GB2494702A - Diagnosis of hypertrophic cardiomyopathy from change in blood oxygen level dependent magnetic resonance signal intensity - Google Patents

Diagnosis of hypertrophic cardiomyopathy from change in blood oxygen level dependent magnetic resonance signal intensity Download PDF

Info

Publication number
GB2494702A
GB2494702A GB1116140.3A GB201116140A GB2494702A GB 2494702 A GB2494702 A GB 2494702A GB 201116140 A GB201116140 A GB 201116140A GB 2494702 A GB2494702 A GB 2494702A
Authority
GB
United Kingdom
Prior art keywords
text
signal intensity
magnetic resonance
subject
hypertrophic cardiomyopathy
Prior art date
Legal status (The legal status is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the status listed.)
Withdrawn
Application number
GB1116140.3A
Other versions
GB201116140D0 (en
Inventor
Stefan Neubauer
Theodoros Karamitsos
Sairia Dass
Hugh Watkins
Current Assignee (The listed assignees may be inaccurate. Google has not performed a legal analysis and makes no representation or warranty as to the accuracy of the list.)
Oxford University Innovation Ltd
Original Assignee
Oxford University Innovation Ltd
Priority date (The priority date is an assumption and is not a legal conclusion. Google has not performed a legal analysis and makes no representation as to the accuracy of the date listed.)
Filing date
Publication date
Application filed by Oxford University Innovation Ltd filed Critical Oxford University Innovation Ltd
Priority to GB1116140.3A priority Critical patent/GB2494702A/en
Publication of GB201116140D0 publication Critical patent/GB201116140D0/en
Priority to PCT/GB2012/051825 priority patent/WO2013041834A1/en
Publication of GB2494702A publication Critical patent/GB2494702A/en
Withdrawn legal-status Critical Current

Links

Classifications

    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61B—DIAGNOSIS; SURGERY; IDENTIFICATION
    • A61B5/00—Measuring for diagnostic purposes; Identification of persons
    • A61B5/05—Detecting, measuring or recording for diagnosis by means of electric currents or magnetic fields; Measuring using microwaves or radio waves 
    • A61B5/055—Detecting, measuring or recording for diagnosis by means of electric currents or magnetic fields; Measuring using microwaves or radio waves  involving electronic [EMR] or nuclear [NMR] magnetic resonance, e.g. magnetic resonance imaging
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61B—DIAGNOSIS; SURGERY; IDENTIFICATION
    • A61B5/00—Measuring for diagnostic purposes; Identification of persons
    • A61B5/02—Detecting, measuring or recording pulse, heart rate, blood pressure or blood flow; Combined pulse/heart-rate/blood pressure determination; Evaluating a cardiovascular condition not otherwise provided for, e.g. using combinations of techniques provided for in this group with electrocardiography or electroauscultation; Heart catheters for measuring blood pressure
    • A61B5/026—Measuring blood flow
    • A61B5/0263—Measuring blood flow using NMR
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61B—DIAGNOSIS; SURGERY; IDENTIFICATION
    • A61B5/00—Measuring for diagnostic purposes; Identification of persons
    • A61B5/145—Measuring characteristics of blood in vivo, e.g. gas concentration, pH value; Measuring characteristics of body fluids or tissues, e.g. interstitial fluid, cerebral tissue
    • A61B5/14542—Measuring characteristics of blood in vivo, e.g. gas concentration, pH value; Measuring characteristics of body fluids or tissues, e.g. interstitial fluid, cerebral tissue for measuring blood gases

Abstract

A method of detecting hypertrophic cardiomyopathy or a gene mutation for hypertrophic cardiomyopathy is described comprising measuring the change in blood oxygen level dependent magnetic resonance signal intensity between rest and cardiac stress. Cardiac stress may be pharmacologically induced, e.g using adenosine, in the heart of a subject. Cardiac stress may alternatively be induced by physical exercise. A corresponding apparatus is also disclosed.

