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The Society for Cardiovascular Magnetic Resonance (SCMR) last published its comprehensive expert panel report of clinical indications for CMR in 2004. This new Consensus Panel report brings those indications up to date for 2020 and includes the very substantial increase in scanning techniques, clinical applicability and adoption of CMR worldwide. We have used a nearly identical grading system for indications as in 2004 to ensure comparability with the previous report but have added the presence of randomized controlled trials as evidence for level 1 indications. In addition to the text, tables of the consensus indication levels are included for rapid assimilation and illustrative figures of some key techniques are provided.

Despite decades of accruing evidence supporting the clinical utility of cardiovascular magnetic resonance (CMR), adoption of CMR in routine cardiovascular practice remains limited in many regions of the world. Persistent use of long scan times of 60 min or more contributes to limited adoption, though techniques available on most scanners afford routine CMR examination within 30 min. Incorporating such techniques into standardize protocols can answer common clinical questions in daily practice, including those related to heart failure, cardiomyopathy, ventricular arrhythmia, ischemic heart disease, and non-ischemic myocardial injury. In this white paper, we describe CMR protocols of 30 min or shorter duration with routine techniques with or without stress perfusion, plus specific approaches in patient and scanner room preparation for efficiency. Minimum requirements for the scanner gradient system, coil hardware and pulse sequences are detailed. Recent advances such as quantitative myocardial mapping and other add-on acquisitions can be incorporated into the proposed protocols without significant extension of scan duration for most patients. Common questions in clinical cardiovascular practice can be answered in routine CMR protocols under 30 min; their incorporation warrants consideration to facilitate increased access to CMR worldwide.

T2-Weighted (T2W) magnetic resonance imaging (MRI) pulse sequences have been used to detect edema in patients with acute myocardial infarction and differentiate acute from chronic infarction. T2W sequences have suffered from several problems including (i) signal intensity variability caused by phased array coils, (ii) high signal from slow moving ventricular chamber blood that can mimic and mask elevated T2 in sub-endocardial myocardium, (iii) motion artifacts, and (iv) the subjective nature of T2W image interpretation. In this work we demonstrate the advantages of a quantitative T2 mapping technique to accurately and reliably detect regions of edematous myocardial tissue without the limitations of qualitative T2W imaging. Methods of T2 mapping were evaluated on phantoms; the best of these protocols was then optimized for in vivo imaging. The optimized protocol was used to study the spatial, view-dependent, and inter-subject variability and motion sensitivity in healthy subjects. Using the insights gained from this, the utility of T2 mapping was demonstrated in a porcine model of acute myocardial infarction (AMI) and in three patients with AMI. T2-prepared SSFP demonstrated greater accuracy in estimating the T2 of phantoms than multi-echo turbo spin echo. The T2 of human myocardium was found to be 52.18 ± 3.4 ms (range: 48.96 ms to 55.67 ms), with variability between subjects unrelated to heart rate. Unlike T2W images, T2 maps did not show any signal variation due to the variable sensitivity of phased array coils and were insensitive to cardiac motion. In the three pigs and three patients with AMI, the T2 of the infarcted region was significantly higher than that of remote myocardium. Quantitative T2 mapping addresses the well-known problems associated with T2W imaging of the heart and offers the potential for increased accuracy in the detection of myocardial edema.

Speckle tracking echocardiography (STE), and more recently, cardiovascular magnetic resonance myocardial feature tracking (CMR-FT) provides insight into all phases of atrial function. The aim of our study was to compare all phases of RA strain using CMR-FT and STE and also assess the relationship between RA and LA strain. A total of 61 healthy volunteers with mean age of 45 ± 13 years had adequate tracking for analysis on CMR-FT and 2D-STE. Females had larger RA reservoir strain (39 ± 15% vs. 32 ± 13%, p = 0.046) and conduit strain (26 ± 12% vs. 20 ± 9%, p = 0.03) when compared to males, but was not the case with booster strain (14 ± 7% vs. 12 ± 6%, p = 0.45). In comparison with STE derived strain, the RA reservoir and conduit strain were not significantly different between CMR-FT and the three echocardiography gating methods (p > 0.05 for all). Noticeably, there were no significant differences in strain and strain rate between RA and LA function using CMR-FT (p > 0.05 for all). RA strain and strain rate using CMR-FT had fair and good intra- and inter-observer reproducibility and had superior reproducibility compared to STE derived strain.

