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In experimental myocardial infarction (MI), a rise in cell counts of circulating monocyte subsets contributes to impaired myocardial healing and to atherosclerotic plaque destabilization. In humans, the prognostic role of monocyte subsets in patients suffering ST-elevation MI (STEMI) is still unclear. In the present study, we aimed to determine the kinetics of the 3 monocyte subsets (classical CD14++CD16-, intermediate CD14++CD16+, and nonclassical CD14+CD16++ monocytes), as well as the subset-specific monocyte-platelet aggregates (MPA), in acute STEMI followed by primary percutaneous coronary intervention (PCI), and their relationships with cardiovascular outcomes during a 2-year follow-up.Monocyte subsets and MPA were measured in 100 STEMI patients receiving primary PCI on days 1, 2, 3, 5, and 7 of symptom onset, which were compared with 60 stable coronary heart disease patients and 35 healthy volunteers. From day 1 to day 7, significant increases in the counts of CD14++CD16+ monocytes and CD14++CD16+ MPA were observed, with peak levels on day 2. During a median follow-up of 2.0 years, 28 first cardiovascular events (defined as cardiovascular death, nonfatal ischemic stroke, recurrent MI, need for emergency or repeat revascularization, and rehospitalization for heart failure) were recorded. After adjustment for confounders, CD14++CD16+ monocytosis (day 1 [HR: 3.428; 95% CI: 1.597-7.358; P = 0.002], day 2 [HR: 4.835; 95% CI: 1.106-21.13; P = 0.04], day 3 [HR: 2.734; 95% CI: 1.138-6.564; P = 0.02], and day 7 [HR: 2.647; 95% CI: 1.196-5.861; P = 0.02]), as well as increased levels of CD14++CD16+ MPA measured on all time points (days 1, 2, 3, 5, and 7), had predictive values for adverse cardiovascular events.In conclusion, our data show the expansion of the CD14++CD16+ monocyte subset during acute phase of STEMI has predictive values for 2-year adverse cardiovascular outcomes in patients treated with primary PCI. Future studies will be warranted to elucidate whether CD14++CD16+ monocytes may become a target cell population for new therapeutic strategies after STEMI.

While single‐shot late gadolinium enhancement (LGE) is useful for imaging patients with arrhythmia and/or dyspnea, it produces low spatial resolution. One approach to improve spatial resolution is to accelerate data acquisition using compressed sensing (CS). Our previous work described a single‐shot, multi‐inversion time (TI) LGE pulse sequence using radial k‐space sampling and CS, but over‐regularization resulted in significant image blurring that muted the benefits of data acceleration. The purpose of the present study was to improve the spatial resolution of the single‐shot, multi‐TI LGE pulse sequence by incorporating view sharing (VS) and k‐space weighted contrast (KWIC) filtering into a GRASP‐Pro reconstruction. In 24 patients (mean age = 61 ± 16 years; 9/15 females/males), we compared the performance of our improved multi‐TI LGE and standard multi‐TI LGE, where clinical standard LGE was used as a reference. Two clinical raters independently graded multi‐TI images and clinical LGE images visually on a five‐point Likert scale (1, nondiagnostic; 3, clinically acceptable; 5, best) for three categories: the conspicuity of myocardium or scar, artifact, and noise. The summed visual score (SVS) was defined as the sum of the three scores. Myocardial scar volume was quantified using the full‐width at half‐maximum method. The SVS was not significantly different between clinical breath‐holding LGE (median 13.5, IQR 1.3) and multi‐TI LGE (median 12.5, IQR 1.6) (P = 0.068). The myocardial scar volumes measured from clinical standard LGE and multi‐TI LGE were strongly correlated (coefficient of determination, R2 = 0.99) and in good agreement (mean difference = 0.11%, lower limit of the agreement = −2.13%, upper limit of the agreement = 2.34%). The inter‐rater agreement in myocardial scar volume quantification was strong (intraclass correlation coefficient = 0.79). The incorporation of VS and KWIC into GRASP‐Pro improved spatial resolution. Our improved 25‐fold accelerated, single‐shot LGE sequence produces clinically acceptable image quality, multi‐TI reconstruction, and accurate myocardial scar volume quantification. [ABSTRACT FROM AUTHOR]