Description

BOLD IMAGING IN HYPERTROPHIC CARDIOMYOPATHY AND ATIILETE'S
HEART
The present invention relates to a detection technique useful in the investigation of S patients with suspected hypertrophic cardiomyopathy (HCM) and in particular to the use of magnetic resonance imaging of the heart to detect conditions associated with HCM.
Iiypertrophic eardiomyopathy (HCM) is a relatively common genetic cardiac disease (1:500 in the general population) and is the commonest cause of sudden cardiac death in the young (including competitive athletes). HCM is a disease of the myocardium (the muscle of the heart) in which a portion of the myocardium is hypertrophicd (thickened).
One of the difficulties in diagnosing HCM is in distinguishing between pathological hypertrophy caused by disease and so-called athlete's heart, namely the normal enlargement of the heart muscle in response to regular exercise. At thc moment it is often only possible to distinguish between these two conditions by recommending a period of detraining, which is unwelcome to most athletes.
Furthermore, with current genetic testing, the genetic mutation responsible for HCM cannot be identified in as many as 40% of patients. Some individuals may carry the genetic mutation, but not have a phenotypical expression of HCM (i.e. the heart muscle may not yet be enlarged). It is therefore difficult conclusively to exclude disease in relatives of patients with HCM. Consequently such individuals are usually offered lifetime clinical follow-up which is both an emotional burden to the subject and their family and a financial burden to the health care system, especially if the subject is actually unaffected by 1-1CM.
The present invention provides a method of detecting hypertrophic cardiomyopathy or the presence of a gene mutation for hypertrophic cardiomyopathy, comprising measuring the change in blood oxygen level depeildent magnetic resonance signal intensity between rest and cardiac stress in the heart of a subject. More specifically, a first aspect provides a method of testing relatives of patients with hypertrophic cardiomyopathy who arc themselves free of hypertrophy, to ref iably differentiate between those who carry the gene (genotype positive phenotype negative) and those who do not (genotype negative phenotype negative). A second aspect provides a method of reliably differentiating between patients with hypertrophic cardiomyopathy (i.e. pathologic hypertrophy) and athletes (i.e. physiological hypertrophy).
Another aspect of the invention provides a method comprising the steps of selecting a subject suspected of suffering from hypertrophic cardiomyopathy or thc presence of a gene mutation for hypertrophic cardiomyopathy and measuring the change in blood oxygen level
I
dependent magnetic resonance signal intensity between rest and cardiac stress in the heart of the subject.
Another aspect of the invention provides a method comprising the steps of comparing a preobtained measurement of the change in blood oxygen level dependent magnetic resonance signal intensity between rest and cardiac stress in the heart of a subject to a predetermined threshold to determine whether the subject is suffering from hypertrophic cardiomyopathy or has a gene mutation for hypertrophic cardiomyopathy.
The blood oxygen level dependent magnetic resonance imaging technique (BOLD-MRI) utiliscs the different MRI signal intensity which is caused by differences in the dcoxyhaemoglobin concentration in an image pixel and the blood volume fraction, both of which affect the MRI apparent transverse relaxation rate T2 or T2*. The BOLD signal intensity observed in a subject's heart will change between the rest and cardiac stress. In accordance with the invention the size of the change from rest to cardiac stress indicates either the presence of 14CM or the presence of the gene mutation for 14CM (despite the absence of hypertrophy).
Preferably the cardiac stress is pharmacologically induced, example by using adenosine. Alternatively other pharmacological stressors (e.g. dipyridamo Ic, regadenoson, dobutamine) can be used or physical exercise (e.g. with an MR compatible bike or treadmill) can be used.
