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Cardiac Imaging - Science topic

The Cardiac Imaging Network
Questions related to Cardiac Imaging
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Which property of an ECG most strongly correlates to sudden cardiac death?
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We now we can take the red flag signs from ECG as suggested by ESC guidelines for syncope 2018, as ECG predictive signs of sudden cardiac death.
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As Feigenbaum said, it takes only five minutes to perform a 2D longitudinal strain evaluation in patients who underwent cardiotoxic chemotherapy. Is it part of your routine cardiac ultrasound examination?
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In recent years one the student of our department had his dissertation on use of 2D strain in follow up of patients undergoing chemotherapy.
We found that it was not difficult on his part to perform 2D strain during the follow up.
(In some studies revealed that, in performaning 2D strain :fellows are better than faculty.)
I think every centre can have a dedicated Echocardiographer for this purpose and possibly 2D strain is a must do part of echocardiographic examination for the patients receiving chemotherapy .
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Appropriateness in medicine, specially in cardiovascular imaging is a wide concept, sometimes difficult to define. Most doctors think they are choosing tests appropriately. I would like to know what "appropriateness" is for you? (Please, forget for a while the concept of "appropriateness" in the Appropriate Use Criteria and the Rand-Ucla Method, if you can).
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The appropriateness for selection of the cardiac images to me based on
1. What is the requirements of a clinician ?
(disgnostic/therapeutic/functional/screenings).
2.Sensitivty and specificity of the part imaging modality.
3.limtation on the part of patients or there diseases in terms capablilty of performing the test
and interpretation.
4. Quality of the expertise available on particular imaging.
5.Potential risks of a imaging test.
Depending on these factor choosing the best imaging will be the appropriate cardiac image for me.
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What is the best strategy - tredamill stress test or chemical stress with dipyridamole or dobutamine?
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Tredamil excercis echocardiographic may be a good choice for detection of CAD. But this test is much operaters skill dependent. The sensitivity and specificity much higher Than DSE.
We keep DSE for patients with Myocardial infarction (post discharge or follow up), for those who can not exercise and for preoperative evaluation.
To us bicycle ergometer echo is preferred when the patients are haveing LVH or if we want to add 2 D strain.
Myocardial contrast echo for detection of CAD is not appealing to us.
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To avoid non- responders to this therapy cardiac imaging has been proposed as a possible solution. But it does not work always...
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Since Echocardiography do not contributes in decisions making nor does it assess the outcome of the CRT. It is our practice only we look at the routine base line echocardiographic parameters only.
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Is it obvious that VR can help medical education? Yes.
Then why are so many academic institutions resistant to implement this technology?
I would like to personally extend an offer to demonstrate hands on to any medical school interested and give a live demo opportunity to anyone in this sphere to learn about this technology.
I will travel anywhere in the world to promote this know how. It’s a rising tides float all boats equation. The VR community is in its diapers stage.
lets collaborate! Please see our progress on www.vral.ca and email me hmaresky@vral.ca
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Hi,
I want to use a MRI images dataset in order to detect heart failure with image processing techniques. In the beginning I should choose the kind of map I need. T1 map or T2 map, I should choose one of them.
But I don’t know what is the differences between them and which one is better for detecting heart failure.
Can anyone share some information about that?
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T1 mapping allows you to quantify extracellular volume (ECV). Normal values for ECV are 25-28%, higher ECV values most usually represent interstitial myocardial fibrosis (as in hypertension, hypertrophic cardiomyopathy, severe aortic stenosis,...), values over 40% represent amyloidosis or infarction-related scar
T2 mapping measures specifically interstitial edema (thus, it is usually employed to detect the acute phase of myocardial infarction or acute myocarditis, as overtime edema will disappear)
One important point, though. Heart failure is defined CLINICALLY not by MRI techniques. MRI can help you to identify the cause of HF, but HF itself is diagnosed clinically (clinical history, physical examination, chest X ray,...)
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Thanks in advance.
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MIT-BIH Arrhythmia Database - PhysioNet
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I am interested to segment it (somehow) and get the motion information from an echo of the heart. Any comment also on this part?