Cardiomyopathy is a leading cause of death in patients with Duchenne muscular dystrophy and myocardial damage precedes decline in left ventricular systolic function. We tested the efficacy of eplerenone on top of background therapy in patients with Duchenne muscular dystrophy with early myocardial disease. In this randomised, double-blind, placebo-controlled trial, boys from three centres in the USA aged 7 years or older with Duchenne muscular dystrophy, myocardial damage by late gadolinium enhancement cardiac MRI and preserved ejection fraction received either eplerenone 25 mg or placebo orally, every other day for the first month and once daily thereafter, in addition to background clinician-directed therapy with either angiotensin-converting enzyme inhibitors (ACEI) or angiotensin receptor blockers (ARB). Computer-generated randomisation was done centrally using block sizes of four and six, and only the study statistician and the investigational pharmacy had the preset randomisation assignments. The primary outcome was change in left ventricular circumferential strain (Ecc) at 12 months, a measure of contractile dysfunction. Safety was established through serial serum potassium levels and measurement of cystatin C, a non-creatinine measure of kidney function. This trial is registered with ClinicalTrials.gov, number NCT01521546. Between Jan 26, 2012, and July 3, 2013, 188 boys were screened and 42 were enrolled. 20 were randomly assigned to receive eplerenone and 22 to receive placebo, of whom 20 in the eplerenone group and 20 in the placebo group completed baseline, 6-month, and 12-month visits. After 12 months, decline in left ventricular circumferential strain was less in those who received eplerenone than in those who received placebo (median ΔEcc 1·0 [IQR 0·3–2·2] vs 2·2 [1·3–3·1]; p=0·020). Cystatin C concentrations remained normal in both groups, and all non-haemolysed blood samples showed normal potassium concentrations. One 23-year-old patient in the placebo group died of fat embolism, and another patient in the placebo group withdrew from the trial to address long-standing digestive issues. All other adverse events were mild: short-lived headaches coincident with seasonal allergies occurred in one patient given eplerenone, flushing occurred in one patient given placebo, and anxiety occurred in another patient given placebo. In boys with Duchenne muscular dystrophy and preserved ejection fraction, addition of eplerenone to background ACEI or ARB therapy attenuates the progressive decline in left ventricular systolic function. Early use of available drugs warrants consideration in this population at high risk of cardiac death, but further studies are needed to determine the effect of combination cardioprotective therapy on event-free survival in Duchenne muscular dystrophy. BallouSkies, Parent Project for Muscular Dystrophy, US National Center for Advancing Translational Sciences, and US National Institutes of Health.

No consensus exists for heart transplant listing for patients who use cannabis. We conducted a web-based survey to assess knowledge, and practice patterns towards patients with heart failure who use cannabis referred for transplant. A total of 140 clinicians (cardiologists (41.4%, n = 58), surgeons (7.1%, n = 10), pharmacists (9.3%, n = 13), advanced practice providers and coordinators) responded and responses were grouped by whether they responded that cannabis is “illegal in my state” (illegal), or “legal for medical and recreational use in my state,” (legal). There was a statistically significant difference in responses between the groups in the frequency of cannabis use that should preclude a patient from HT listing p = 0.0330) with respondents where cannabis is legal tending to answer that higher frequencies were acceptable. The groups in the “legal group” responded that a validated cannabis screening questionnaire could evaluate HT eligibility (p = 0.0111). A majority in the illegal group responding “No” as to whether their program allows pre- or post-transplant patients to use prescribed cannabis products (p < 0.0001). A majority in the illegal group responding “No” while the majority in the legal group responded “Yes” to “Does your HT center’s current selection criteria policy address medical cannabis use in potential transplant candidates?” (p = 0.0001). Health care providers generally agreed that a validated cannabis use disorder screening questionnaire would be useful and that 6 months of abstinence from cannabis is sufficient prior to HT listing. Significant heterogeneity exists regarding cannabis use as it relates to heart transplantation.