The change in signal intensity is preferably measured transmurally in the heart. One way of achieving this is to draw endocardial and epicardial contours on the BOLD images.
The myocardial walls are then divided into segments by delineating the inferior or anterior left/right ventricular junction. Any segmentation is possible, however, in clinical practice, if 3 BOLD slices are acquired, then the AHA 17 segmentation model (excluding segment 17-true apex) is preferably used. Further segmentation into subendocardial/subepicardial layers is possible with the use of commercial software such as QMass.
The signal intensity may be measured in an image representing a single slice through the heart, or altematively in three slices (as mentioned above), such as the basal, mid ventricular and apical positions.
The MR sequence is preferably a T2 or T2t weighted magnetic resonance sequence and preferably using a magnetic field strength B0 of at least 1.5 Tesla, more preferably at least 3 Tesla.
In accordance with the invention, subjects potentially suffering from HCM or potentially having the gene mutation for HCM can be discriminated from normal subjects or athletes on the basis of a change in signal intensity from rest to cardiac stress of less than 15%, more preferably less than 12%, more preferably less than 10%. Typically normal subjects and athletes will exhibit an increase in BOLD signal intensity of more than 15% when cardiac stress is induced.
Another aspect of the invention provides apparatus for detecting hypertrophic cardiomyopathy or the presence of a gene mutation for hypertrophic cardiomyopathy, comprising a processor adapted to receive a measurement of the blood oxygen level dependent magnetic resonance signal intensity in the heart of a subject at rest, to receive a measurement of the blood oxygen level dependent magnetic resonance signal intensity in the heart of a subject under cardiac stress, and to determine from the two measurements whether or not the subject is suffering from hypertrophic cardiomyopathy or the presence of a gene mutation for hypertrophic cardiomyopathy. The processor may be adapted to determine whether or not the subject is suffering from hypertrophic cardiomyopathy or the presence of a gene mutation for hypertrophic cardiomyopathy by comparing the difference in blood oxygen level dependent magnetic resonance signal intensity at rest and under cardiac stress to a threshold. The threshold, for measurements in a 3 Tesla field, is 15%, more preferably 12%, more preferably 10%. Alternatively, the processor may be adapted to determine whether or not the subject is suffering from hypertrophic cardiomyopathy or the presence of a gene mutation for hypertrophic cardiomyopathy by comparing the change in blood oxygen level dependent magnetic resonance signal intensity from rest to cardiac stress of the subject with the change for a non-sufferer of hyperfrophic cardiomyopathy. For example the change in blood oxygen level dependent magnetic resonance signal intensity from rest to cardiac stress of an HCM sufferer is less than 60% of the change for a a non-sufferer of hypertrophic cardiomyopathy.
Because the BOLD method is an MR1 technique, it involves no harmful radiation and there is no need for administration of a contrast agent. It is a non-invasive imaging tcst and is thus extremely safe for use as a screening method.
The invention will be further described by way of an example with reference to the accompanying drawing in which:-Figure 1 shows the difference in BOLD signal intensity percentage change from rest to cardiac stress in normal subjects, athletes, patients with HCM and those who arc phenotype negative for HCM but carry the genetic mutation; Figures 2 a and b are rest and stress BOLD-MR cardiac images, respectively; and Figure 3 shows the epicardial and endocardial boundaries and six myocardial segments drawn on a BOLD MR image.
In one embodiment the invention can use the following MRI protocol.
