Use of β-blockade and nitroglycerin administration before CT improve diagnostic performance of FFRCT. Diagnostic accuracy of FFRCT is significantly reduced in the setting of misalignment artifacts.

Background There is concern regarding the administration of iodinated contrast to patients with impaired renal function because of the increased risk of contrast-induced nephropathy. Objective Evaluate image quality and feasibility of a protocol with a reduced volume of iodinated contrast and utilization of dual-energy coronary CT angiography (DECT) vs a standard iodinated contrast volume coronary CT angiography protocol (SCCTA). Methods A total of 102 consecutive patients were randomized to SCCTA (n = 53) or DECT with rapid kVp switching (n = 49). Eighty milliliters and 35 mL of iodinated contrast were administered in the SCCTA and DECT cohorts, respectively. Two readers measured signal and noise in the coronary arteries; signal-to-noise ratio (SNR) and contrast-to-noise ratio (CNR) were calculated. A 5-point signal/noise Likert scale was used to evaluate image quality; scores of <3 were nondiagnostic. Agreement was assessed through kappa analyses. Results Demographics and radiation dose were not significantly different; there was no difference in CNR between both cohorts (P = .95). A significant difference in SNR between the groups (P = .02) lost significance (P = .13) when adjusted for body mass index. The median Likert score was inferior for DECT for reader 1 (3.6 ± 0.6 vs 4.3 ± 0.6; P < .001) but not reader 2 (4.1 ± 0.6 vs 4.3 ± 0.5; P = .06). Agreement in diagnostic interpretability in the DECT and SCCTA groups was 91% (95% confidence interval, 86%–100%) and 96% (95% confidence interval, 90%–100%), respectively. Conclusion DECT resulted in inferior image quality scores but demonstrated comparable SNR, CNR, and rate of diagnostic interpretability without a radiation dose penalty while allowing for >50% reduction in contrast volume compared with SCCTA.

Summary Dendritic cells (DC) have a key role in controlling the immune response, by determining the outcome of antigen presentation to T cells. Through costimulatory molecules and other factors, DC are involved in the maintenance of peripheral tolerance through modulation of the immune response. This modulation occurs both constitutively, and in inflammation, in order to prevent autoimmunity and to control established immune responses. Dendritic cell control of immune responses may be mediated through cytokine or cell-contact dependent mechanisms. The molecular and cellular basis of these controls is being understood at an increasingly more complex level. This understanding is reaching a level at which DC-based therapies for the induction of immune regulation in autoimmunity can be tested in vivo . This review outlines the current state of knowledge of DC in immune tolerance, and proposes how DC might control both T cell responses, and themselves, to prevent autoimmunity and maintain peripheral tolerance.