Diagnostic performance of prospectively ECG triggered versus retrospectively ECG gated 64-slice computed tomography coronary angiography in a heterogeneous patient population

Objective

To compare diagnostic performance and applicability of prospectively versus retrospectively gated 64-slice computed tomography coronary angiography (pro-CTCA vs. retro-CTCA) in a heterogeneous patient population compared to invasive coronary angiography.

Methods

77 patients referred to an ECG-gated-CT of the chest were retrospectively included. Pro-CTCA was applied, whenever possible, alternatively retro-CTCA was performed. All coronary artery segments ≥1.5 mm were analysed and image quality was assessed.

Results

In 39 patients retro-CTCA and in 38 patients pro-CTCA was applied, mean heart rate (HR) was 69.5 ± 9.1 min⁻¹ and 62.8 ± 5.9, respectively. For a stenosis ≥50% segment-based (patient-based) analysis revealed a sensitivity, specificity, positive (PPV) and negative predictive value (NPV) of 97%, 98%, 71%, 100% (91%, 82%, 67%, 96%) using retro-CTCA and 94%, 97%, 75%, 99% (93%, 96%, 93%, 96%) using pro-CTCA. Sensitivity and NPV increased in the pro-CTCA group in patients with a HR < 65. Vessel-based analysis showed lower diagnostic performance for the right coronary artery (RCA) using pro-CTCA, which increased when HR < 65. Image quality did not differ significantly in both groups.

Conclusions

Prospectively triggered CTCA in a heterogeneous patient group has a very high diagnostic accuracy and image quality, when used in HR ≤ 65. A low HR is of special importance for the evaluation of the RCA.     

To see or not to see – Ambiguous findings on post-mortem cross-sectional imaging in a case of ruptured abdominal aortic aneurysm

We present a case of a ruptured abdominal aortic aneurysm (AAA) with ambiguous accessory findings on post-mortem computed-tomography (PMCT), post-mortem magnetic resonance (PMMR) imaging, and PMCT-angiography (PMCTA) suggestive of thoracic aortic dissection. The diagnosis of ruptured AAA was confirmed by autopsy; however, there was no aortic dissection. The imaging findings that mimicked the presence of aortic dissection might have been an atypical presentation of post-mortem clotting or sedimentation. This case is an ideal example to illustrate benefits, limitations, and challenges of post-mortem cross-sectional imaging. It serves as a reminder that both, training as well as correlation of imaging findings with autopsy are fundamental to improve our understanding of radiologic findings on post-mortem cross-sectional imaging.     

Altered serotonin transporter availability in patients with multiple sclerosis

Purpose

Modulation of the immune system by the CNS may involve serotonergic regulation via the brain serotonin transporters (SERT). This regulation may be disturbed in patients with CNS disorders including multiple sclerosis (MS). Central serotonergic mechanisms have not been investigated in MS by in vivo imaging. The objective of the study was to assess the availability of SERT in antidepressant-naive patients with MS by means of PET.

Methods

Included in this study were 23 patients with MS and 22 matched healthy volunteers who were investigated with PET and the SERT-selective marker [¹¹C]DASB, and distribution volume ratios were determined. Clinical assessment of the patients included the expanded disability status scale, the MS fatigue scale Würzburger Erschöpfungsinventar bei MS (WEIMuS) and the Beck Depression Inventory (BDI). The PET data were analysed with both volume-of-interest and voxel-based analyses to determine regional SERT availability.

Results

Patients had lower SERT availability in the cingulate cortex, the thalamus and the insula, and increased availability in the orbitofrontal cortex. Patients with relapsing/remitting MS tended to have lower SERT in the hippocampus, whereas patients with primary progressive disease showed increased SERT availability in prefrontal regions. There was a positive correlation between SERT availability in the insula and both depression and fatigue scores (r?=?0.56 vs. BDI, p?=?0.02; r?=?0.49 vs. WEIMuS, p?=?0.05).

Conclusion

Serotonergic neurotransmission in MS patients is altered in limbic and paralimbic regions as well as in the frontal cortex that this appears to contribute to psychiatric symptoms of MS.     

CD11c‐positive cells from brain,spleen, lung,and liver exhibit site‐specific immune phenotypes and plastically adapt to new environments