S The BOLD-MRI is performed on a MR scanner of at least 1.5 Tesla (ideally 3 Tesla and above) preferably with the subject instructed to refrain from caffeine-containing drinks and food in the 24 hours preceding the scan. Images are acquired with the patient supine, using anterior and posterior phased-array surface coils. In a single slice scan a single mid-ventricular slice can be acquired at mid-diastole using a T2-prepared ECG-gated SSFP sequence with the following parameters: repetition time/echo time 2.86ms/1.43 ms, T2 preparation time 4Oms, matrix 168 x 192, FOV 340 x 340mm, slice thickness 8mm, flip angle 440 Each BOLD image is obtained during a single breath-hold over 6 heart beats. A set of 2-6 images is acquired at rest and during the infusion of adenosine (140 jig/kg/mm).
The acquisition of stress BOLD images should commence at peak stress about 90 seconds after the initiation of adenosine infusion. If necessary, shimming and centre frequency adjustments can be performed, as well-known in the art, before BOLD imaging, to generate images free from off-resonance artefacts.For a multi-slice technique 3 or more slices can be acquired. For the data analysis, QMass software (version 6.2.3 or above, Medis, Netherlands) can be used. Myoeardial signal intensity is measured after manually tracing the endocardial and epicardial contours as shown in Figure 3. This figure shows the eridocardial (inner) and epicardial (outer) contours of a BOLD image in a patient with hypertrophic cardiomyopathy.
The cross marked at the inferior left/right ventricular junction is the reference point for dividing the myocardium into 6 segments according to thc AHA 17-segment model (starting clockwise from the cross is inferior septum, anterior septum, anterior, anterolateral, inferolateral and inferior segment). One mid-ventricular slice is shown here. The same process is repeated for all slices at stress and rest and then mean signal intensities are calculated for resting and stress conditions by averaging signal measurements from all of the segments in the images during rest and adenosine stress, respectively. For a 3-slice technique, the basal and mid-ventricular slices are divided in 6 segments each, whereas the apical slice is divided in 4 segments (total 16 segments) In this cardiac gated sequence, variations of heart-rate also affect the signal intensity due to its effect on Tl relaxation and the following equation is used for correction: with Ti = 1220 ms (for 3 Tesla) and f3=0.59 (determined empirically for this sequence) where So is the measured signal intensity, S is the corrected signal intensity and TR is the image dependent time between acquisitions of sections of k-space, governed by the heart rate. TR is replaced by the RR interval.
S The relative signal intensity change is calculated as follows: ASI(%) = Mean SI (stress)-mean SI (rest)x 100 Mean SI (rest) where SI is the corrected signal intensity.
An example of a BOLD scan in a patient with HCM is shown in Figure 2 (panel A is the rest BOLD image, panel B isthc stress BOLD image).
Table 1 below shows the change in BOLD signal intensity from rest during adenosine stress in normal subjects, athletes and patients with hypertrophie eardiomyopathy (phenotype positive and negative). The difference between athletes and HCM is clearly shown and on the basis of these results the test distinguishes between normal or athlete on the one hand and HCM on the other hand with a sensitivity of 94.6% and a specificity of 58.1%.
Table 1: Mean BOLD± standard deviation in the studied population.
Normal Athlete Phenotype Phenotype posHCM negHClSl Sample size 16 12 26 11 BOLD SI 18.3±14 16.6±10 7.9±10 9.8±11 change Furthermore, within the HCM cohort the change in BOLD signal intensity is evident even for individuals who are phenotype negative for HCM but carry the genetic mutation.
These results are illustrated graphically in Figure 1. Therefore, the technique of the invention can distinguish between HCM and physiological (athletes) hypertrophy and it can detect underlying pathology in 1-1CM mutation carriers before the onset of hypertrophy.

