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T1 Mapping and ECV | Physics Webinar Q&A

Posted By Administration, Monday, October 19, 2020

Dr. Andreas Sigfridsson answers your questions from the September Physics Webinar. To view the recording, visit:

  1. Can you explain how standard deviations are generated from native T1 measurements?

    • A: Do you think of the error maps? Please check Peter Kellman's paper: doi 10.1186/1532-429X-15-56 

  2. I have one more of a basic question regarding the MOLLI approach, actually, it's known that T1 is specific for every individual tissue but when you acquire the signal it would be from the entire slice, that being said, how do you distinguish T1 values for every individual tissue? is there some sort of phase encoding/frequency-encoding here?

    • A: Yes, using slice selective imaging with phase and frequency encoding, you can measure T1 on a per pixel basis. 

  3. Why the SAT time is different in each cardiac cycle for the SASHA method? Thank you for the clarification in advance.

    • A: This is to sample the recovery curve at different times. With a 2-parameter fit, one could in principle just use one TS (saturation time), and this can be beneficial in some cases to sample this point several time. Please see Kellman's paper on this: doi 10.1186/s12968-014-0055-3

  4.  MOLLI-Sequence: should I use the same heart beat pattern in pre and post GD? Or should I change the heart beat pattern?

    • A: It is good do adapt with different patterns, due to the expected shorter T1 post Gd. We use 5(3)3 pre and 4(1)3(1)2 post.

  5. NIST, the US National Institute of Science and Technology, has produced a 'System Phantom' containing traceable vials with known T1 properties. Could this phantom be used to allow sites to confidently compare T1 mapping measurements with published values, or is there still a need for developing local reference ranges as per the SCMR consensus document?"
    • A: Well, it could be useful to some extent. However, it will not be possible to simulate MT effects, and motion / heart rate effects, for example. A pulse sequence optimized using a phantom is not necessarily better than another when moving in-vivo.
  6. Can you please briefly comment on how to report the T1 and ECV values e.g., which slices, which segments etc?
    •  A: This varies in different sites. We acquire a full stack in short axis and three long axis images, but are moving to a three or five slice short axis stack.

  7. How recent does the hematocrit have to be? Does location of blood draw matter?
    • A: I'm not the authority on this, but I would recommend same day. Not sure about location.

  8. For patients with pacemakers, do you generally recommend not to trust our T1 values?
    • A: Exactly. I would not trust MOLLI values. There might be some specially tuned variant less off-resonance sensitivity.

  9. Can you transfer colour maps to a PACS system?
    • A: Yes, at least some PACS systems support this. Ours started supporting them a couple of years ago.

  10. Sometimes the wall is thin in diastole. Any difference in T1 or T2 measurements if acquire images in systole?
    • A: Yes, there might be changes due to the blood content in the myocardium. I cannot answer how big these changes are.

  11. Do you do segmental ECV? or global ECV?
    •  A: Segmental, since we can expect focal variations.

  12. We can't compare native T1 value in different magnitude (1.5T vs 3T) or different vendors (philips vs GE vs Siemens) MR scanners. Can we compare ECV in different magnitude/vendors MR scanners?
    • A: Regarding comparing ECV, it all comes down to expected biases. The individual T1 measurements may have bias, but the combined ECV value has much less bias due to some of these partially cancelling out. It is hard to say how much these would vary - MOLLI ECV and SASHA ECV probably differ, but similar acquisitions between vendors could actually be close.
  13. Do you consider T1 mapping valuable for the assessment of microvascular disfunction?
    • A: I'm not an expert on the clinical application, but I believe this is a field where T1 mapping is being explored.

  14. T1 mapping is not longitudinal relaxation? Is it different?
    • A:T1 mapping measures the T1 (longitudinal) relaxation time per pixel.

  15. Do you have any experience you would like to share working with Philips or GE on T1 mapping?
    • A: Yes

  16. Can you use a sample small ROI in the septum to quickly assess native T1 time?
    • A:Yes

  17. In case of transmural scar in the septum, where you advise T1 to be measure, in which other segment that the septum?
    • A: I advise to measure T1 in several regions, for example using a 16 segment AHA model.

  18. Can we choose between molli and shasha sequences during or after acquisition?
    • A: This has to be decided before acquisition. One can acquire both sequences in the same exam (but don't expect the values to be the same).

