Left Ventricular Noncompaction, or Is It?

Editoria

Fractal frontiers in cardiovascular magnetic resonance: towards clinical implementation

This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.JCM: Higher Education Funding Council for England and the UK National Institute for Health Research, University College London, Biomedical Research Centre; GC: NIHR BRC University College London. DAB: Intramural research program, National Institutes of Health

Physical activity and left-ventricular trabeculation in the UK Biobank community-based cohort study

Objective: Vigorous physical activity (PA) in highly trained athletes has been associated with heightened left ventricular (LV) trabeculation extent. It has therefore been hypothesised that LV trabeculation extent may participate in exercise-induced physiological cardiac remodelling. Our cross-sectional observational study aimed to ascertain whether there is a ‘dose–response’ relationship between PA and LV trabeculation extent and whether this could be identified at opposite PA extremes. Methods: In a cohort of 1030 individuals from the community-based UK Biobank study (male/female ratio: 0.84, mean age: 61 years), PA was measured via total metabolic equivalent of task (MET) min/week and 7-day average acceleration, and trabeculation extent via maximal non-compaction/compaction ratio (NC/C) in long-axis images of cardiovascular magnetic resonance studies. The relationship between PA and NC/C was assessed by multivariate regression (adjusting for potential confounders) as well as between demographic, anthropometric and LV phenotypic parameters and NC/C. Results: There was no significant linear relationship between PA and NC/C (full adjustment, total MET-min/week: ß=−0.0008, 95% CI −0.039 to –0.037, p=0.97; 7-day average acceleration: ß=−0.047, 95% CI −0.110 to –0.115, p=0.13, per IQR increment in PA), or between extreme PA quintiles (full adjustment, total MET-min/week: ß=−0.026, 95% CI −0.146 to –0.094, p=0.67; 7-day average acceleration: ß=−0.129, 95% CI −0.299 to –0.040, p=0.49), across all adjustment levels. A negative relationship was identified between left ventricular ejection fraction and NC/C, significantly modified by PA (ß difference=−0.006, p=0.03). Conclusions: In a community-based general population cohort, there was no relationship at, or between, extremes, between PA and NC/C, suggesting that at typical general population PA levels, trabeculation extent is not influenced by PA changes.British Heart Foundation (BHF) (PG/14/89/31194)National Institute for Health Research (NIHR) Barts Biomedical Research Centre’SmartHeart’ Engineering and Physical Sciences Research Council programme grant (EP/P001009/1

Evaluation of splenic switch off in a tertiary imaging centre: validation and assessment of utility.

Aims: Adenosine can induce splenic vasoconstriction (splenic switch-off, SSO). In this study, we aim to evaluate the utility of identifying a lack of SSO for detecting false-negative adenosine stress perfusion cardiac magnetic resonance (CMR) scans. Methods and results: We visually analysed 492 adenosine stress perfusion CMR scans reported as negative in a cohort of patients with no previous history of coronary artery disease. A lack of SSO was identified in 11%. We quantified the phenomenon by drawing regions of interest on the spleen and comparing intensity between stress and rest scans, the spleen intensity ratio (SIR). Inter-rater agreement for qualitative determination of SSO was κ = 0.81 and inter-class correlation for quantitative determination of SSO was 0.94. The optimal threshold for SIR as an indicator of SSO was 0.40 (sensitivity = 82.5%, specificity = 92.3%, AUC = 0.91). 23 065 CMR scans and 9926 invasive coronary angiogram reports were retrospectively examined to identify patients with negative CMR scans who required coronary intervention in the subsequent 12 months (false negatives). We compared these scans with true positives who had positive adenosine stress perfusion CMR scans followed by coronary intervention. The rate of lack of SSO was 20.7% in the false-negative group versus 13.1% in true positives (P = 0.37). Conclusion: The lack of SSO is prevalent, easily measureable, and has potential to improve on haemodynamic criteria as a marker of adenosine understress in CMR perfusion scans.This work forms part of the research areas contributing to the translational research portfolio of the Cardiovascular Biomedical Research Unit at Barts which is supported and funded by the National Institute for Health Research. C.M. is partially funded by support from the National Institute for Health Research University College London Hospitals Biomedical Research Centre

