Really interesting question. As far as I know T1 mapping/ECV is not a "daily practice" tool in CMR lab and it is more focus on clinical trials and studies. Some useful points as clinical potential applications are in:
- Acute myocardial injury: In patients with acute myocardial infarction, T1 value by pre-contrast T1 mapping showed a significantly lower variability than T2-weighted image (T2WI) and accurately detected acutely injured myocardium.
- Myocardial fibrosis: T1 mapping can be a useful method to detect and quantify diffuse infiltrative pathology in the myocardium as amyloidosis.
- Myocarditis: With combination of pre-contrast and post-contrast T1 mapping, early detection and quantification of water contents or extracellular space will be feasible in myocarditis.
In conclusion, I think T1 mapping is becoming an useful tool in some inflammatory/infiltrative/fibrosis entities but we need a clear cut-off value.
The normal data for native T1 values are starting to be published (Piechnik, S. et al. Normal variation of magnetic resonance T1 relaxation times in the human population at 1.5T using ShMOLLI. Journal of Cardiovascular Magnetic Resonance 15, 13 (2013), but more larger datasets are always useful.
I agree that T1 mapping shows potential in:
1. Diffuse fibrosis - not only amyloidosis, but also in patients with aortic stenosis, where it could have a role in assessing disease progression and prognosis, and in HCM - where it could detect abnormal myocardium before LGE imaging.
2. Myocarditis - to assess oedema, particularly diffuse oedema.
3. Myocardial Infarction - both acute (native T1 values) where it has shown to closely reflect the area of injury as defined by microspheres (Ugander M, et al. Myocardial edema as detected by pre-contrast t1 and t2 cmr delineates area at risk associated with acute myocardial infarction. JACC. Cardiovascular imaging. 2012;5:596-603) and chronic (post gadolinium contrast)
ECV measurement may play a role in increasing the use of T1 mapping. Multiple factors (field strength, sequence etc.) influence post-contrast myocardial T1. By normalizing myocardial T1 in relation to blood T1, these factors can be minimised. ECV has the advantage of being a physiologically intuitive unit of measurement, and is more accessible to the general cardiology community
The normals work is coming - as above, the Oxford group have published for ShMOLLI a large cohort over three centres using Siemens 1,5T magnets. However the different vendors, different field strengths and different sequences mean that any centre doing this at present are likely to need to scan some healthy volunteers to make up their normal range.
There is exponentially growing interest in this field - both pre contrast T1 assessment and ECV. I understand that Siemens now have a WIP with ShMOLLI and MOLLI (and possibly SASHA?) .
There is some great physicis work going on with Stefan Piechnik (Oxford, UK), Peter Kellman (NIH, USA) and the SASHA groups to make the sequences more accurate and robust - however they are already very good - cetrtainly MOLLI and ShMOLLI (which we use) in most patients will give excellent image quality straight "out of the box" which is nice.
Without meaning to plug my own research, we have just published in circ imaging pre contrast T1 mapping is incredibly useful in the assessment of LVH - it has extremely high sensitivity and specificity for the identification of Anderson Fabry Disease (low T1) and Cardiac Amyloid. We actually found an absolute cut off between the highest T1 in Fabry and the lowest T1 in hypertension, HCM, Amyloid and AS. T1 mapping also allows earlier idendtification of cardiac invovlement in AFD and amyloid (JACC imaging paper from Oxford from 2013 for the amyloid specific work) than other clinical methods. Nice advatange in amyloid and Fabry that you dont need contrast to get all of this information and hence renal failure not an issue.
In other disease, the T1 and T2 mapping sequences allow you to idenify "global" myocarditis - we now have seen a number of cases where there is no LGE (no doubt because there is diffuse oedema), but clearly high T1 and T2 signal (this can be missed on STIR if the operator / reporter are not careful, but is easy to see on mapping).
In the ECV, there is work going on in various centres in Aortic Stenosis, HCM (where I wonder whether ECV maybe a better measure than LGE for all the reasons on a previous thread), Amyloid, Myocardial Infaction, Diabetes, Hypertension, Myocarditis, Lupus, Normal Volunteers and of course the technical development work. No doubt there are people looking at other things too.
An international T1 mapping group has been set up by my CMR mentor (James Moon) which aims to address the issues that we have with multiple sequences and multiple methods. This along with the research that will be forthcoming in the next few years should give a better idea as to where the clinical uses of the techniques will be...
The most important contribution of T1-mapping is, in my opinion, to live the dicotomic LGE assessment (normal= no LGE) which has been used as a strong prognostic tool in many cardiac diseases, to enter in a new era of quantitative assessment (normal = 960 ms). There is a lot of work to do to standardize sequences, methods and to get normal reference values in different populations (gender and age are important issues). The final result could be great.