Background Troponin elevation is common in hospitalized COVID-19 patients, but underlying aetiologies are ill-defined. We used multi-parametric cardiovascular magnetic resonance (CMR) to assess myocardial injury in recovered COVID-19 patients. Methods and results One hundred and forty-eight patients (64 ± 12 years, 70% male) with severe COVID-19 infection [all requiring hospital admission, 48 (32%) requiring ventilatory support] and troponin elevation discharged from six hospitals underwent convalescent CMR (including adenosine stress perfusion if indicated) at median 68 days. Left ventricular (LV) function was normal in 89% (ejection fraction 67% ± 11%). Late gadolinium enhancement and/or ischaemia was found in 54% (80/148). This comprised myocarditis-like scar in 26% (39/148), infarction and/or ischaemia in 22% (32/148) and dual pathology in 6% (9/148). Myocarditis-like injury was limited to three or less myocardial segments in 88% (35/40) of cases with no associated LV dysfunction; of these, 30% had active myocarditis. Myocardial infarction was found in 19% (28/148) and inducible ischaemia in 26% (20/76) of those undergoing stress perfusion (including 7 with both infarction and ischaemia). Of patients with ischaemic injury pattern, 66% (27/41) had no past history of coronary disease. There was no evidence of diffuse fibrosis or oedema in the remote myocardium (T1: COVID-19 patients 1033 ± 41 ms vs. matched controls 1028 ± 35 ms; T2: COVID-19 46 ± 3 ms vs. matched controls 47 ± 3 ms). Conclusions During convalescence after severe COVID-19 infection with troponin elevation, myocarditis-like injury can be encountered, with limited extent and minimal functional consequence. In a proportion of patients, there is evidence of possible ongoing localized inflammation. A quarter of patients had ischaemic heart disease, of which two-thirds had no previous history. Whether these observed findings represent pre-existing clinically silent disease or de novo COVID-19-related changes remain undetermined. Diffuse oedema or fibrosis was not detected.

I n North America most clinical MRI is performed at 1.5 T or 3.0 T, and some research applications have moved to 7.0 T. High field is motivated by higher polarization, promising increased signal-to-noise ratio (SNR), and resolution. However, this causes image distortion, constrained imaging efficiency, increased specific absorption rate, and higher cost. For some applications, low field strength may offer intrinsic advantages (1,2). At low field strength, short T1 and long T2* allow more efficient pulse sequence design; imaging near air-tissue interfaces is improved by virtue of reduced susceptibility gradients; and specific absorption rate is reduced, which can diminish heating of conductive devices and implants, and can eliminate pulse sequence parameter constraints (3). Commercial lower field systems have been largely overlooked as hardware and software have improved over the last 2 decades, and therefore are not well-suited for technically demanding imaging. We developed and evaluated a custom 0.55-T MRI system equipped with contemporary

BackgroundQuantification of myocardial blood flow requires knowledge of the amount of contrast agent in the myocardial tissue and the arterial input function (AIF) driving the delivery of this contrast agent. Accurate quantification is challenged by the lack of linearity between the measured signal and contrast agent concentration. This work characterizes sources of non-linearity and presents a systematic approach to accurate measurements of contrast agent concentration in both blood and myocardium.MethodsA dual sequence approach with separate pulse sequences for AIF and myocardial tissue allowed separate optimization of parameters for blood and myocardium. A systems approach to the overall design was taken to achieve linearity between signal and contrast agent concentration. Conversion of signal intensity values to contrast agent concentration was achieved through a combination of surface coil sensitivity correction, Bloch simulation based look-up table correction, and in the case of the AIF measurement, correction of T2* losses. Validation of signal correction was performed in phantoms, and values for peak AIF concentration and myocardial flow are provided for 29 normal subjects for rest and adenosine stress.ResultsFor phantoms, the measured fits were within 5% for both AIF and myocardium. In healthy volunteers the peak [Gd] was 3.5 ± 1.2 for stress and 4.4 ± 1.2 mmol/L for rest. The T2* in the left ventricle blood pool at peak AIF was approximately 10 ms. The peak-to-valley ratio was 5.6 for the raw signal intensities without correction, and was 8.3 for the look-up-table (LUT) corrected AIF which represents approximately 48% correction. Without T2* correction the myocardial blood flow estimates are overestimated by approximately 10%. The signal-to-noise ratio of the myocardial signal at peak enhancement (1.5 T) was 17.7 ± 6.6 at stress and the peak [Gd] was 0.49 ± 0.15 mmol/L. The estimated perfusion flow was 3.9 ± 0.38 and 1.03 ± 0.19 ml/min/g using the BTEX model and 3.4 ± 0.39 and 0.95 ± 0.16 using a Fermi model, for stress and rest, respectively.ConclusionsA dual sequence for myocardial perfusion cardiovascular magnetic resonance and AIF measurement has been optimized for quantification of myocardial blood flow. A validation in phantoms was performed to confirm that the signal conversion to gadolinium concentration was linear. The proposed sequence was integrated with a fully automatic in-line solution for pixel-wise mapping of myocardial blood flow and evaluated in adenosine stress and rest studies on N = 29 normal healthy subjects. Reliable perfusion mapping was demonstrated and produced estimates with low variability.Electronic supplementary materialThe online version of this article (doi:10.1186/s12968-017-0355-5) contains supplementary material, which is available to authorized users.

BackgroundDisturbances in the myocardial extracellular volume fraction (ECV), such as diffuse or focal myocardial fibrosis or edema, are hallmarks of heart disease. Diffuse ECV changes are difficult to assess or quantify with cardiovascular magnetic resonance (CMR) using conventional late gadolinium enhancement (LGE), or pre- or post-contrast T1-mapping alone. ECV measurement circumvents factors that confound T1-weighted images or T1-maps, and has been shown to correlate well with diffuse myocardial fibrosis. The goal of this study was to develop and evaluate an automated method for producing a pixel-wise map of ECV that would be adequately robust for clinical work flow.MethodsECV maps were automatically generated from T1-maps acquired pre- and post-contrast calibrated by blood hematocrit. The algorithm incorporates correction of respiratory motion that occurs due to insufficient breath-holding and due to misregistration between breath-holds, as well as automated identification of the blood pool. Images were visually scored on a 5-point scale from non-diagnostic (1) to excellent (5).ResultsThe quality score of ECV maps was 4.23 ± 0.83 (m ± SD), scored for n = 600 maps from 338 patients with 83% either excellent or good. Co-registration of the pre-and post-contrast images improved the image quality for ECV maps in 81% of the cases. ECV of normal myocardium was 25.4 ± 2.5% (m ± SD) using motion correction and co-registration values and was 31.5 ± 8.7% without motion correction and co-registration.ConclusionsFully automated motion correction and co-registration of breath-holds significantly improve the quality of ECV maps, thus making the generation of ECV-maps feasible for clinical work flow.