Publications
463 results found
Halliday BP, Tayal U, Prasad S, 2018, Role of Cardiovascular Magnetic Resonance in Dilated Cardiomyopathy, Cardiovascular Magnetic Resonance: A Companion to Braunwald’s Heart Disease, Pages: 383.e4-390.e4, ISBN: 9780323415613
Dilated cardiomyopathy (DCM) is defined as a disease of the myocardium characterized by left ventricular dilatation and systolic impairment that cannot be exclusively explained by abnormal loading conditions (such as hypertension or valvular heart disease) or coronary artery disease. The true prevalence is debated because of a lack of large contemporary population studies. The original Olmsted County study, performed between 1975 and 1984, estimated the prevalence to be in the region of 1 in 2700 individuals. However, the calculated prevalence of hypertrophic cardiomyopathy in the same study has since been shown to be a gross underestimate, possibly explained by the fact that echocardiography was still a developing technique. Recent reports have estimated the prevalence to be closer to 1 in 400 people in the United States. Nevertheless, DCM is a commonly encountered condition, representing the most frequent indication for cardiac transplantation and a common cause of heart failure and sudden cardiac death. Despite therapeutic advances, 3-year treated mortality rates are estimated to be 12% to 20%. Definitive early investigation giving a prompt and accurate diagnosis is therefore essential for the expedient introduction of targeted therapy. We will discuss the benefits of cardiovascular magnetic resonance in the investigation of DCM after a brief overview of our current understanding of the disease.
Balaban G, Halliday BP, Costa CM, et al., 2018, The Effects of Non-ischemic Fibrosis Texture and Density on Mechanisms of Reentry, 45th Computing in Cardiology Conference (CinC), Publisher: IEEE, ISSN: 2325-8861
Halliday BP, Pennell DJ, Prasad SK, 2017, Response by Halliday et al to letter regarding article, "Association between midwall late gadolinium enhancement and sudden cardiac death in patients with dilated cardiomyopathy and mild and moderate left ventricular systolic dysfunction", Circulation, Vol: 137, Pages: 101-102, ISSN: 0009-7322
Walsh R, Buchan R, Wilk A, et al., 2017, Defining the genetic architecture of hypertrophic cardiomyopathy: re-evaluating the role of non-sarcomeric genes, European Heart Journal, Vol: 38, Pages: 3461-3468, ISSN: 1522-9645
Aim: Hypertrophic cardiomyopathy (HCM)exhibits genetic heterogeneity that is dominated by variation in eight sarcomericgenes.Genetic variation in a large number of non-sarcomeric genes has also been implicated in HCM but not formally assessed. Here we used very large case and control cohorts to determine the extent to which variation in non-sarcomeric genes contributes to HCM.Methods and results: We sequenced known and putative HCM genes ina new large prospective HCM cohort (n=804) and analysed data alongside the largest published series of clinically genotyped HCM patients (n=6179), previously published HCM cohorts and reference population samples from the Exome Aggregation Consortium (ExAC, n=60,706) to assess variation in 31 genes implicated in HCM. We foundno significant excess of rare (minor allele frequency < 1:10,000 in ExAC)protein-alteringvariants over controls for most genes tested and conclude that novel variantsin these genes are rarely interpretable, even for genes with previous evidence of co-segregation (e.g. ACTN2). To provide an aid for variant interpretation, weintegratedHCM gene sequencedata with aggregatedpedigreeand functional data and suggest ameans of assessing genepathogenicity in HCMusing this evidence. Conclusions: We show that genetic variation in the majority of non-sarcomeric genes implicated in HCM is not associated with the condition, reinforce the fact that the sarcomeric gene variation is the primary cause of HCM known to date and underscore that the aetiology of HCM is unknown in the majority ofpatients.