  19. In recent years, there have been some studies in trying to correct cardiac T1 values for things like readout signal loss using Bloch equation simulations. Do these approaches have much clinical use nowadays?
    • A: My general feeling is that the effects are so interdependent in MOLLI that it will probably be very difficult to tackle all issues. I think most people either use MOLLI and accept the biases (i.e. find their own cutoff values) or use SASHA if the correct T1 value is of importance.

  20. What are your normal ranges in ECV map?Is it different in MOLLI and SASHA?
    • A: Our normal range is 20%-30%. They would be different between MOLLI and SASHA generated ECV.

  21. How do we deal with images captured in various phases of heart cycle with time based MOLLI sequence?
    • A: MOLLI (and SASHA) are usually acquired in a fixed cardiac phase (as opposed to the older cardiac Look-Locker sequence).

  22. Since MOLLI has more data points to map than shMOLLI, would one expect a better fit if the heart rate is irregular or bradycardic?
    • A: Yes, the precision and SNR would be worsened with fewer data points, but including bad points would deteriorate the accuracy.

  23. Which T1 mapping sequence is the most clinically validated against e.g. histopathology?
    • A: I think MOLLI has been more widely validated.

  24. Where are the error maps located?
    • A: This might depend on the system used. On our system, the user can select to have them generated. They then appear as a separate image series next to the others.

  25. Could a reference image in molli prior to the inversion pulse aid in correction, similar to as done in sasha?
    what's the acquisition scheme of MOLLI in commercially available GE, Siemens, Philips T1 map? Is it a 3(3)3(3)5 or something else?  Important for multiinstitutional trials Mark DeLano I
 don't know, but I believe these could be user selectable. I agree this is very important, but I also think any multicenter/multivendor trials have this parameter the same. It is more unclear, however, whether the RF pulses are the
 same, the approach into "steady state", and other factors are the same as these parameters or details are less transparentCould a reference image in molli prior to the inversion pulse aid in correction, similar to as done in

    • A: Potentially. I have seen at least one abstract with such an idea.

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Posted By lauren small, Wednesday, July 8, 2020

This webinar took place live on June 24, 2020 and was presented by Dr. Peter Kellman and moderated by Dr. Marcus Carlsson. Over 400 individuals attended the webinar live and asked over 30 questions! Click into the comments area of this blog post to see written responses by Dr. Kellman and Dr. Carlsson to each question asked live. 

Have more questions after watching the webinar? Ask them in this thread.

To watch the webinar recording visit:

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Cardio-Oncology - CMR CASE-BASED WEBINAR - Q&A

Posted By Administration, Tuesday, June 30, 2020

This webinar recording can be found here.

Questions & Answers

Q: Is GLS by CMR comparable to echo?  

A: There are different methods of obtaining deformation data using Cardiac MRI (CMR). Myocardial tagging (MT) is an established method of measuring strain which has been extensively validated (Swoboda J. Magn. Reson. Imaging, 2014). Currently, a number of MT-based techniques are available for strain evaluation (spatial modulation of magnetization (SPAMM); Displacement encoding with simulated echoes (DENSE); and more recently fast strain encoding (SENC)) – the latter allowing strain data acquisition from a single heart beat. In the case presented we demonstrated the use of Feature tracking (FT) CMR which unlike myocardial tagging methods mentioned above does not require the use of a dedicated sequence and can be performed on previously acquired cine imaging. Global longitudinal strain (GLS) obtained from FT CMR and speckle tracking echocardiography are comparable, but the values are not interchangeable. Feature tracking CMR allows acquisition of deformation parameters such as GLS though tissue voxel motion tracking, a process which is analogous to speckle tracking performed with echocardiography. A number of studies have shown good correlation with speckle tracking echocardiography (Onishi et al. J Am Soc Echocardiogr. 2015; Obokata et al, Eur Heart J Cardiovasc Imaging. 2016). Furthermore, meta-analysis data (Vo et al, JACC Cardiovasc Imaging. 2018) looking at the normal range of GLS obtained from FT CMR in healthy subjects showed a mean GLS -20.1% (95% CI: -20.9% to -19.3%) which is comparable to normal GLS range from speckle tracking echocardiography.


Q: How frequent you do CMR, is it yearly or every 6 months?      

A: Current guidelines propose the use of echocardiography as a first line test for evaluation of LV function in the context of trastuzumab-induced cardiotoxicity monitoring, with 3 monthly monitoring during treatment (2016 ESC position statement European Heart Journal (2016)37, 2768–2801). The argument made in the first case presented, was that the superior precision (test: re-test variability in LVEF estimation) associated with CMR allows us to avoid the fluctuations in LVEF and unnecessary treatment interruptions, seen particularly in patients with poor echocardiographic windows, as shown in this case.  It is worth highlighting that the CMR studies performed on this patient, were focused, short CMR studies (under 15 minutes duration, no requirement for contrast administration) focusing on cardiac function.




