standard resolution which is easily achievable with modern scanners is around 2.0x2.0mm in plane. With hybrid-PEI or KT Acceleration you may be able to get down to 1.0x1.0mm in plane. Personally 2.0x2.0 is fine for most standard clinical uses.


Q: When should be considered stress CT favorable over stress CMR considering the larger amount of contrast medium and radiations              ?

A: Could be a good alternative in cases where patients are claustrophobic or do not have access to stress CMR and are not good candidates for a stress echo. Moreover, it saves time and resources as could be done on the spot after a CTCA in patients with moderate disease who would otherwise be referred for another functional scan. Radiation dose with the new scanners and protocols is not that high, but of course should be taken into consideration.


Q: What do you do first? Stress or Rest?

A: Stress


Q: Why did you decide to proceed to invasive angio? Was the perfusion defect not explained by HCM?

A: Perfusion CMR is not particularly helpful for patients with HCM, as you are unable to differentiate between LAD defect and HCM-induced defects. The most appropriate test would be an anatomical one in order not to miss underlying CAD, especially in the LAD territory.


Q: Any situation where CMR preferred in CM in this kind of context? ie over anatomical imaging

A: Great test for cardiac structure and function, but not for detecting flow limiting CAD in the context of HCM. LAD defects could be easier missed.


Q: Do perfusion defects due to coronary disease and HCM look different?             

A: They do. Defects due to CAD are better delineated and not that fluffy and patchy.  However, CAD and HCM can coexist and thus it is not easy to differentiate (especially for LAD territory).


Q: Mark, would you talk about role on CMR in microvascular disease?

A: So, I am not the greatest believer in the role of CMR in the assessment of microvascular or small vessel disease. Some groups say that small vessel disease causes slow subendocardial perfusion, but I have rarely seen this, and you must remember that this would be very similar in appearance to dark rim artefact.


Q: Any difference in MFR CMR between CAD and HCM?

A: Yes, as was covered in the case. You can get a REDUCTION in perfusion in HCM during stress compared to rest which you do not see in coronary disease


Q: Mark Westwood - Is this the same mechanism where perfusion defects are seen in children with dilated coronaries in Kawasaki disease?

A: There is variable perfusion in areas of LGE with minimal wall motion defects... I have very little experience in this area as we do not do congenital work at Barts. In Kawasaki disease you can get perfusion defects which appear (I believe) like those seen in coronary artery disease but treatment is different and difficult so I would not be best placed to comment in this very specific disease of the value of CMR.


Q: What is the difference about frames in distant coronary territories talk about intensity of ischemia?

A: For clinical then I personally count around 5-7 frames after when you first see any contrast in the LV myocardium in the context of good LV function. With visual analysis I would be careful about trying to infer severity of lesions based on intensity of perfusion defect as there a many think which can affect this (such as the presence of collaterals etc). However, perfusion defects which last more than 10 frames and remain very dark as usually due to occlusions or near total occlusions.


Q: Great cases!  This last 2xV disease case--the LAD lesion might have more easily been picked up by quantitative perfusion, no?

A: Assessment is done based on a combination of visual analysis, first pass perfusion semi-quantitative maps, and the LGE sequences.


Q: Nice case, do you use a semi quantitative approach? 

A: Assessment is done based on a combination of visual analysis, first pass perfusion semi-quantitative maps, and the LGE sequences.


Q: If an angiogram will be done in order to confirm ischemic damage speculated from perfusion MRI, then why should perfusion MRI be done at all?

A: Revascularization should be guided by ischemic testing as per the 2014 ESC/EACTS guidelines (albeit some time ago now and pre-ISCHAEMIA trial), and MR stress perfusion is an appropriate choice of ischemia testing given its proven non-inferiority in the MR INFORM trial from 2019.


Q: Mark Westwood—  do you report CFR on stress perfusion studies? Particularly in patients that present with MINOCA.

A: I generally don't do that although there is research in this area so one to watch for the future.