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I've implemented a GE/Kretz 3D ultrasound image reader in 3D Slicer. After you have loaded the image you can use all the awesome tools in 3D Slicer to visualize and process it (for example, to create a 3D-printable model). You can see a demo here:
It's not perfect yet (spherical to Cartesian conversion is not fully accurate), but it's completely free and open-source - fixes and improvements are welcome. For further details and questions please post to the 3D Slicer forum:
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For example, can we use information on pulse sequences available in articles  to perform T1 mapping and how easy is it to implement?
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In theory, that's easy: You can use any generic inversion-recovery or saturation-recovery imaging pulse sequence to perform T1 mapping. Now acquire data with varying inversion times (TI) or saturation times (keeping all other sequence parameters constant) and calculate T1 (pixel by pixel) by fitting the measured signal to an exponential recovery function (or, e.g., the magnitude of an inversion-recovery function). If possible, use non-selective magnetization preparation to minimize any perfusion-related bias. A simple and relatively quick technique for T1 mapping are saturation-recovery single-shot fast-spin-echo (FSE or TSE) sequences (i.e. RARE or HASTE sequences).
However, your question is tagged with "Cardiac MRI", which means that simple approaches will probably not work satisfyingly. Cardiac T1 mapping should be performed with appropriate ECG triggering (and typically, the inversion times are chosen depending on the ECG signal). I'm afraid that most generic pulse sequence types will not provide a sufficiently flexible interface to combine magnetization preparation and ECG triggering and a segmented readout (cf. the figures in the attached publications). So, you should check whether your cardiac pulse sequences allow the additional application of magnetization preparation, but probably you will have to either purchase or implement yourself (in terms of low-level pulse sequence programming) a dedicated cardiac T1 mapping sequence.
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For Cardiac Innervation Imaging 123-mIBG is used. Due to its non-availability, can I-131-mIBG with proper Thyroid block be used. 
-It may be cost effective for the patient.
-Has got a long half life ?
Kindly provide references, if any.
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Dear Dr. Adams thanks for your input.
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With the increasing use of echocardiographic contrast for both endocardial border delineation , and in the evaluation of myocardial perfusion , we are faced with the indication for the procedure in pregnant women. Logically the contraindication due to the use of medication in the first quarter is present , but from there in situations where the examination is absolutely necessary. What to do? How far is safe use of echocardiographic contrast ?
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Placental imaging, placental dysfunction?
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I'm currently researching on left ventricle motion quantification. Can anyone suggest me any heart or left ventricle localization method in tagged cardiac MRI images? Appreciate if you can provide me references too. Thanks.
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Thanks all. I'm looking for an automated method to define the ROI (left ventricle) for tagged MR images.
To Aymeric Histace, I think the paper you recommended me is useful to me. I'm interested with the mean-std image method which I have personally tried to apply. But I ran into some problem. I've attached the image of the mean-std image below. The mean-std image i generated does not show a a significant contrast between the cavity and the left ventricle wall. I think I'm doing it wrong or missing some steps.
Here are the steps I have taken using Matlab to process the image.
1) compute local mean image using 'conv2' with kernel size N=11
2) compute local std image using 'stdfilt' with kernel size N=11
3) compute uendomap(i,j)=wm.mN(i,j) - wo.ON(i,j) with wm=1/3 and wo=2/3 where wm+wo=1 and wo/wo=2.
Any help is appreciated as I might adopt this method to localize my tagged MR images for my coming paper. Thanks.
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Just choice those more relevant papers published during last year in the topic of heart failure and cardiac imaging?
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Thanks a lot Fernando. Obviously I don´t want to do that. But when talking about this topic it would be useful for me just to compare my perceptions: Year 2014 in this field has been a year of guidelines and consensus, they both are relevant in our daily practice. Also the consensus document of the EACVI-ASE-Industry in definitions for a Common Standard for 2D Speckle Tracking Echocardiography should be important for those who believe in that modality.
What about for those who need expert reviews?  I have no doubt that there are excellent papers as that state of the art paper from Voigt just reviewing in depth the contribution of left atrium and how to measure it.