Q: Any experience with CMR- strain software?

A: The software used in our department is CVI42 (Circle Cardiovascular Imaging Inc, Calgary, Canada). Strain analysis is primarily used as a research tool rather than for clinical purposes. As with speckle tracking echocardiography inter-vendor differences have been reported among different CMR analysis software (Barreiro-Perez et al, Eur Radiol, 2018). Among deformation parameters, left ventricular GLS appears to have reasonable inter-vendor agreement in some reports  (Gertz et al, PLoS One. 2018).


Q: Which software was used to measure strain in this case?         

A: As above.


Q: I think We should implement CMR prior starting chemotherapy as suggested. But the question come of the time interval? And would you abandon Echo?         

A: As above.


Q: Do you have any experience with immune check point inhibitors medication?

A: The cardio oncology service at the Barts Heart Centre in actively involved in the care of patients receiving immune checkpoint inhibitors (ICI) for both the surveillance and management of ICI-related cardiotoxicity - the case presented as part of the webinar was an example. ICI myocarditis is the most significant cardiotoxicity and although its incidence of 1% makes it relatively uncommon compared to the other ICI-induced complications, it carries the highest risk of mortality at 40%. The presentation is varied, and can include asymptomatic elevations in serum troponin on one hand, to decompensated cardiac failure and the accumulation of pericardial effusions, and on the most severe end of the spectrum, cardiogenic shock and serious arrhythmias such as advanced conduction disease or ventricular tachycardia. High dose corticosteroids are the mainstay of therapy, with reports or case series of success with intravenous immunoglobulin, myocophenolate, infliximab, anti-thymocyte globulin, plasmapheresis, atemtuzumab, and abatacept in those refractory to corticosteroids. The meta-analysis by Wang et al in JAMA Oncology in 2018, analysis by Zhang in EHJ in 2020, and review by Palasakas et al in JAHA in 2020 are useful references.


Q: In patients with impaired cardiac function, how do you differentiate myocarditis from infarction?          

A: Contrast enhanced CMR is particularly helpful for differentiating myocarditis from infarction. The characteristic pattern of late gadolinium enhancement (LGE) due to infarction is either subendocardial or transmural following a coronary artery territory. In contrast, the characteristic pattern of LGE due to myocarditis is patchy or multifocal in a subepicardial or mid wall distribution, often involving (but not limited to) the lateral wall. In addition, T2 weighted imaging and parametric mapping techniques including T1 and T2 mapping offer the ability to detect and quantify myocardial oedema, enabling an assessment of active myocardial inflammation.


Q: Have you seen many cases LGE - and myocardial fibrosis by endomyocardial biopsy?   

A: Endomyocardial biopsy (EMB) remains the gold standard for definite myocarditis, as outlined by the European Society of Cardiology (ESC) Working Group on Myocardial and Pericardial Diseases position paper in 2013. Non invasive imaging techniques such as CMR offer value for diagnosis especially in centres where there are state-of-the-art facilities and expertise as they may obviate the requirement for an invasive biopsy, and also can be performed serially to track disease and response to treatments. As with many centres in Europe, EMB is generally performed second line following CMR in conjunction with clinical, biochemical and immunological markers. In addition, where systemic toxicity secondary to immunotherapies is seen, extra-cardiac biopsy may yield diagnostic utility and reduce risk. In the important analysis of ICI myocarditis patients provided by Zhang et al in EHJ this year, the diagnosis of myocarditis included both EMB-proven and clinically proven (per ESC criteria in the 2013 position paper) cases. However, in all the patients who underwent both CMR and EMB, 98% had abnormal histopathology (lymphocytic infiltration); conversely, of this subset of patients with pathology-proven ICI myocarditis, only 64% demonstrated abnormal CMR tissue characterisation (LGE or increased T2-weighted STIR signal). Zhang et al therefore advocate for broader use of EMB within their diagnostic algorithm, especially if the T2-weighted STIR signal is normal.


Q: How sensitive is cardiac biopsy in ICI myocarditis?       

A: As above.


Q: Checkpoint inhibitors are now being used in refractory pediatric solid tumors. What do we know about CMR in pediatric checkpoint induced myocardial toxicity or inflammation?   