Kouranos V, Tzelepis GE, Rapti A, et al., 2017, Complementary Role of CMR to Conventional Screening in the Diagnosis and Prognosis of Cardiac Sarcoidosis, JACC-CARDIOVASCULAR IMAGING, Vol: 10, Pages: 1437-1447, ISSN: 1936-878X
- Author Web Link
- Cite
- Citations: 124
Corden B, Jarman J, Whiffin N, et al., 2017, Titin Truncating Variants Predict Life-threatening Arrhythmias in Patients With Dilated Cardiomyopathy, Scientific Sessions of the American-Heart-Association / Resuscitation Science Symposium, Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0009-7322
Corden B, Jarman J, Whiffin N, et al., 2017, Titin Truncating Variants Predict Life-threatening Arrhythmias in Patients With Dilated Cardiomyopathy, Scientific Sessions of the American-Heart-Association / Resuscitation Science Symposium, Publisher: American Heart Association, Pages: E96-E96, ISSN: 0009-7322
Introduction: There is an urgent need for better arrhythmic risk stratification in non-ischaemic dilated cardiomyopathy (DCM), where the benefit of ICD implantation is unclear. Titin truncating variants (TTNtv) are the commonest genetic cause of DCM and are associated with early onset non-sustained ventricular tachycardia (NSVT) and atrial fibrillation (AF) in these patients.Hypothesis: We hypothesize that TTNtv status can predict potentially life threatening ventricular tachycardia (VT) or fibrillation (VF) and development of new persistent AF in DCM patients with CRT-D or ICD devices.Methods: We studied 117 DCM patients with an ICD or CRT-D and documented device-recorded arrhythmia over a median period of 4.2 years. Patients were stratified by TTN genotype (28 positive for a TTNtv, 89 negative). The primary outcome was time to first device-treated VT >200bpm or VF. Secondary outcome measures included time to first development of persistent AF.Results: TTNtv predicted the risk of receiving an appropriate ICD therapy for VT/VF (hazard ratio [HR] = 4.9, 95% confidence interval [CI]=2.3-10.7, P<0.0001). This association was independent of all covariates, including replacement fibrosis measured by late-gadolinium enhancement (LGE), (adjusted HR = 8.2, 95% CI 1.9-36.5, P=0.005). Individuals with both a TTNtv and fibrosis had a markedly greater risk for appropriate device therapy than those with neither (HR = 16.6, CI 3.5-79.3, P<0.0001). TTNtv were also a risk factor for developing new persistent AF (HR = 4.4, 95% CI = 1.45-13.1, P=0.006).Conclusion: TTNtv status is an important risk factor for clinically significant arrhythmia in patients with DCM and CRT-D or ICD devices. TTNtv status alone, or more powerfully in combination with fibrosis imaging by MRI, may provide an effective approach for risk stratifying the need for ICD therapy in DCM patients.
Eijsvogels TMH, Oxborough DL, O'Hanlon R, et al., 2017, Global and regional cardiac function in lifelong endurance athletes with and without myocardial fibrosis., Eur J Sport Sci, Vol: 17, Pages: 1297-1303
The aim of the present study was to compare cardiac structure as well as global and regional cardiac function in athletes with and without myocardial fibrosis (MF). Cardiac magnetic resonance imaging with late gadolinium enhancement was used to detect MF and global cardiac structure in nine lifelong veteran endurance athletes (58 ± 5 years, 43 ± 5 years of training). Transthoracic echocardiography using tissue-Doppler and myocardial strain imaging assessed global and regional (18 segments) longitudinal left ventricular function. MF was present in four athletes (range 1-8 g) and not present in five athletes. MF was located near the insertion points of the right ventricular free wall on the left ventricle in three athletes and in the epicardial lateral wall in one athlete. Athletes with MF demonstrated a larger end diastolic volume (205 ± 24 vs 173 ± 18 ml) and posterior wall thickness (11 ± 1 vs 9 ± 1 mm) compared to those without MF. The presence of MF did not mediate global tissue velocities or global longitudinal strain and strain rate; however, regional analysis of longitudinal strain demonstrated reduced function in some fibrotic regions. Furthermore, base to apex gradient was affected in three out of four athletes with MF. Lifelong veteran endurance athletes with MF demonstrate larger cardiac dimensions and normal global cardiac function. Fibrotic areas may demonstrate some co-localised regional cardiac dysfunction, evidenced by an affected cardiac strain and base to apex gradient. These data emphasize the heterogeneous phenotype of MF in athletes.