Claims (1)

  1. <claim-text>CLAIMS1. A method of detecting hypertrophic cardiomyopathy or the presence of a gene mutation for hypertrophic cardiomyopathy, comprising measuring the change in blood oxygen level dependent magnetic resonance signal intensity between rest and cardiac stress in the heart of a subject.</claim-text> <claim-text>2. A method comprising the steps of selecting a subject suspected of suffering from hypertrophic cardiomyopathy or the presence of a gene mutation for hypertrophic cardiomyopathy and measuring the change in blood oxygen level dependent magnetic resonance signal intensity between rest and cardiac stress in the heart of the subject.</claim-text> <claim-text>3. A method according to claim I or 2 further comprising the step of comparing the change in blood oxygen level dependent magnetic resonance signal intensity to a predetermined threshold.</claim-text> <claim-text>4. A method comprising the steps of comparing a preobtained measurement of the change in blood oxygen level dependent magnetic resonance signal intensity between rest and cardiac stress in the heart of a subject to a predetermined threshold to determine whether the subject is suffering from hypertrophic eardiomyopathy or has a gene mutation for hypertrophic cardio myopathy.</claim-text> <claim-text>5. A method according to any one of the preceding claims wherein thc cardiac stress is pharmacologically induced stress.</claim-text> <claim-text>6. A method according to any one of the preceding claims wherein the cardiac stress is induced using adenosine, dipyridamole, regadenoson or dobutamine.</claim-text> <claim-text>7. A method according to any one of claims I to 4 wherein the cardiac stress is induced by physical exercise.</claim-text> <claim-text>S. A method according to any one of the preceding claims wherein the change in blood oxygen level dependent magnetic resonance signal intensity is measured in multiple segments of the myocardium.</claim-text> <claim-text>9. A method according to any one of the preceding claims wherein the change in blood oxygen [eve! dependent magnetic resonance signal intensity is measured in a single s!ice scan through the heart.</claim-text> <claim-text>10. A method according to any one of claims Ito 8 wherein the change in blood oxygen level dependent magnetic resonance signal intensity is measured in a three scan slices through the heart.</claim-text> <claim-text>II. A method according to claim 10 wherein the three slices are at the basal, midventrieu!ar and apical positions of the subject's heart.</claim-text> <claim-text>12. A method according to any one of the preceding claims wherein the measurement is made using a T2 or T2* weighted magnetic resonance sequence.</claim-text> <claim-text>13. A method according to any one of the preceding claims wherein the measurement is made using a magnetic field strength BO of at least 1.5 Tesla, more preferably at least 3 Tesla.</claim-text> <claim-text>14. A method according to any one of the preceding claims comprising discriminating a change in signal intensity, for a 3 Tesla magnetic field, from rest to cardiac stress of less than 15%, more preferab!y less than 12%, more preferably less than l0%.</claim-text> <claim-text>15. A method of testing relatives of patients with hypertrophic cardiomyopathy who are themselves free of hypertrophy, to differentiate between those who carry the gene (genotype positive phenotype negative) and those who do not (genotype negative phenotype negative)., comprising executing the method of any one of the preceding claims.</claim-text> <claim-text>16. A method of differentiating between patients with hypertrophic cardiomyopathy(i.e.pathologic hypertrophy) and athletes (i.e. physiological hypertrophy) comprising executing the method of any one of c!aims Ito 14.</claim-text> <claim-text>17. Apparatus for detecting hypertrophie eardiomyopathy or the presence of a gene mutation for hypertrophic cardiomyopathy, comprising a processor adapted to receive a measurement of the blood oxygen level dependent magnetic resonance signal intensity in the heart of a subject at rest, to receive a measurement of the blood oxygen level dependent magnetic resonance signal intensity in the heart of a subject under cardiac stress, and to determine from the two measurements whether or not the subject is suffering from hypertrophic cardiomyopathy or the presence of a gene mutation for hypertrophic cardiomyopathy.</claim-text> <claim-text>18. Apparatus according to claim 18 wherein the processor is adapted to determine whether or not the subject is suffering from hypertrophic cardiomyopathy or the presence of a gene mutation for hypertrophic eardiomyopathy by comparing the difference in blood oxygen level dependent magnetic resonance signal intensity at rest and under cardiac stress to a threshold.</claim-text> <claim-text>19. Apparatus according to claim 17 wherein the threshold, for measurements made at a magnetic field strength of 3 Tesla, is 15%, more preferably 12%, more preferably 10%.</claim-text> <claim-text>20. Apparatus according to claim 18 wherein the processor is adapted to determine whether or not the subject is suffering from hypertrophic cardiomyopathy or the presence of a gene mutation for hypertrophic cardiomyopathy by comparing the comparing the change in blood oxygen level dependent magnetic resonance signal intensity from rest to cardiac stress of the subject with the change for a non-sufferer ofhypertrophic cardiomyopathy.</claim-text> <claim-text>21. Apparatus according to claim 20 wherein the processor is adapted to determine that the subject is suffering from hypertrophic cardiomyopathy or the presence of a gene mutation for hypertrophic cardiomyopathy if the change in blood oxygen level dependent magnetic resonance signal intensity from rest to cardiac stress of the subject is less than 60% of the change for a non-sufferer of hypertrophic cardio myopathy.</claim-text>
GB1116140.3A 2011-09-19 2011-09-19 Diagnosis of hypertrophic cardiomyopathy from change in blood oxygen level dependent magnetic resonance signal intensity Withdrawn GB2494702A (en)