Purpose: To develop and evaluate a flexible, Bloch‐equation based framework for retrospective T2∗ correction to the arterial input function (AIF) obtained with quantitative cardiac perfusion pulse sequences. Methods: Our framework initially calculates the gadolinium concentration [Gd] based on T1 measurements alone. Next, T2∗ is estimated from this initial calculation of [Gd] while assuming fast water exchange and using the literature native T2 and static magnetic field variation (ΔB0) values. Finally, the [Gd] is recalculated after performing T2∗ correction to the Bloch equation signal model. Using this approach, we performed T2∗ correction to historical phantom and in vivo, dual‐imaging perfusion data sets from 3 different patient groups obtained using different pulse sequences and imaging parameters. Images were processed to quantify both the AIF and resting myocardial blood flow (MBF). We also performed a sensitivity analysis of our T2∗ correction to ±20% variations in native T2 and ΔB0. Results: Compared with the ground truth [Gd] of phantom, the normalized root‐means‐square‐error (NRMSE) in measured [Gd] was 5.1%, 1.3%, and 0.6% for uncorrected, our corrected, and Kellman's corrected, respectively. For in vivo data, both the peak AIF (7.0 ± 3.0 mM vs. 8.6 ± 7.1 mM, 7.2 ± 0.9 mM vs. 8.6 ± 1.7 mM, 7.7 ± 1.8 mM vs. 10.3 ± 5.1 mM, P <.001) and resting MBF (1.3 ± 0.1 mL/g/min vs. 1.1 ± 0.1 mL/g/min, 1.3 ± 0.1 mL/g/min vs. 1.1 ± 0.1 mL/g/min, 1.2 ± 0.1 mL/g/min vs. 0.9 ± 0.1 mL/g/min, P <.001) values were significantly different between uncorrected and corrected for all 3 patient groups. Both the peak AIF and resting MBF values varied by <5% over the said variations in native T2 and ΔB0. Conclusion: Our theoretical framework enables retrospective T2∗ correction to the AIF obtained with dual‐imaging, cardiac perfusion pulse sequences. [ABSTRACT FROM AUTHOR]

Purpose Myocardial perfusion can be quantified using the 'dual bolus' technique, which uses two separate contrast boluses to avoid signal nonlinearity in the blood pool. This technique relies on knowing the precise ratio of contrast concentrations between the two boluses. In this study, we investigated the variability found in these ratios, as well as the error it introduces, and developed a method for correction. Methods Five dogs received dual bolus myocardial perfusion MRI scans. Perfusion was calculated separately using assumed contrast dilution ratios and empirically determined contrast ratios. Perfusion was compared with reference standard fluorescent microspheres. The same technique was then applied to a cohort of six patients with no significant coronary artery stenosis by cardiac catheterization. Results Assumed contrast dilution ratios were 10:1 for all animal and patient scans. Empirically derived contrast ratios were significantly different for animal (8.51:1 ± 1.53:1, P < 0.001) and patient scans (7.32:1 ± 2.27:1, P < 0.01). Incorporating empirically derived ratios for animal scans improved correlation with microspheres from 0.84 to 0.90 ( P < 0.05). Conclusion Variability in dual bolus contrast concentration ratios is an important source of experimental error, especially outside of a carefully controlled laboratory setting. Empirically deriving the correct ratio is feasible and improves the accuracy of quantitative perfusion measurements. Magn Reson Med 77:2347-2355, 2017. © 2016 International Society for Magnetic Resonance in Medicine [ABSTRACT FROM AUTHOR]

Aims To apply 4D flow cardiac magnetic resonance (CMR) for the volumetric measurement of 3D left atrial (LA) blood flow to evaluate its potential to detect altered LA flow in patients with atrial fibrillation (AF) and to investigate associations of changes in systolic and diastolic LA flow with the current clinical risk score (CHA2DS2-VASc) used for the assessment of thromboembolic risk in AF. Methods and results 4D flow CMR was performed in 40 patients with a history of AF (in sinus rhythm during CMR scan, age = 61±11 years), 20 age-appropriate controls (59±7 years), and 10 young healthy volunteers (24±2 years) to measure in vivo time-resolved 3D LA blood flow. LA velocities were characterized with respect to atrial function and timing by calculating normalized LA flow velocity histograms during ventricular systole, early diastole, mid-late diastole, and the entire cardiac cycle. Mean, median, and peak LA velocity steadily decreased when comparing young volunteers, age-appropriate controls, and AF patients by 10-44% and 8-26% for early diastole and the entire cardiac cycle, respectively (P < 0.01 for all comparisons except median velocity for young vs. older volunteers and peak velocity for older volunteers and AF patients). There were moderate but significant inverse relationships between increased CHA2DS2-VASc score and reduced mean LA velocity (early diastole: r = -0.37, P < 0.001; entire RR-interval: r = -0.33, P = 0.005), median LA velocity (r = -0.33, P = 0.003; r = -0.25, P = 0.017), and peak velocity (r = -0.36, P = 0.001; r = -0.45, P < 0.001). LA flow indices also correlated significantly with age and LA volume (R² = 0.44-0.62, P < 0.001), but not with left ventricular ejection fraction. Conclusion Left atrial 4D flow CMR demonstrated significantly reduced LA blood flow velocities in patients with AF. Further study is needed to determine whether these measures can improve upon the CHA2DS2-VASc score for stroke risk prediction and enhance individual decisions on anticoagulation in patients with AF. [ABSTRACT FROM AUTHOR]

An abstract of the article "Assessment of diffuse myocardial fibrosis in systemic sclerosis by cardiac magnetic resonance imaging," by Daniel C. Lee, Roberto Sarnari, Brandon Benefield, Alejandro Aquino, James Carr, John Varga, Monique Hinchcliff, Edwin Wu and Sanjiv Shah is presented.