Tayal U, Newsome S, Buchan R, et al., 2017, Phenotype and clinical outcomes of titin cardiomyopathy, Journal of the American College of Cardiology, Vol: 70, Pages: 2264-2274, ISSN: 0735-1097
Background Improved understanding of dilated cardiomyopathy (DCM) due to titin truncation (TTNtv) may help guide patient stratification.Objectives The purpose of this study was to establish relationships among TTNtv genotype, cardiac phenotype, and outcomes in DCM.Methods In this prospective, observational cohort study, DCM patients underwent clinical evaluation, late gadolinium enhancement cardiovascular magnetic resonance, TTN sequencing, and adjudicated follow-up blinded to genotype for the primary composite endpoint of cardiovascular death, and major arrhythmic and major heart failure events.Results Of 716 subjects recruited (mean age 53.5 ± 14.3 years; 469 men [65.5%]; 577 [80.6%] New York Heart Association function class I/II), 83 (11.6%) had TTNtv. Patients with TTNtv were younger at enrollment (49.0 years vs. 54.1 years; p = 0.002) and had lower indexed left ventricular mass (5.1 g/m2 reduction; padjusted = 0.03) compared with patients without TTNtv. There was no difference in biventricular ejection fraction between TTNtv+/− groups. Overall, 78 of 604 patients (12.9%) met the primary endpoint (median follow-up 3.9 years; interquartile range: 2.0 to 5.8 years), including 9 of 71 patients with TTNtv (12.7%) and 69 of 533 (12.9%) without. There was no difference in the composite primary outcome of cardiovascular death, heart failure, or arrhythmic events, for patients with or without TTNtv (hazard ratio adjusted for primary endpoint: 0.92 [95% confidence interval: 0.45 to 1.87]; p = 0.82).Conclusions In this large, prospective, genotype-phenotype study of ambulatory DCM patients, we show that prognostic factors for all-cause DCM also predict outcome in TTNtv DCM, and that TTNtv DCM does not appear to be associated with worse medium-term prognosis.
Delle Donne G, Rosés Noguer F, Till J, et al., 2017, Ivabradine in Postural Orthostatic Tachycardia Syndrome: Preliminary Experience in Children., Am J Cardiovasc Drugs
OBJECTIVE: Ivabradine is a selective and specific inhibitor of the I(f) current in the sinoatrial and atrioventricular nodes. It decreases heart rate and myocardial oxygen consumption at rest and during exercise. It is used in adults for management of heart failure and angina, but promising results have been obtained in postural orthostatic tachycardia syndrome (POTS). There is little experience of ivabradine in childhood, although it is used on a compassionate basis. Our aim was to review our experience of ivabradine in a retrospective evaluation of pediatric patients with POTS. METHODS: We evaluated all patients younger than 18 years for whom ivabradine had been prescribed for this indication, from February 2008 to June 2014. RESULTS: Twenty-two patients were identified (15 female). Median age was 14.5 years (11-17 years). The ivabradine dosage after up-titration was 0.1 mg/kg per dose twice daily. In 15 (68%) symptoms improved. Ivabradine was suspended in five, but only in one for worsening of symptoms. There was a reduction in heart rate on resting electrocardiogram (EKG) from a mean (standard deviation) of 82.5 (13.6) bpm to a mean of 71 (16.5) bpm (p = 0.007). No patient had increased duration of QTc (p = 0.44). One (4.5%) experienced phosphenes. CONCLUSIONS: From this initial experience, ivabradine is safe in patients younger than 18 years with POTS. We observed improvement of symptoms in 68% and phosphenes in less than 5%. Further studies are needed to assess the safety in a randomized control setting.