The aim of this document is to provide general guidance and specific recommendations on the practice of cardiovascular magnetic resonance (CMR) in the era of the COVID-19 pandemic. There are two major considerations. First, continued urgent and semi-urgent care for the patients who have no known active COVID-19 should be provided in a safe manner for both patients and staff. Second, when necessary, CMR on patients with confirmed or suspected active COVID-19 should focus on the specific clinical question with an emphasis on myocardial function and tissue characterization while optimizing patient and staff safety.

People with HIV (PWH) are at increased risk for atherosclerotic cardiovascular disease (ASCVD). Proportions of vascular homing monocytes are enriched in PWH; however, little is known regarding monocyte-derived macrophages (MDMs) that may drive atherosclerosis in this population. We isolated PBMCs from people with and without HIV, and cultured these cells for 5 days in medium containing autologous serum to generate MDMs. Differential gene expression (DGE) analysis of MDMs from PWH identified broad alterations in innate immune signaling (IL-1β, TLR expression, PPAR βδ) and lipid processing (LXR/RXR, ACPP, SREBP1). Transcriptional changes aligned with the functional capabilities of these cells. Expression of activation markers and innate immune receptors (CD163, TLR4, and CD300e) was altered on MDMs from PWH, and these cells produced more TNFα, reactive oxygen species (ROS), and matrix metalloproteinases (MMPs) than did cells from people without HIV. MDMs from PWH also had greater lipid accumulation and uptake of oxidized LDL. PWH had increased serum levels of free fatty acids (FFAs) and ceramides, with enrichment of saturated FAs and a reduction in polyunsaturated FAs. Levels of lipid classes and species that are associated with CVD correlated with unique DGE signatures and altered metabolic pathway activation in MDMs from PWH. Here, we show that MDMs from PWH display a pro-atherogenic phenotype; they readily form foam cells, have altered transcriptional profiles, and produce mediators that likely contribute to accelerated ASCVD.

Background Cardiomyopathy is a leading cause of morbidity and mortality in boys with Duchenne muscular dystrophy (DMD). We recently showed in a 12-month double-blind randomized controlled trial that adding eplerenone to background medical therapy was cardioprotective in this population. The objective of this study was to evaluate the safety and efficacy of longer-term eplerenone therapy in boys with DMD. Results Eleven subjects (phase 1 baseline median [range] age: 13 [7 – 25] years) from the original 12-month trial at a single participating center were enrolled. Importantly, those who entered the extension study who had been on eplerenone previously were significantly older than those who had originally been on placebo (median age 10.5 vs. 18.0 years, p  = 0.045). During an additional 24-month open-label extension study, all boys received eplerenone 25 mg orally once daily to treat preclinical DMD cardiomyopathy, defined as evident myocardial damage by late gadolinium enhancement cardiac magnetic resonance (LGE) with preserved ejection fraction (EF). The threshold for potassium level, the primary safety measure, was not exceeded in any non-hemolyzed blood sample. Over 24 months, left ventricular (LV) systolic strain, a more sensitive marker whose more negative values indicate greater contractility significantly improved (median change -4.4%, IQR -5.8 to -0.9%) in younger subjects whereas older subjects’ strain remained stable without significant worsening or improvement (median change 0.2%, IQR -1.1 to 4.3%). EF and extent of myocardial damage by LGE remained stable in both groups over 2 years. Conclusions Eplerenone offers effective and safe cardioprotection for boys with DMD, particularly when started at a younger age. Eplerenone is a useful clinical therapeutic option, particularly if treatment is initiated earlier in life when cardiac damage is minimal. Trial registration http://ClinicalTrials.gov identifier NCT01521546. Registered 26 January 2012.