And finally, what about original investigations, is there any original contribution that should be considered more relevant? For instance I should remind that one from Kraigher-Krainer E, published in J Am Coll Cardiol 2014;63:447 – 456, assessing the role of GLS in patients with heart failure and preserved ejection fraction. So it seems to be a matter of individual perception and that was exactly I want to compare. 
Once again, thank you very much. Your contributions are extremely useful for me. 
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My group is trying to develop digital phantoms that will ultimately be useful when quantitatively characterizing scar tissue after cardiac ablation.  I have found several papers on scar tissue in the cornea following refractive eye surgery et al, but nothing for cardiac tissue.
Alternatively, does anyone know the general composition of cardiac scar tissue (e.g., proportion of different types of collagen, muscle, etc.)?  Many thanks in advance!
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Hi John, try this link to an article it may be of some use!
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As far as I know, within several min after injection activity absorption would be in the highest value possible. What is "the" value in (Mbq/ml or mCi/ml) ?
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Quantification in terms of Bq/ml is usually only performed by a solid state camera (rotating heads are not fast enough to pick up the dynamics involved). Using a DSPECT system with 99mTc-MIBI, peak myocardial activity concentration is on the order of 5 Bq/ml (with injection of 800 MBq), while of course the input function from the ventricle should be much higher. These numbers are patient-dependent, but are certainly on the order of Bq/ml for SPECT (only 2% of MIBI is taken up in the myocardium), even in PET studies a maximum of few hundred kBq/ml are to be expected (depending on tracer of course)
A recent paper from UCL in London explains myocardial perfusion quantification in SPECT further:
Hope it helps
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Recent studies have shown to be feasible the use of thrombolysis by ultrasound. This is really a new therapeutic window? What we need to move forward to achieve this purpose?
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I don't know
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In some papers they say dynamic SPECT provides a better contrast between normal and decreased flow regions than can be obtained from static imaging. what are the other advantages,if any?
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Well, in recents papers (such as Glenn Wells et al. 10.2967/jnumed.114.139782) the potential of fast cardiac SPECT cameras to acquire in a dynamic way to "track" the delivery  and uptake of perfusion agents is investigated (i.e. the tracer is injected while the patient is sitting/lying in/under the camera). Based on such data, quantification of absolute myocardial blood flow similar to PET would be possible. Theoretically this allows - amongst others advantages - the detection of balanced three vessel disease as the stress flow is reduced in absolute terms (ml/min/gram) but the (static) images look almost normal. The problem, however, is that conventional SPECT tracers are much less extracted by the myocardium as typical PET agents - thus this quantification is much less reliable.
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Thank you!
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Don't know please
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K1 and k2 are cardiac kinetic parameters which define wash-in and wash-out rate in a compartmental model of the cardiac muscle. j1 and j2 are two coefficients which are related to K1 and k2. using equation Count=-C1.exp(-j1.t)+C2.exp(-j2.t) time-acitivity curve for myocardium can be plotted which shows washin and washout rate of myocardium, but as far as I know K1 and k2 are somehow different from j1 and j2.
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Dear Etienne,
as far as I know in a one compartment model, input function must be convolved with K1.exp(-k2.t) which is transfer function of the model.
how many TACs are there in a one compartment model of myocardium? I think in this model there is just one TAC which can be described by the equation C1.exp(-j1.t)+C2.exp(-j2.t)
also,the shape of input function is the way that it can be plotted using this equation. so maybe to have myocardium TAC the equation C1.exp(-j1.t)+C2.exp(-j2.t) must be convolved with the transfer function.
I would be glad if you let me know what you think about it.
M.Reza
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I would like what is the methods you are using to evaluate paradoxical low flow low gradient aortic stenosis
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1. First, doublecheck the LVOT diameter on Echo and the aortic gradients (use a stand alone CW probe), to avoid potential source of error. Evaluate energy loss index in case the ascending aorta has a diameter <3cm to adjust for pressure recovery.
2. Evaluate the afterload: valvuloarterial impedance Zva, usually elevated.
3. Look at the left ventricle. It should be concentrically remodelled (thick walls and small cavity) and the systolic fuction impaired when assessed by speckle tracking GLS (global longitudinal strain). 
