43 research outputs found

    Erratum to: Assessment of myocardial injury after reperfused infarction by T1ρ cardiovascular magnetic resonance

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    BackgroundThe evolution of T1ρ and of other endogenous contrast methods (T2, T1) in the first month after reperfused myocardial infarction (MI) is uncertain. We conducted a study of reperfused MI in pigs to serially monitor T1ρ, T2 and T1 relaxation, scar size and transmurality at 1 and 4 weeks post-MI.MethodsTen Yorkshire swine underwent 90 min of occlusion of the circumflex artery and reperfusion. T1ρ, T2 and native T1 maps and late gadolinium enhanced (LGE) cardiovascular magnetic resonance (CMR) data were collected at 1 week (n = 10) and 4 weeks (n = 5). Semi-automatic FWHM (full width half maximum) thresholding was used to assess scar size and transmurality and compared to histology. Relaxation times and contrast-to-noise ratio were compared in healthy and remote myocardium at 1 and 4 weeks. Linear regression and Bland-Altman was performed to compare infarct size and transmurality.ResultsRelaxation time differences between infarcted and remote myocardial tissue were ∆T1 (infarct-remote) = 421.3 ± 108.8 (1 week) and 480.0 ± 33.2 ms (4 week), ∆T1ρ = 68.1 ± 11.6 and 74.3 ± 14.2, and ∆T2 = 51.0 ± 10.1 and 59.2 ± 11.4 ms. Contrast-to-noise ratio was CNRT1 = 7.0 ± 3.5 (1 week) and 6.9 ± 2.4 (4 week), CNRT1ρ = 12.0 ± 6.2 and 12.3 ± 3.2, and CNRT2 = 8.0 ± 3.6 and 10.3 ± 5.8. Infarct size was not significantly different for T1ρ, T1 and T2 compared to LGE (p = 0.14) and significantly decreased from 1 to 4 weeks (p < 0.01). Individual infarct size changes were ∆T1ρ = -3.8%, ∆T1 = -3.5% and ∆LGE = -2.8% from 1 - 4 weeks, but there was no observed change in infarct size for T2 or histologically.ConclusionsT1ρ was highly correlated with alterations left ventricle (LV) pathology at 1 and 4 weeks post-MI and therefore it may be a useful method endogenous contrast imaging of infarction

    User-initialized active contour segmentation and golden-angle real-time cardiovascular magnetic resonance enable accurate assessment of LV function in patients with sinus rhythm and arrhythmias

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    BACKGROUND: Data obtained during arrhythmia is retained in real-time cardiovascular magnetic resonance (rt-CMR), but there is limited and inconsistent evidence to show that rt-CMR can accurately assess beat-to-beat variation in left ventricular (LV) function or during an arrhythmia. METHODS: Multi-slice, short axis cine and real-time golden-angle radial CMR data was collected in 22 clinical patients (18 in sinus rhythm and 4 patients with arrhythmia). A user-initialized active contour segmentation (ACS) software was validated via comparison to manual segmentation on clinically accepted software. For each image in the 2D acquisitions, slice volume was calculated and global LV volumes were estimated via summation across the LV using multiple slices. Real-time imaging data was reconstructed using different image exposure times and frame rates to evaluate the effect of temporal resolution on measured function in each slice via ACS. Finally, global volumetric function of ectopic and non-ectopic beats was measured using ACS in patients with arrhythmias. RESULTS: ACS provides global LV volume measurements that are not significantly different from manual quantification of retrospectively gated cine images in sinus rhythm patients. With an exposure time of 95.2 ms and a frame rate of > 89 frames per second, golden-angle real-time imaging accurately captures hemodynamic function over a range of patient heart rates. In four patients with frequent ectopic contractions, initial quantification of the impact of ectopic beats on hemodynamic function was demonstrated. CONCLUSION: User-initialized active contours and golden-angle real-time radial CMR can be used to determine time-varying LV function in patients. These methods will be very useful for the assessment of LV function in patients with frequent arrhythmias

    Magnetic resonance myocardial T1ρ mapping

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    Abstract The potential of cardiac magnetic resonance to improve cardiovascular care and patient management is considerable. Myocardial T1-rho (T1ρ) mapping, in particular, has emerged as a promising biomarker for quantifying myocardial injuries without exogenous contrast agents. Its potential as a contrast-agent-free (“needle-free”) and cost-effective diagnostic marker promises high impact both in terms of clinical outcomes and patient comfort. However, myocardial T1ρ mapping is still at a nascent stage of development and the evidence supporting its diagnostic performance and clinical effectiveness is scant, though likely to change with technological improvements. The present review aims at providing a primer on the essentials of myocardial T1ρ mapping, and to describe the current range of clinical applications of the technique to detect and quantify myocardial injuries. We also delineate the important limitations and challenges for clinical deployment, including the urgent need for standardization, the evaluation of bias, and the critical importance of clinical testing. We conclude by outlining technical developments to be expected in the future. If needle-free myocardial T1ρ mapping is shown to improve patient diagnosis and prognosis, and can be effectively integrated in cardiovascular practice, it will fulfill its potential as an essential component of a cardiac magnetic resonance examination

    Pulse sequence and magnetization trajectory for single-shot cardiac T<sub>1ρ</sub> MRI in humans.