Tayal U, Prasad SK, 2017, Myocardial remodelling and recovery in dilated cardiomyopathy, JRSM Cardiovascular Disease, Vol: 6, Pages: 1-7, ISSN: 2048-0040
Myocardial reverse remodeling has been reported to occur in 25–70% of patients with dilated cardiomyopathy. It is not yet fully understood whether remodeling represents disease remission or cure and which hearts retain this capacity to recover. In this review article we discuss the capacity for recovery in DCM, the prognostic implications of this recovery and potential clinical and imaging predictors for myocardial remodeling.
Prasad SK, Lota AS, 2017, Right Ventricle Dysfunction in Cardiomyopathy To Measure Is to Know, JACC-CARDIOVASCULAR IMAGING, Vol: 10, Pages: 1237-1239, ISSN: 1936-878X
- Author Web Link
- Cite
- Citations: 4
Cleland JGF, Halliday BP, Prasad SK, 2017, Selecting Patients With Nonischemic Dilated Cardiomyopathy for ICDs Myocardial Function, Fibrosis, and What's Attached?, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Vol: 70, Pages: 1228-1231, ISSN: 0735-1097
- Author Web Link
- Cite
- Citations: 10
Liew A, Raphael CE, Mitchell F, et al., 2017, Prognostic value of cardiovascular magnetic resonance in the prediction of atrial fibrillation in hypertrophic cardiomyopathy (HCM), Publisher: OXFORD UNIV PRESS, Pages: 946-947, ISSN: 0195-668X
Raphael CE, Mitchell F, Kanaganayagam GS, et al., 2017, Risk factors for the development of heart failure in hypertrophic cardiomyopathy: a cardiovascular magnetic resonance study, Publisher: OXFORD UNIV PRESS, Pages: 944-944, ISSN: 0195-668X
Tayal U, Newsome S, Walsh R, et al., 2017, Defining the genetic architecture of dilated cardiomyopathy- insights from population genetic variation and the role of titin, Publisher: OXFORD UNIV PRESS, Pages: 821-822, ISSN: 0195-668X
Everett R, Chin CWL, Kwiencinski J, et al., 2017, Longitudinal cardiac magnetic resonance assessment in patients with aortic stenosis, Congress of the European-Society-of-Cardiology (ESC), Publisher: OXFORD UNIV PRESS, Pages: 65-65, ISSN: 0195-668X
Vassiliou VS, Flynn PD, Raphael CE, et al., 2017, Lipoprotein(a) in patients with aortic stenosis: insights from cardiovascular magnetic resonance, PLOS One, Vol: 12, ISSN: 1932-6203
BackgroundAortic stenosis is the most common age-related valvular pathology. Patients with aortic stenosis and myocardial fibrosis have worse outcome but the underlying mechanism is unclear. Lipoprotein(a) is associated with adverse cardiovascular risk and is elevated in patients with aortic stenosis. Although mechanistic pathways could link Lipoprotein(a) with myocardial fibrosis, whether the two are related has not been previously explored. In this study, we investigated whether elevated Lipoprotein(a) was associated with the presence of myocardial replacement fibrosis.MethodsA total of 110 patients with mild, moderate and severe aortic stenosis were assessed by late gadolinium enhancement (LGE) cardiovascular magnetic resonance to identify fibrosis. Mann Whitney U tests were used to assess for evidence of an association between Lp(a) and the presence or absence of myocardial fibrosis and aortic stenosis severity and compared to controls. Univariable and multivariable linear regression analysis were undertaken to identify possible predictors of Lp(a).ResultsThirty-six patients (32.7%) had no LGE enhancement, 38 (34.6%) had midwall enhancement suggestive of midwall fibrosis and 36 (32.7%) patients had subendocardial myocardial fibrosis, typical of infarction. The aortic stenosis patients had higher Lp(a) values than controls, however, there was no significant difference between the Lp(a) level in mild, moderate or severe aortic stenosis. No association was observed between midwall or infarction pattern fibrosis and Lipoprotein(a), in the mild/moderate stenosis (p = 0.91) or severe stenosis patients (p = 0.42).ConclusionThere is no evidence to suggest that higher Lipoprotein(a) leads to increased myocardial midwall or infarction pattern fibrosis in patients with aortic stenosis.