A: To our knowledge, there remains a paucity of data around ICI myocarditis and its incidence, mortality, diagnosis, and CMR phenotype within the paediatric population in the literature. Furthermore, whilst the utility of CMR in myocarditis has been extrapolated to paediatric patients, mapping techniques have not been systematically analysed in this age group. Cornicelli et al have provided an analysis of a small cohort of childrenwith myocarditis which suggests abnormalities in native T1 and T2 mapping and extracellular volume (ECV) are associated with a high sensitivity and specificity for the diagnosis of myocarditis. However, it is evident that further research into the utility of CMR in ICI myocarditis in children will be required to better understand the entity.


Q: LGE negative I meant

A: As above.


Q: If this patient developed cardiomyopathy with systolic dysfunction, would you give him 5FU?            

A: There is plenty to be considered in this situation. Firstly, it would depend on the degree of his systolic dysfunction alongside his cardiac symptoms. For patients with complex cardiac histories, our usual practice is to discuss them in our dedicated Cardio-Oncology MDTs, where detailed discussions about the potential risks and benefits of 5FU is addressed in the presence of oncologists and cardiologists. If deemed suitable, our potential management strategy would include optimizing heart failure treatment with ACE-I and Beta blockers, and commencing medications such as calcium channel blockers and nitrates to reduce the likelihood of coronary artery vasospasm. Careful cardiac monitoring in cardio-oncology clinics are essential for such patients, although left ventricular dysfunction is a less common complication than coronary spasm with fluoropyrimidine chemotherapy agents.


Questions answered during the webinar:

Q: Do you have any pointers on the use of CMR in pediatric oncology patients?

Q: Could it be possible to combine myostrain with T2 mapping in cardio-oncology?

Q: Which region we should focus for edema evaluation? Septum?             

Q: Thank you for these presentations. What are the best methods for T1/T2 mapping on CMR images?     

Q: For edema evaluation it would be interesting to do longitudinal acquisitions? 

Q: My concern is about the reason of the myocarditis such in HIV for example, is it the agents or infections. CMR could help diagnose myocarditis but not the etiology that affects the management?            


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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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HCM AND HYPERTOPHIC PHENOTYPES - CMR Case-Based Webinar - Post Your Questions

Posted By lauren small, Friday, June 5, 2020
Post your questions for this webinar via the comment section.

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Myocarditis - CMR Case-Based Webinar - Post Your Questions

Posted By lauren small, Monday, June 1, 2020

We're excited for tomorrow's webinar (June 2, 2020) for our next Case-Based webinar that will cover Myocarditis. Register here.

Join us from 11:00 am - 12:00 pm ET with presenters: Dr. Jeanette Schulz-Menger, Dr.  Maximilian Fenski, and Dr. Edyta Blaszczyk of University Medicine Berlin

Moderator: Dr. Jadranka Stojanovska


Have questions on Myocarditis that you would like for our presenters to touch on tomorrow live? Leave your question(s) as a comment in this thread and the presenters will respond either live or via a reply comment.

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CMR for Functionally Single Ventricle: Decision Making in Borderline LV & CMR Approach for the Cyanotic Fontan

Posted By lauren small, Thursday, May 28, 2020

Post your questions on the CMR for Functionally Single Ventricle: Decision Making in Borderline LV & CMR Approach for the Cyanotic Fontan webinar by commenting below.


The recording will be posted in the webinar section of the Online Learning Portal soon after the live webinar.

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Posted By lauren small, Thursday, May 21, 2020

Post your questions on the Right Heart webinar by commenting below.


The recording will be posted in the webinar section of the Online Learning Portal soon after the live webinar. Register for the live webinar here:

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Posted By lauren small, Thursday, May 21, 2020

Post your questions on the Right Heart webinar by commenting below.


The recording will be posted in the webinar section of the Online Learning Portal soon after the live webinar on May 21 at 10 am EDT. 

Tags:  Excellent talk  Thank you 

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CMR in Patients with Pacemaker/ICD | CMR Case-Based Webinar

Posted By lauren small, Monday, May 18, 2020
Updated: Monday, May 18, 2020

We will now using the SCMR Blog to keep a thread of questions from the CMR Case-Based Webinars. On May 19, Drs. Mushabbar Syed and Menhel Kinno of Loyola University Medical Center will present on CMR in patients with a pacemaker/ICD. If you have questions, please leave a comment in this thread.

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