4. Dobutamine stress echo to evaluate projected aortic valve area at normal flow conditions.
5. Apart from echo, use non-contrast MDCT to measure aortic valve calcium in Agatston units (severity cut-off recently published by Clavel et al. JACC 2013). 
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Cardiac stress MRI is commonly performed by administering dobutamine or adenosine. Is it useful to employ an ergometer for this issue?
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There are very now and then publications on it over the last two decades such as http://www.ncbi.nlm.nih.gov/pubmed/22423637. However, the image degradation due to added motion is not worth the effort, IMHO.
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I would like to know about the strategies that are being developed to evaluate the role of peri-coronary fat in the development of coronary artery disease, mainly on the use of cardiac imaging and biochemical markers.
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The criteria for evaluation of peri-renal fat is well established?
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My department has recently purchased the Philips EPIQ which is the latest echo machine from them. I am now proactively using Speckle Tracking (mainly Radial and Longitudinal). However, I did not find any document (even by PHILIPS) which gives a clear idea of standardised parameters for global strain (age/sex/BMI adjusted). If anyone has come across this, I would really appreciate their input and suggestions.
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Unfortunately there are no normal values for strain rates mainly due to the reason that the values still differ dependent by the vendor of the ultrasound machines. Either you look for an article which is describing values assessed by a Philips machine or you have to assess values in a control group by yourself.
Perhaps those articles can help:
Variability of global left ventricular deformation analysis using vendor dependent and independent two-dimensional speckle-tracking software in adults.
Risum N, Ali S, Olsen NT, Jons C, Khouri MG, Lauridsen TK, Samad Z, Velazquez EJ, Sogaard P, Kisslo J. J Am Soc Echocardiogr. 2012 Nov;25(11):1195-203.
Perk G, Tunick PA, Kronzon I. Non-Doppler two-dimensional strain imaging by echocardiography—from technical considerations to clinical applications. J Am Soc Echocardiogr 2007;20:234–243.
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What intensity of ultrasound energy is used to dissolve thrombi and is there a standard protocol available?
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And for peripheral arterial disease someone has a great experience?
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I am interested in starting a collaboration on processing cardiac DW-MRI sequences. Our research group has experience in brain DW-MRI processing.
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Searching for a related topic to pursue research on.
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We worked with systolic mitral annulus displacement (SMAD) instead. SMAD is a simple surrogate measure for stroke volume index to detect low-flow low-gradient aortic stenosis with preserved ejection fraction. Longitudinal strain might be another one.
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I am being protected stenting about 8 years in Symptomatic Carotid Disease. Because there is continuing debate inthis topic and I want to know the common idea in RG scientists.
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It is a very complex sometimes very individual story.
I would suggest an experienced vascular board team/ center which provides both options.
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ECHO is not raccomended in the guidelines for CRT selection, but in many centers still has a role especially in borderline situations
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i think SCI is usuless for CRT planing,
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I need to measure length and size of heart cell branching. Normal HE histology sections cannot be used (too many artifacts and not possible to measure length with enough accuracy).
Is there any (2D or 3D) images that shows length and/or size of the branchings in a measurable way?
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I would try with the method of Welsch very quick running and valid for the fibers of the myocardium normal and pathological.
1) Bouin fixation.
2) Inclusion and paraffin sections of 5-6 microns.
After bringing water sections colorize 1 minute with thionine (CI 52,000) at 0.1% in ethanol 20 °.
3) Differentiate controlling the microscope in ethanol 80 ° (about 2 minutes).
4) Dehydrate ethanol 95 ° (3 minutes)
5) Ethanol 100 ° (6 minutes).
6) Xylene 10 minutes and close the slides with synthetic resin Eukitt.
best regards
Fabio
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For which clinical scenarios are you using T1 mapping by cardiac magnetic resonance in "daily practice"?
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My COI is that is my main research interest.
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...
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Many young patients are referred to cardiac MRI because of reduced exercise performance after infection. In these cases, we detect often an early enhancement, a small pericardial effusion and a small late enhancement. Left ventricular function is usually in the lower normal range.