The brain's immune privilege has been also attributed to the lack of dendritic cells (DC) within its parenchyma and the adjacent meninges, an assumption, which implies maintenance of antigens rather than their presentation in lymphoid organs. Using mice transcribing the green fluorescent protein under the promoter of the DC marker CD11c (itgax), we identified a juxtavascular population of cells expressing this DC marker and demonstrated their origin from bone marrow and local microglia. We now phenotypically compared this population with CD11c/CD45 double‐positive cells from lung, liver, and spleen in healthy mice using seven‐color flow cytometry. We identified unique, site‐specific expression patterns of F4/80, CD80, CD86, CX3CR1, CCR2, FLT3, CD103, and MHC‐II. Furthermore, we observed the two known CD45‐positive populations (CD45^high and CD45^int) in the brain, whereas liver, lung, and spleen exhibited a homogeneous CD45^high population. CD11c‐positive microglia lacked MHC‐II expression and CD45^high/CD11c‐positive cells from the brain have a lower percentage of MHC‐II‐positive cells. To test whether phenotypical differences are fixed by origin or specifically develop due to environmental factors, we transplanted brain and spleen mononuclear cells on organotypic slice cultures from brain (OHSC) and spleen (OSSC). We demonstrate that adaption and ramification of MHC‐II‐positive splenocytes is paralleled by down‐regulation of MHC‐II, whereas brain‐derived mononuclear cells neither ramified nor up‐regulated MHC‐II in OSSCs. Thus, brain‐derived mononuclear cells maintain their MHC‐II‐negative phenotype within the environment of an immune organ. Intraparenchymal CD11c‐positive cells share immunophenotypical characteristics of DCs from other organs but remain unique for their low MHC‐II expression. GLIA 2015;63:611–625     

Long-term outcome of endoscopic therapy in patients with bile duct injury after cholecystectomy

Background and Aim:  Bile duct lesions, including leaks and strictures, are immanent complications of open or laparoscopic cholecystectomy. Endoscopic procedures have gained increasing potential as the treatment of choice in the management of postoperative bile duct injuries.
Methods:  Between January 1996 and December 2006, 44 patients with biliary leakages and 12 patients with biliary strictures after cholecystectomy were identified by analyzing the endoscopic retrograde cholangiopancreatography database, clinical records, and cholangiograms. The long-term follow up of endoscopic treatment in biliary lesions after cholecystectomy was evaluated by this retrospective study.
Results:  In 34 of 35 patients (97%) with peripheral bile duct leakages, endoscopic therapy was successful. Transpapillary endoprothesis and/or nasobiliary drainage were removed after 31 (5–399) days. After stent removal, the median follow-up period was 81 (11–137) months. In patients with central bile duct leakages, the success rate after median 90 (4–145) days of endoscopic therapy was 66.7% (6/9 patients). The median follow up after stent removal in six successfully treated patients was 70 (48–92) months. Eleven of 12 patients (91.6%) with bile duct strictures had successfully completed stent therapy. The follow-up period of this patient group was 99 (53–140) months.
Conclusions:  Endoscopic treatment of bile duct lesions after cholecystectomy is effective, particularly in patients with peripheral bile duct leakages and bile duct strictures. Therefore, it should be the first-line therapy used in these patients. Although endoscopic management is less successful in patients with central bile duct leakages, an attempt is warranted.     

Visceral artery aneurysms—follow-up of 23 patients with 31 aneurysms after surgical or interventional therapy

Purpose  

Visceral artery aneurysms (VAA) are rare forms of vascular pathology, with an incidence of 0.1% to 0.2% in routine autopsies [1–4]. They frequently present as a life-threatening, often fatal, emergency, if associated with rupture and intra- or retroperitoneal bleeding. The clinical symptoms, natural history, and mortality of VAAs vary depending on the vessels involved. The mortality rates range from 8.5% up to 25% and, in pregnant women, up to 75% [1, 4, 6, 7]. A retrospective analysis of all VAAs diagnosed at our institution from 1991 to 2006 was performed. The presentation, management, and outcome of therapy was evaluated for each patient.     

GDF15 promotes simultaneous astrocyte remodeling and tight junction strengthening at the blood–brain barrier

Perivascular astrocyte processes (PAP) surround cerebral endothelial cells (ECs) and modulate the strengthening of tight junctions to influence blood–brain barrier (BBB) permeability. Morphologically altered astrocytes may affect barrier properties and trigger the onset of brain pathologies. However, astrocyte-dependent mediators of these events remain poorly studied. Here, we show a pharmacologically driven elevated expression and release of growth/differentiation factor 15 (GDF15) in rat primary astrocytes and cerebral PAP. GDF15 has been shown to possess trophic properties for motor neurons, prompting us to hypothesize similar effects on astrocytes. Indeed, its increased expression and release occurred simultaneously to morphological changes of astrocytes in vitro and PAP, suggesting modulatory effects of GDF15 on these cells, but also neighboring EC. Administration of recombinant GDF15 was sufficient to promote astrocyte remodeling and enhance barrier properties between ECs in vitro, whereas its pharmacogenetic abrogation prevented these effects. We validated our findings in male high anxiety-related behavior rats, an animal model of depressive-like behavior, with shrunk PAP associated with reduced expression of the junctional protein claudin-5, which were both restored by a pharmacologically induced increase in GDF15 expression. Thus, we identified GDF15 as an astrocyte-derived trigger of astrocyte process remodeling linked to enhanced tight junction strengthening at the BBB.