Halliday BP, Cleland JGF, Goldberger JJ, et al., 2017, Personalizing Risk Stratification for Sudden Death in Dilated Cardiomyopathy:The Past, Present, and Future, Circulation, Vol: 136, Pages: 215-231, ISSN: 0009-7322
Results from the DANISH Study (Danish Study to Assess the Efficacy of ICDs in Patients with Non-ischemic Systolic Heat Failure on Mortality) suggest that, for many patients with dilated cardiomyopathy (DCM), implantable cardioverter defibrillators (ICD) do not increase longevity. Accurate identification of patients who are more likely to die of an arrhythmia and less likely to die from other causes is required to ensure improvement in outcomes and wise use of resources. Until now, left ventricular ejection fraction (LVEF) has been used as a key criterion for selecting patients with DCM for an ICD for primary prevention purposes. However, registry data suggest that many patients with DCM and an out-of-hospital cardiac arrest do not have a markedly reduced LVEF. Additionally, many patients with reduced LVEF die from non-sudden causes of death. Methods to predict a higher or lower risk of sudden death include the detection of myocardial fibrosis (a substrate for ventricular arrhythmia), microvolt T-wave alternans (MTWA; a marker of electrophysiological vulnerability) and genetic testing. Mid-wall fibrosis is identified by late gadolinium enhancement cardiovascular magnetic resonance imaging in around 30% of patients and provides incremental value in addition to LVEF for the prediction of SCD events. MTWA represents another promising predictor, supported by large meta-analyses that have highlighted the negative predictive value of this test. However, neither of these strategies have been routinely adopted for risk stratification in clinical practice. More convincing data from randomized trials are required to inform the management of patients with these features. Understanding of the genetics of DCM and how specific mutations affect arrhythmic risk is also rapidly increasing. The finding of a mutation in LMNA, the cause of around 6% of idiopathic DCM, commonly underpins more aggressive management due to the malignant nature of the associated phenotype. With the expansi
Selvanayagam JB, Hartshorne T, Billot L, et al., 2017, Cardiovascular magnetic resonance-GUIDEd management of mild to moderate left ventricular systolic dysfunction (CMR GUIDE): Study protocol for a randomized controlled trial., Ann Noninvasive Electrocardiol, Vol: 22
BACKGROUND: The majority of sudden cardiac death (SCD) in patients with heart failure occurs in those with mild-moderate left ventricular (LV) systolic dysfunction (LVEF 36-50%) who under current guidelines are ineligible for primary prevention implantable cardiac defibrillator (ICD) therapy. Recent data suggest that cardiac magnetic resonance (CMR) evidence of replacement fibrosis forms a substrate for malignant arrhythmia and therefore potentially identifies a subgroup at increased risk of SCD. Our hypothesis is that among patients with mild-moderate LV systolic dysfunction, a CMR-guided management strategy for ICD insertion based on the presence of scar or fibrosis is superior to a current strategy of standard care. METHODS/DESIGN: CMR GUIDE is a prospective, multicenter randomized control trial enrolling patients with mild-moderate LV systolic dysfunction and CMR evidence of fibrosis on optimal heart failure therapy. Participants will be randomized to receive either a primary prevention ICD or an implantable loop recorder (ILR). The primary endpoint is the time to SCD or hemodynamically significant ventricular arrhythmia (VF or VT) during an average 4-year follow-up. Secondary endpoints include quality of life assessed by Minnesota Living with Heart Failure Questionnaire, heart failure related hospitalizations, and a cost-utility analysis. Clinical trials.gov identifier NCT01918215. DISCUSSION: CMR GUIDE trial will add substantially to our understanding of the role of myocardial fibrosis and the risk of developing life-threatening ventricular arrhythmias. If the superiority of a CMR-guided approach over standard care is proven, it may change international clinical guidelines, with the potential to considerably increase survival in this growing patient population.
