Indications for MRI have grown considerably in recent years. However, many patients with cardiac implantable electronic devices are denied imaging due to physician misinterpretation of the risks associated with MRI. This review discusses the theoretical basis for the perceived risk by exploring preclinical literature. It then presents a detailed examination of the true rates of adverse events in clinical studies across both MR nonconditional (legacy) and MR conditional devices. Indeed, many of these adverse events are rare, nonexistent, and/or clinically insignificant in the wealth of published data. The authors then address image quality and the constituents of a safety checklist that institutions should consider when performing MRI in patients with a cardiac implantable electronic device. Lastly, the authors conclude with an overview of future directions for advancement in the field.

BackgroundEpicardial adipose tissue (EAT) is hypothesized to alter atherosclerotic plaque composition, with potential development of high‐risk plaque (HRP). EAT can be measured by volumetric assessment (EAT‐v) or linear thickness (EAT‐t). We performed a systematic review and random‐effects meta‐analysis to assess the association of EAT with HRP and whether this association is dependent on the measurement method used.Methods and ResultsElectronic databases were systematically searched up to October 2016. Studies reporting HRP by computed tomography or intracoronary imaging and studies measuring EAT‐v or EAT‐t were included. Odds ratios were extracted from multivariable models reporting the association of EAT with HRP and described as pooled estimates with 95% confidence intervals (CIs). Analysis was stratified by EAT measurement method. Nine studies (n=3772 patients) were included with 7 measuring EAT‐v and 2 measuring EAT‐t. Increasing EAT was significantly associated with the presence of HRP (odds ratio: 1.26 [95% CI, 1.11–1.43]; P<0.001). Patients with HRP had higher EAT‐v than those without (weighted mean difference: 28.3 mL [95% CI, 18.8–37.8 mL]; P<0.001). EAT‐v was associated with HRP (odds ratio: 1.19 [95% CI, 1.06–1.33]; P<0.001); however, EAT‐t was not (odds ratio: 3.09 [95% CI, 0.56–17]; P=0.2). Estimates remained significant when adjusted for small‐study effect bias (odds ratio: 1.13 [95% CI, 1.03–1.28]; P=0.04).ConclusionsIncreasing EAT is associated with the presence of HRP, and patients with HRP have higher quantified EAT‐v. The association of EAT‐v with HRP is significant compared with EAT‐t; however, a larger scale study is still required, and further evaluation is needed to assess whether EAT may be a potential therapeutic target for novel pharmaceutical agents.Clinical Trial Registration URL: https://www.crd.york.ac.uk/. Unique identifier: CRD42017055473.

Background Epicardial adipose tissue ( EAT ) is in immediate apposition to the underlying myocardium and, therefore, has the potential to influence myocardial systolic and diastolic function or myocardial geometry, through paracrine or compressive mechanical effects. We aimed to review the association between volumetric EAT and markers of myocardial function and geometry. Methods and Results PubMed, Medline, and Embase were searched from inception to May 2018. Studies were included only if complete EAT volume or mass was reported and related to a measure of myocardial function and/or geometry. Meta‐analysis and meta‐regression were used to evaluate the weighted mean difference of EAT in patients with and without diastolic dysfunction. Heterogeneity of data reporting precluded meta‐analysis for systolic and geometric associations. In the 22 studies included in the analysis, there was a significant correlation with increasing EAT and presence of diastolic dysfunction and mean e′ (average mitral annular tissue Doppler velocity) and E/e′ (early inflow / annular velocity ratio) but not E/A (ratio of peak early (E) and late (A) transmitral inflow velocities), independent of adiposity measures. There was a greater EAT in patients with diastolic dysfunction (weighted mean difference, 24.43 mL; 95% confidence interval, 18.5–30.4 mL; P <0.001), and meta‐regression confirmed the association of increasing EAT with diastolic dysfunction ( P =0.001). Reported associations of increasing EAT with increasing left ventricular mass and the inverse correlation of EAT with left ventricular ejection fraction were inconsistent, and not independent from other adiposity measures. Conclusions EAT is associated with diastolic function, independent of other influential variables. EAT is an effect modifier for chamber size but not systolic function.

The safety profile of AF ablation has improved significantly in less than a decade.