Q: Can you use dipyridamole instead of adenosine due to cost consideration?      

A: Yes, you can use both.


Q: Practical question, we stopped beta block before stress test, but patient BP is often very high during the perfusion scan, how to prepare the patient for that?              

A: Our perfusion MRIs are almost exclusively with adenosine, so no need to stop beta-blockers. For dobutamine I would say the same rules apply as for stress echo i.e. interrupt if uncontrolled hypertension


Q: Utility of SSO for regadenoson?

A: None as discussed.


Q: Do you have any bibliographic reference about SSO in CMR stress?

A: Charlotte Manisty 2015 paper in RSNA


Q: How frequent you see cases of myocarditis associated with COVID-19 at your center      

A: We have seen it but not sure of the prevalence. It is the subject of a different talk and one where many centres based on which country they are in and when they look, I presume will get very different answers….


Q: Why CMR as a first choice? STEMI and troponine raise…Why not coronarography?      

A: This patient presented with chest pain in the context of coryzal symptoms. The pain settled when the patient arrived in the emergency department. She had no coronary risk factors. Her ECG showed transient ST elevation, which is unusual in pericarditis. This was not a "barn dorn" STEMI. This patient was reviewed by the local cardiology team and the decision was made to refer her for a CMR scan.


Q: Does black blood LGE confuse us in case of amyloidosis?          

A: Amyloidosis is associated with diffuse deposition of amyloid is myocardium and other tissues. This increases extracellular volume and therefore "attracts" gadolinium agents. LGE imaging may seem difficult, but this difficulty in imaging is so characteristic to point towards amyloid that it makes scanning very easy. Conventional imaging may seem tricky, but not impossible. T1 mapping and other findings add to the diagnostic spectrum. I would not rely on one sequence (LGE) only).


Q: Can you speak about your stress protocol? What do you do first?

A: The stress protocol we use in our centre comprises of: localisers, white blood and black blood transverse imaging od the chest, long-axis cine, (T1 and T2 maps if indicted), stress perfusion, SAX cine, rest perfusion, early gadolinium enhancement, LVOT cine, aortic cine, LGE


Q: Do you have any experience in use BB-LGE in endocarditis? Is it better than conventional?   

A: CMR is not the modality of choice to diagnose or manage infective endocarditis (IE) or in fact in the assessment of valves due to suboptimal temporal and spatial resolution. Transthoracic and transoesophageal echocardiography with clinical picture should be used in IE. CMR may have a role in assessing for underlying heart muscle disease or some of the complications - embolic infarction mostly.


Q: Has the ISCHEMIA trial influenced your practice / case selection?

A: Not yet though of course the results are very interesting.


Q: What’s the role of magnitude image of LGE in ischemic cardiomyopathy.

A: Very difficult to work out as LGE is like most CMR techniques a relative technique so what you see is based on certain assumptions about how to apply a grey scale to the raw data and therefore the individual pixels have units, but they are not absolute. If you want to look at extent of scarring and measure it T1 mapping would be better to get around this. There is some data to suggest that high levels of scarring in HCM are more associated with developing heart failure (Moon et at in JACC I believe).


Q: Could you comment on a standardized approach to viability assessment (non-viable, hibernating myocardium) for revascularization planning?

A: For each segment: >50% viable myocardium, segment viable, >50% scar, segment non-viable as per the Kim paper I mentioned. Viable and impaired contraction on cine imaging is potentially hibernating.


Q: How much ischemia is considered significant on perfusion scans? Is there an equivalent of the 10percent figure widely quoted in nuclear imaging literature?

A: The study has not been done but certainly evidence of a perfusion defect in more than 1 AHA segment I would say is significant. In terms of planning treatment important to discuss with the patient, clarify symptoms etc.


Q: What does a cardiac surgeon need to know before CABG?

A: This is a huge question but for surgeons about to operate I would say RV function and any RV infarction (if seen - often hard to be sure on LGE imaging) as this will determine the risk of not being able to get the patient off the pump and then viability of segments would be a good start.

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