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I don't think that myocarditis is overdiagnosed. Based on lots of data, we have to assume that more than 50% of all systemic viral diseases (remember the last severe cold or flu you had?) come with myocardial involvement. Up to about 8 of 100 people have a severe (with necrosis) myocarditis in their lifetime, without knowing about it.
Early enhancement may stay positive after myocarditis, so it should be used in combination with the other CMR consensus markers for myocarditis ("Lake Louise Criteria"; Myocarditis White Paper; Friedrich et al. JACC. 2009;53:1475–1487.).
In fact, compared with other clinical markers, the limitation of CMR is rather UNDER- not overcalling, since the sensitivity and negative predictive value are only 67% and 69%, respectively. For Early enhancement this would be 74% and 70%.
We have had many cases with non-specific symptoms, sometimes combined with ventricular ectopy, which was associated with edema (assessed by T2-weighted CMR) and early enhancement.
It looks like the myocardium is not much different to other tissue (muscle ache in influenza is very common), yet may be more sensitive to viral injury because it cannot go into "resting" (as we all can do when we have inflamed muscles. Animal models have shown that exercise during inflammation may cause a DCM phenotype.
Persisting early enhancement indicates a worse prognosis (Wagner et al., MAGMA 2003;16:17-20 and Mavrogeni et al., European Journal of Heart Failure 2011;13:830–837.). While we have to get a more robust image quality (or use T1 mapping in the future instead of signal intensity analysis), the concept of visualizing hyperemia in myocardial inflammation is solid.
I think we are identifying real disease. Luckily, myocarditis is usually a benign course and thus, the value for most patients is in its explanation for non-specific symptoms, while in patients with heart failure it is the best gatekeeper to decide on endomyocardial biopsies.
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According to the ADA´s guidelines from 1998, asymptomatic diabetic patients with risk factors should be subjected to a test to detect cardiac ischemia. However, these recommendations were not based on scientific evidence. What is your opinion on what should be done to these patients?
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Dear Lorenzo,
In my opinion I would not send any asymptomatic patients for any tests to detect "cardiac ischaemia", neither non-diabetics nor diabetics. As BARI-2D has shown, there is no benefit of revascularisation over optimal medical treatment for many initially symptomatic patients, let alone for asymptomatic ones! Just get there glycaemia, cholesterol and blood pressure optimally controlled and tell them to stop smoking. Non-invasive tests are often false positive, both imaging and functional tests and I don't find them helpful at all. A good history and optimal primary prevention is far more useful!
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Current ACC/AHA/ESC guidelines do recommend implantation of an ICD in patients with hypertrophic cardiomyopathy (HCM) with 1 or more of the clasical risk factors for SCD (wall thickness greater than 30 mm, syncope, abnormal blood pressure during exercise test, asymptomatic non-sustained ventricular tachycardia and family history of sudden cardiac death-SCD-). Other factors such as age, diastolic dysfunction, left ventricular outflow tract gradient, and myocardial ischemia (myocardial bridging) have not been clearly identified as independent risk factors for SCD. Late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging, which appears to reflect fibrosis, is being proposed as a possible risk factor for SCD. In your opinion, when will LGE appear in guidelines as a risk factor for SCD in patients with HCM?
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There is already very good evidence for a predictive value for combined endpoints and heart failure, and borderline values for sudden death (Bruder et al. J Am Coll Cardiol. 2010; 56:875–887.; O'Hanlon et al. J Am Coll Cardiol. 2010; 56:867–874.; Editorial: Salerno et al. J Am Coll Cardiol. 2010; 56:888–889. Green et al. JACC: Cardiovasc Img. 2012; 5:370–377.), yet for definitive answers a larger multi-center trial will have to be implemented. Such initiatives are underway.
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For my research on Coronary Artery Calcium Scoring I want to calculate the CAC mass score. Therefore I need a calibration factor for 100 kV CT scans. Does a standardized calibration factor exist for 100 kV Coronary Artery Calcium scans?
I found a log summary through google in which such calibration factors where considered. See the attached document.
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You can use 100 and 80 kV scans with specific calibration , the result are similar to 120 kv, every one must make the own machine calibration, own stratification according results.