Vassiliou V, Wassilew K, Cameron D, et al., 2017, Identification of myocardial diffuse fibrosis by 11 heartbeat MOLLI T1 mapping: Averaging to improve precision and correlation with collagen volume fraction, Magnetic Resonance Materials in Physics Biology and Medicine, Vol: 31, Pages: 101-113, ISSN: 0968-5243
ObjectivesOur objectives involved identifying whether repeated averaging in basal and mid left ventricular myocardial levels improves precision and correlation with collagen volume fraction for 11 heartbeat MOLLI T1 mapping versus assessment at a single ventricular level.Materials and methodsFor assessment of T1 mapping precision, a cohort of 15 healthy volunteers underwent two CMR scans on separate days using an 11 heartbeat MOLLI with a 5(3)3 beat scheme to measure native T1 and a 4(1)3(1)2 beat post-contrast scheme to measure post-contrast T1, allowing calculation of partition coefficient and ECV. To assess correlation of T1 mapping with collagen volume fraction, a separate cohort of ten aortic stenosis patients scheduled to undergo surgery underwent one CMR scan with this 11 heartbeat MOLLI scheme, followed by intraoperative tru-cut myocardial biopsy. Six models of myocardial diffuse fibrosis assessment were established with incremental inclusion of imaging by averaging of the basal and mid-myocardial left ventricular levels, and each model was assessed for precision and correlation with collagen volume fraction.ResultsA model using 11 heart beat MOLLI imaging of two basal and two mid ventricular level averaged T1 maps provided improved precision (Intraclass correlation 0.93 vs 0.84) and correlation with histology (R2 = 0.83 vs 0.36) for diffuse fibrosis compared to a single mid-ventricular level alone. ECV was more precise and correlated better than native T1 mapping.ConclusionT1 mapping sequences with repeated averaging could be considered for applications of 11 heartbeat MOLLI, especially when small changes in native T1/ECV might affect clinical management.
Halliday BP, Gulati A, Ali A, et al., 2017, Association between mid-wall late gadolinium enhancement and sudden cardiac death in patients with dilated cardiomyopathy and mild and moderate left ventricular systolic dysfunction, Circulation, Vol: 135, Pages: 2106-2115, ISSN: 0009-7322
Background—Current guidelines only recommend the use of an implantable cardioverter defibrillator (ICD) in patients with dilated cardiomyopathy (DCM) for the primary prevention of sudden cardiac death (SCD) in those with a left ventricular ejection fraction (LVEF)<35%. However, registries of out-of-hospital cardiac arrests demonstrate that 70-80% of such patients have a LVEF>35%. Patients with a LVEF>35% also have low competing risks of death from non-sudden causes. Therefore, those at high-risk of SCD may gain longevity from successful ICD therapy. We investigated whether late gadolinium enhancement cardiovascular magnetic resonance (LGE-CMR) identified patients with DCM without severe LV systolic dysfunction at high-risk of SCD.Methods—We prospectively investigated the association between mid-wall late gadolinium enhancement (LGE) and the pre-specified primary composite outcome of SCD or aborted SCD amongst consecutive