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    <p><b>A</b>, RF pulse diagram, showing magnetization preparation and spatial encoding periods with HR = 60 bpm. The spatial encoding period includes a flip angle ramp to stabilize the transverse magnetization, during which the magnetization is not spatially encoded. <b>B</b>, extended RF graph depicting 8 single-shot T<sub>1ρ</sub>-weighted images with varying spin lock duration to create a T<sub>1ρ</sub> map. <b>C</b>, longitudinal <i>M</i><sub><i>Z</i></sub> and transverse |<i>M</i><sub><i>x</i></sub> + <i>iM</i><sub><i>y</i></sub>| magnetization for the period in <b>A. D</b>, magnetization for 8 shots at 60 bpm. <b>E</b>, longitudinal <i>M</i><sub><i>Z</i></sub> and transverse |<i>M</i><sub><i>x</i></sub> + <i>iM</i><sub><i>y</i></sub>| magnetization at 80 bpm. and <b>F</b>, 80 bpm. The acquisition of parallel imaging reference data is not shown and occurs in a separate heartbeat. The arrows in <b>C</b> and <b>D</b> indicate that the transverse magnetization is different after the spin lock and after the ramp.</p

    DSC quantification of motion correction for large, moderate and no motion T<sub>1ρ</sub> datasets.

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    <p><b>A</b>, Overall DSC for large motion datasets. <b>B</b>, Overall DSC for moderate motion datasets. <b>C</b>, Overall DSC for moderate motion datasets. For the large motion category, the DSC values are significantly improved after correction. In the case of moderate motion datasets, DSC values improved slightly after the registration. In the datasets without heart motion, the DSC values were similar before and after registration.</p

    Pulse sequence and magnetization trajectory for single-shot cardiac T<sub>1ρ</sub> MRI in humans.

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    <p><b>A</b>, RF pulse diagram, showing magnetization preparation and spatial encoding periods with HR = 60 bpm. The spatial encoding period includes a flip angle ramp to stabilize the transverse magnetization, during which the magnetization is not spatially encoded. <b>B</b>, extended RF graph depicting 8 single-shot T<sub>1ρ</sub>-weighted images with varying spin lock duration to create a T<sub>1ρ</sub> map. <b>C</b>, longitudinal <i>M</i><sub><i>Z</i></sub> and transverse |<i>M</i><sub><i>x</i></sub> + <i>iM</i><sub><i>y</i></sub>| magnetization for the period in <b>A. D</b>, magnetization for 8 shots at 60 bpm. <b>E</b>, longitudinal <i>M</i><sub><i>Z</i></sub> and transverse |<i>M</i><sub><i>x</i></sub> + <i>iM</i><sub><i>y</i></sub>| magnetization at 80 bpm. and <b>F</b>, 80 bpm. The acquisition of parallel imaging reference data is not shown and occurs in a separate heartbeat. The arrows in <b>C</b> and <b>D</b> indicate that the transverse magnetization is different after the spin lock and after the ramp.</p

    T<sub>1ρ</sub> pulse sequence designed for use in humans using breath-hold and electrocardiogram (ECG)-triggering.

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    <p>The pulse sequence is synchronized to the R-wave using a MRI- compatible vector ECG. The spin lock pulse cluster shown here is a spin lock, spin echo (90<sub>x</sub>-SL<sub>y</sub>-180<sub>+y</sub>-SL<sub>-y</sub>-90<sub>-x</sub>), consisting of a pair of continuous RF spin locking pulses with opposite phase ±y to refocus magnetization in a heterogeneous B<sub>1</sub> magnetic field and a refocusing pulse to refocus B<sub>0</sub>. TSL is total spin lock time. After the T<sub>1ρ</sub> pulse cluster, a crusher gradient is delivered to eliminate remaining transverse signal and then a second magnetization preparation period employing a bSSFP flip angle ramp to stabilize the transverse magnetization prior to spatial encoding. The readout sequence employed is a single-shot bSSFP.</p

    T<sub>1ρ</sub> relaxation times in normal myocardial tissue and dependence on pulse sequence parameters.

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    <p><b>A</b>, heart rate variability causes the first shot (black arrow) to be inconsistent with our signal intensity measurements and overestimation of T<sub>1ρ</sub> relaxation times. <b>B</b>, Reproducibility and bias with and without an initial ‘dummy’ shot (D+ or D-) and for centric and linear encoding (C,L). <b>C</b>, Reproducibility and bias of 3 models for T<sub>1ρ</sub> relaxation.</p
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