Priority Applications (2)

Application Number Priority Date Filing Date Title
GB1116140.3A GB2494702A (en) 2011-09-19 2011-09-19 Diagnosis of hypertrophic cardiomyopathy from change in blood oxygen level dependent magnetic resonance signal intensity
PCT/GB2012/051825 WO2013041834A1 (en) 2011-09-19 2012-07-27 Bold imaging in hypertrophic cardiomyopathy and athlete's heart

Applications Claiming Priority (1)

Application Number Priority Date Filing Date Title
GB1116140.3A GB2494702A (en) 2011-09-19 2011-09-19 Diagnosis of hypertrophic cardiomyopathy from change in blood oxygen level dependent magnetic resonance signal intensity

Publications (2)

Publication Number Publication Date
GB201116140D0 GB201116140D0 (en) 2011-11-02
GB2494702A true GB2494702A (en) 2013-03-20

Family

ID=44937480

Family Applications (1)

Application Number Title Priority Date Filing Date
GB1116140.3A Withdrawn GB2494702A (en) 2011-09-19 2011-09-19 Diagnosis of hypertrophic cardiomyopathy from change in blood oxygen level dependent magnetic resonance signal intensity

Country Status (2)

Country Link
GB (1) GB2494702A (en)
WO (1) WO2013041834A1 (en)

Families Citing this family (2)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
WO2017059302A1 (en) 2015-09-30 2017-04-06 Cedars-Sinai Medical Center Robust myocardial blood oxygen level dependent magnetic resonance imaging with long-acting coronary vasodilators
CA3092698A1 (en) * 2018-04-26 2019-10-31 Cedars-Sinai Medical Center Highly-time resolved myocardial blood-oxygen-level-dependent magnetic resonance imaging

Citations (1)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
WO2002068930A2 (en) * 2001-02-23 2002-09-06 Allos Therapeutics, Inc. Methods and reagents to acquire mri signals and images

Family Cites Families (1)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
US6687528B2 (en) * 2001-09-28 2004-02-03 Ge Medical Systems Global Technology Company Llc Analysis of cardic MR relaxation time images with application to quantifying myocardial perfusion reserve indexes

Patent Citations (1)

* Cited by examiner, † Cited by third party
Publication number Priority date Publication date Assignee Title
WO2002068930A2 (en) * 2001-02-23 2002-09-06 Allos Therapeutics, Inc. Methods and reagents to acquire mri signals and images

Non-Patent Citations (5)

* Cited by examiner, † Cited by third party
Title
Gadolinium-Enhanced Cardiovascular Magnetic Resonance and Exercise Capacity in Hypertrophic Cardiomyopathy, REVISTA ESPANOLA DE CARDIOLOGIA, 2008-01-01, doi:10.1016/S1885-5857(08)60233-9, Romero-Puche A et al., ISSN 1885-5857, VOL 61, NR 8, PG 853-860, XP025648598 *
MR perfusion and delayed enhancement imaging in the heart, CLINICAL RADIOLOGY, 2006-03-01, doi:10.1016/j.crad.2005.09.010, Crean A et al., ISSN 0009-9260, VOL 61, NR 3, PG 225-236, XP025059230 *
Myocardial fibrosis in a patient with apical hypertrophic cardiomyopathy detected by delayed-enhanced maxgnetic resonance imaging, INTERNATIONAL JOURNAL OF CARDIOLOGY, 2008-12-17, doi:10.1016/j.ijcard.2007.07.062, Sato Y et al., ISSN 0167-5273, VOL 131, NR 1, PG e41-e43, XP025690942 *
Navigator-Gated 3D Blood Oxygen Level Dependent CMR at 3.0-T for Detection of Stress-Induced Myocardial Ischemic Reactions, Cosima Jahnke MD et al., JACC: Cardiovascular Imaging, Vol 3, Iss 4, April 2010, Pages 375 384 *
The Case for Myocardial Ischemia in Hypertrophic Cardiomyopathy, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2009-08-25, doi:10.1016/j.jacc.2009.04.072, Maron M S et al., ISSN 0735-1097, VOL 54, NR 9, PG 866-875, XP026494791 *