referrals with DCM and a LVEF≥40% to our center between January 2000 and December 2011, who did not have a pre-existing indication for ICD implantation.Results—Of 399 patients (145 women, median age 50 years, median LVEF 50%, 25.3% with LGE) followed for a median of 4.6 years, 18 of 101 (17.8%) patients with LGE reached the pre-specified end-point, compared to 7 of 298 (2.3%) without (HR 9.2; 95% CI 3.9-21.8; p<0.0001). Nine patients (8.9%) with LGE compared to 6 (2.0%) without (HR 4.9; 95% CI 1.8-13.5; p=0.002) died suddenly, whilst 10 patients (9.9%) with LGE compared to 1 patient (0.3%) without (HR 34.8; 95% CI 4.6-266.6; p<0.001) had aborted SCD. Following adjustment, LGE predicted the composite end-point (HR 9.3; 95% CI 3.9-22.3; p<0.0001), SCD (HR 4.8; 95% CI 1.7-13.8; p=0.003) and aborted SCD (HR 35.9; 95% CI 4.8-271.4; p<0.001). Estimated hazard ratios for the primary end-point for patients with a LGE extent of 0-2.5%, 2.5-5% and >5% compared to those without LGE were 10.6 (95%CI 3.9-29.4), 4.9 (9
Tayal U, Newsome S, Buchan R, et al., 2017, Truncating variants in titin independently predict early arrhythmias in patients with dilated cardiomyopathy, Journal of the American College of Cardiology, Vol: 69, Pages: 2466-2468, ISSN: 1558-3597
Lota A, Wassall R, Scott A, et al., 2017, T2 mapping by cardiovasular magnetic resonance in acute and recovered myocarditis: potential role in clinical surveillance, European Journal of Heart Failure, Supplement, Vol: 19, Pages: 258-258, ISSN: 1567-4215
Halliday BP, Chiew K, Newsome S, et al., 2017, Incremental prognostic value of cardiopulmonary exercise testing in non-ischemic dilated cardiomyopathy, EUROPEAN JOURNAL OF HEART FAILURE, Vol: 19, Pages: 435-435, ISSN: 1388-9842
Vassiliou V, Perperoglou A, Raphael CE, et al., 2017, Midwall fibrosis and 5-Year outcome in patients with moderate and severe aortic stenosis, Journal of the American College of Cardiology, Vol: 69, Pages: 1755-1756, ISSN: 1558-3597
Tayal U, Newsome S, Voges I, et al., 2017, MULTIMODALITY ASSESSMENT OF RISK IN DILATED CARDIOMYOPATHY-THE IMPORTANCE OF CMR, 12th Annual Meeting of the British-Society-of-Cardiovascular-Magnetic-Resonance (BSCMR), Publisher: BMJ PUBLISHING GROUP, Pages: A4-A4, ISSN: 1355-6037
Lota AS, Wassall R, Scott AD, et al., 2017, T2 MAPPING IN ACUTE AND RECOVERED MYOCARDITIS: POTENTIAL ROLE IN CLINICAL SURVEILLANCE, 12th Annual Meeting of the British-Society-of-Cardiovascular-Magnetic-Resonance (BSCMR), Publisher: BMJ PUBLISHING GROUP, Pages: A22-A24, ISSN: 1355-6037
Tayal U, Newsome S, Whiffin N, et al., 2017, PRECISE PHENOTYPING WITH CMR IDENTIFIES MODERATE ALCOHOL CONSUMPTION AS AN IMPORTANT PHENOTYPIC MODIFIER OF TITIN CARDIOMYOPATHY, 12th Annual Meeting of the British-Society-of-Cardiovascular-Magnetic-Resonance (BSCMR), Publisher: BMJ PUBLISHING GROUP, Pages: A2-A3, ISSN: 1355-6037
Halliday BP, Gulati A, Ali A, et al., 2017, SUDDEN CARDIAC DEATH RISK STRATIFICATION IN PATIENTS WITH MILD DILATED CARDIOMYOPATHY, 12th Annual Meeting of the British-Society-of-Cardiovascular-Magnetic-Resonance (BSCMR), Publisher: BMJ PUBLISHING GROUP, Pages: A2-A2, ISSN: 1355-6037
This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.