No abstract

epicardial adipose tissue (eAt) is associated with cardiovascular risk. the longitudinal change in eAt volume (eAtv) and density (eAtd), and potential modulators of these parameters, has not been described. We prospectively recruited 90 patients with non-obstructive coronary atherosclerosis on baseline computed tomography coronary angiography (ctcA) performed for suspected coronary artery disease to undergo a repeat research CTCA. EATv in millilitres (mL) and EATd in Hounsfield units (HU) were analysed and multivariable regression analysis controlling for traditional cardiovascular risk factors (cVRf) performed to assess for any predictors of change. Secondary analysis was performed based on statin therapy. The median duration between CTCA was 4.3years. Mean EATv increased at follow-up (72 ± 33 mL to 89 ± 43 mL, p < 0.001) and mean EATd decreased (baseline −76 ± 6 HU vs. −86 ± 5 HU, p < 0.001). There were no associations between baseline variables of body mass index, age, sex, hypertension, hyperlipidaemia, diabetes or smoking on change in EATv or EATd. No difference in baseline, follow-up or delta EATv or EATd was seen in patients with (60%) or without baseline statin therapy. in this select group of patients, eAtv consistently increased and eAtd consistently decreased at long-term follow-up and these changes were independent of cVRf, age and statin use. together with the knowledge of strong associations between EAT and cardiac disease, these findings may suggest that eAt is an independent parameter rather than a surrogate for cardiovascular risk. open Scientific RepoRtS | (2020) 10:7109 | https://doi.org/10.1038/s41598-020-63135-z www.nature.com/scientificreports www.nature.com/scientificreports/ Scientific RepoRtS | (2020) 10:7109 | https://doi.org/10.1038/s41598-020-63135-zwww.nature.com/scientificreports www.nature.com/scientificreports/ however, this is reflective of the current literature in examining relevant associations of EAT. Finally, there is potential for error in using delta EAT values with potential overlap from test-retest variability. Our previous work has demonstrated limits of agreement up to 10 mL higher or lower between observers with a mean bias however of only 1 mL, however our inter-observer correlation was excellent at 0.98 with assessors blinded to scan timing and patient details. conclusion Epicardial adipose tissue volume and density demonstrate significant longitudinal changes in patients with non-obstructive coronary artery disease with a consistent increase in EAT volume and consistent decrease in EAT density. There are no clinical risk factors that appear to associate with the change in EAT parameters and this effect is also independent of statin therapy. This finding may suggest that EAT is an independent marker, rather than surrogate of cardiovascular risk.

Automated LV entropy measurement is a novel marker for risk stratification toward ventricular arrhythmia in patients with DCM.

Background--Epicardial adipose tissue (EAT) is hypothesized to alter atherosclerotic plaque composition, with potential development of high-risk plaque (HRP). EAT can be measured by volumetric assessment (EAT-v) or linear thickness (EAT-t). We performed a systematic review and random-effects meta-analysis to assess the association of EAT with HRP and whether this association is dependent on the measurement method used.Methods and Results--Electronic databases were systematically searched up to October 2016. Studies reporting HRP by computed tomography or intracoronary imaging and studies measuring EAT-v or EAT-t were included. Odds ratios were extracted from multivariable models reporting the association of EAT with HRP and described as pooled estimates with 95% confidence intervals (CIs). Analysis was stratified by EAT measurement method. Nine studies (n=3772 patients) were included with 7 measuring EAT-v and 2 measuring EAT-t. Increasing EAT was significantly associated with the presence of HRP (odds ratio: 1.26 [95% CI, 1.11-1.43]; P<0.001). Patients with HRP had higher EAT-v than those without (weighted mean difference: 28.3 mL [95% CI, 18.8-37.8 mL]; P<0.001). EAT-v was associated with HRP (odds ratio: 1.19 [95% CI, 1.06-1.33]; P<0.001); however, EAT-t was not (odds ratio: 3.09 [95% CI, 0.56-17]; P=0.2). Estimates remained significant when adjusted for small-study effect bias (odds ratio: 1.13 [95% CI, 1.03-1.28]; P=0.04).Conclusions--Increasing EAT is associated with the presence of HRP, and patients with HRP have higher quantified EAT-v. The association of EAT-v with HRP is significant compared with EAT-t; however, a larger scale study is still required, and further evaluation is needed to assess whether EAT may be a potential therapeutic target for novel pharmaceutical agents.