Also Published As

Publication number Publication date
GB201116140D0 (en) 2011-11-02
WO2013041834A1 (en) 2013-03-28

Similar Documents

Publication Publication Date Title
Mordi et al. T 1 and T 2 mapping for early diagnosis of dilated non-ischaemic cardiomyopathy in middle-aged patients and differentiation from normal physiological adaptation
Greenman et al. Foot small muscle atrophy is present before the detection of clinical neuropathy
Klinke et al. Quality assessment of cardiovascular magnetic resonance in the setting of the European CMR registry: description and validation of standardized criteria
Messroghli et al. Myocardial T1 mapping: application to patients with acute and chronic myocardial infarction
Tandri et al. Role of magnetic resonance imaging in arrhythmogenic right ventricular dysplasia: insights from the North American arrhythmogenic right ventricular dysplasia (ARVD/C) study
Rasoanandrianina et al. Region‐specific impairment of the cervical spinal cord (SC) in amyotrophic lateral sclerosis: a preliminary study using SC templates and quantitative MRI (diffusion tensor imaging/inhomogeneous magnetization transfer)
Gräβel et al. Wallerian degeneration of pyramidal tract after paramedian pons infarct
Georgoff et al. Hydrogen-1 MR spectroscopy for measurement and diagnosis of hepatic steatosis
Liu et al. Myocardial fat quantification in humans: evaluation by two‐point water‐fat imaging and localized proton spectroscopy
Clique et al. 3D myocardial T1 mapping at 3T using variable flip angle method: pilot study
Tyler et al. Reproducibility of 31P cardiac magnetic resonance spectroscopy at 3 T
Dabir et al. Cardiac magnetic resonance including parametric mapping in acute Takotsubo syndrome: preliminary findings
Kumar et al. CMR imaging of edema in myocardial infarction using cine balanced steady-state free precession
Keller et al. Diffusion tensor imaging combined with T2 mapping to quantify changes in the skeletal muscle associated with training and endurance exercise in competitive triathletes
Okujava et al. Measurement of temporal lobe T2 relaxation times using a routine diagnostic MR imaging protocol in epilepsy
Hollingsworth et al. Subepicardial dysfunction leads to global left ventricular systolic impairment in patients with limb girdle muscular dystrophy 2I
Guo et al. Free‐breathing whole‐heart multi‐slice myocardial T1 mapping in 2 minutes
Ma et al. Cardiac magnetic resonance imaging in arrhythmogenic right ventricular cardiomyopathy: correlation to the QRS dispersion
Reynolds et al. Quantification of DTI in the pediatric spinal cord: application to clinical evaluation in a healthy patient population
Goykhman et al. Reproducibility of myocardial perfusion reserve-variations in measurements from post processing using commercially available software
Wenserski et al. Human Immmunodeficiency Virus 1–associated Minor Motor Disorders: Perfusion-weighted MR Imaging and 1H MR Spectroscopy
Bellm et al. Reproducibility of myocardial T1 and T2 relaxation time measurement using slice‐interleaved T1 and T2 mapping sequences
Nelles et al. Combined 3T diffusion tensor tractography and 1H-MR spectroscopy in motor neuron disease
George et al. Magnetic-resonance-imaging-derived indices for the normalization of left ventricular morphology by body size
GB2494702A (en) Diagnosis of hypertrophic cardiomyopathy from change in blood oxygen level dependent magnetic resonance signal intensity

Legal Events

Date Code Title Description
WAP Application withdrawn, taken to be withdrawn or refused ** after publication under section 16(1)