Non-invasive characterization of pleural and pericardial effusions using T1 mapping by magnetic resonance imaging

AIMS: Differentiating exudative from transudative effusions is clinically important and is currently performed via biochemical analysis of invasively obtained samples using Light's criteria. Diagnostic performance is however limited. Biochemical composition can be measured with T1 mapping using cardiovascular magnetic resonance (CMR) and hence may offer diagnostic utility for assessment of effusions. METHODS AND RESULTS: A phantom consisting of serially diluted human albumin solutions (25-200 g/L) was constructed and scanned at 1.5 T to derive the relationship between fluid T1 values and fluid albumin concentration. Native T1 values of pleural and pericardial effusions from 86 patients undergoing clinical CMR studies retrospectively analysed at four tertiary centres. Effusions were classified using Light's criteria where biochemical data was available (n = 55) or clinically in decompensated heart failure patients with presumed transudative effusions (n = 31). Fluid T1 and protein values were inversely correlated both in the phantom (r = -0.992) and clinical samples (r = -0.663, P < 0.0001). T1 values were lower in exudative compared to transudative pleural (3252 ± 207 ms vs. 3596 ± 213 ms, P < 0.0001) and pericardial (2749 ± 373 ms vs. 3337 ± 245 ms, P < 0.0001) effusions. The diagnostic accuracy of T1 mapping for detecting transudates was very good for pleural and excellent for pericardial effusions, respectively [area under the curve 0.88, (95% CI 0.764-0.996), P = 0.001, 79% sensitivity, 89% specificity, and 0.93, (95% CI 0.855-1.000), P < 0.0001, 95% sensitivity; 81% specificity]. CONCLUSION: Native T1 values of effusions measured using CMR correlate well with protein concentrations and may be helpful for discriminating between transudates and exudates. This may help focus the requirement for invasive diagnostic sampling, avoiding unnecessary intervention in patients with unequivocal transudative effusions

Extracellular volume quantification in isolated hypertension - changes at the detectable limits?

The funding source (British Heart Foundation and UK National Institute for Health Research) provided salaries for research training (FZ, TT, DS, SW), but had no role in study design, collection, analysis, interpretation, writing, or decisions with regard to publication. This work was undertaken at University College London Hospital, which received a proportion of funding from the UK Department of Health National Institute for Health Research Biomedical Research Centres funding scheme. We are grateful to King’s College London Laboratories for processing the collagen biomarker panel

Left Atrial Structure in Relationship to Age, Sex, Ethnicity, and Cardiovascular Risk Factors MESA (Multi-Ethnic Study of Atherosclerosis)

This research was supported by contracts N01-HC-95159, N01-HC-95160, N01-HC-95161, N01- HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01- HC-95168 and N01-HC-95169 from the National Heart, Lung, and Blood Institute and by grants UL1-TR-000040 and UL1-TR-001079 from the National Center for Research Resources. Prof. Petersen and Drs. Zemrak and Mohiddin gratefully acknowledge funding from the National Institute for Health Research Cardiovascular Biomedical Research Unit at Barts. Prof. Petersen’s work is supported by awards establishing the Farr Institute of Health Informatics Research at University College London Partners from the Medical Research Council, in partnership with Arthritis Research United Kingdom, the British Heart Foundation, Cancer Research United Kingdom, the Economic and Social Research Council, the Engineering and Physical Sciences Research Council, the National Institute of Health Research, the National Institute for Social Care and Health Research (Welsh Assembly Government), the Chief Scientist Office (Scottish Government Health Directorates), and the Wellcome Trust (MR/K006584/1)