Institutional transition from invasive to non-invasive imaging in children with univentricular heart defects: safety and cost savings.

OBJECTIVES: Patients with univentricular heart defects require lifelong imaging surveillance. Recent advances in non-invasive imaging have enabled replacing these patients' routine catheterisation. Our objective was to describe the safety and cost savings of transition of a tertiary care children's hospital from routine invasive to routine non-invasive imaging of low-risk patients with univentricular heart defects. METHODS: This single-centre cohort study consists of 1) a retrospective analysis of the transition from cardiac catheterisation (n = 21) to CT angiography (n = 20) before bidirectional Glenn operation and 2) a prospective study (n = 89) describing cardiac magnetic resonance before and after the total cavopulmonary connection in low-risk patients with univentricular heart defects. RESULTS: Pre-Glenn: The total length of CT angiography was markedly shorter compared to the catheterisation: 30 min (range: 20-60) and 125 min (range: 70-220), respectively (p < 0.001). Catheterisation used more iodine contrast agents than CT angiography, 19 ± 3.9 ml, and 10 ± 2.4 ml, respectively (p < 0.001). Controlled ventilation was used for all catheterised and 3 (15%) CT angiography patients (p < 0.001). No complications occurred during CT angiography, while they emerged in 19% (4/21) catheterisation cases (p < 0.001). CT angiography and catheterisation showed no significant difference in the radiation exposure. Pre-/post-total cavopulmonary connection: All cardiac magnetic resonance studies were successful, and no complications occurred. In 60% of the cardiac magnetic resonance (53/89), no sedation was performed, and peripheral venous pressure was measured in all cases. Cost analysis suggests that moving to non-invasive imaging yielded cost savings of at least €2500-4000 per patient. CONCLUSION: Transition from routine invasive to routine non-invasive pre-and post-operative imaging is safely achievable with cost savings.

Clinical experience of magnetic resonance imaging in patients with cardiac pacing devices: unrestricted patient population.

Background: Magnetic resonance imaging (MRI) in patients with cardiac pacing devices has become available despite previously being considered absolutely contraindicated. However, most institutional safety protocols have included several limitations on patient selection, leaving MRI unavailable for many patients. Purpose: To evaluate the first 1000 MRI examinations conducted on patients with cardiac pacing devices at Helsinki University Hospital for any potential safety hazards and also to evaluate the long-term functionality of the safety protocol in "real-life" clinical practice. Material and Methods: A total of 1000 clinically indicated MRI scans were performed with a 1.5-T MRI scanner according to the safety protocol. The following information was collected from the electronic medical record (EMR): patients' date of birth; sex; pacing device generator model; date of MRI scan; date of the latest pacing device generator implantation; and the body region scanned. The EMR of these patients was checked and especially searched for any pacing device related safety hazards or adverse outcomes during or after the MRI scan. Results: Only one potentially dangerous adverse event was noted in our study group. In addition, patients with abandoned leads, temporary pacing devices, and newly implanted pacing device generators were scanned successfully and safely. Conclusion: MRI scans can be performed safely in patients with cardiac pacing devices if the dedicated safety protocol is followed.

[The effect of public defense of a doctoral thesis on the heart rate of the doctoral candidate]. / Väitöstilaisuuden vaikutus väittelijän sydämen syketaajuuteen.

The effect of public defense of a doctoral thesis on the heart rate of the doctoral candidate Most doctoral candidates find the public defense of a doctoral thesis an exciting and stressful experience. In this study, Holter recording during the defense was made for four doctoral candidates of the Faculty of Medicine. Maximum heart rate among the subjects was on the average 172 beats/min with a median heart rate of 116 beats/min. Sympathicotonia and release of stress hormones associated with the defense raise the heart rate to levels that may be very high for several hours. This is a risk factor for a coronary event and should be considered, if the doctoral candidate has coronary heart disease, carries risk factors for coronary heart disease, or is an elderly person.

Vascular adhesion protein-1 is involved in both acute and chronic inflammation in the mouse.

Vascular adhesion protein-1 (VAP-1) is an endothelial molecule that possesses both adhesive and enzymatic properties in vitro. So far, however, elucidation of its in vivo function has suffered from the lack of function-blocking reagents that are suitable for use in animal models. In this work we produced monoclonal antibodies against murine VAP-1 and characterized them using in vitro binding assays. We then examined whether the antibodies could prevent leukocyte migration in in vivo inflammation models, including two acute models (peritonitis induced with proteose peptone and interleukin-1 and air pouch inflammation enhanced by CCL21) and one chronic model (autoimmune diabetes in nonobese diabetic mice). Antibodies 7-88 and 7-106 inhibited migration of granulocytes and monocytes in both acute models of inflammation. Strikingly, antibody 7-88 significantly prevented diabetes in a subset of nonobese diabetic mice. The results show for the first time that in mouse models of inflammation, VAP-1 mediates leukocyte trafficking to sites of inflammation and thus is a potential target for anti-inflammatory therapies.

Diabetogenic T cells are primed both in pancreatic and gut-associated lymph nodes in NOD mice.

Activation of an islet-specific immune response is an early yet essential step in autoimmune diabetes. The immune cells and antigen(s) involved in this early step and its anatomical site remain incompletely understood. To directly evaluate the site where islet-specific and diabetogenic lymphocytes are activated, we isolated lymphocytes from spleen and from pancreas-draining, gut-associated and subcutaneous lymph nodes of diabetic NOD mice and of young NOD mice, and transferred these into NOD scid/scid recipients devoid of endogenous islet-specific immune responses themselves. Although spleen lymphocytes from diabetic NOD mice induced diabetes more rapidly than lymphocytes from any other lymphoid tissue, spleen lymphocytes from young NOD donors were not superior to other lymphocytes from the same donors. At a donor-age of 6 weeks, the most-diabetogenic lymphocytes were found in pancreas-draining lymph node whereas gut-associated lymph nodes and the spleen were sources of intermediate diabetogenic activity. Lymphocytes from peripheral lymph nodes were only weakly diabetogenic at this age, and also remained the least efficient later. Surprisingly, lymphocytes isolated even from 3-week-old NOD mice had diabetogenic potential. However, such cells were almost exclusively found in gut-associated lymph nodes. This suggests that initial priming of diabetogenic cells takes place in the gut whereas pancreas-draining lymph nodes may serve as the site of amplification of the autoimmune response.

Ly6C induces clustering of LFA-1 (CD11a/CD18) and is involved in subtype-specific adhesion of CD8 T cells.

Ly6C is a hemopoietic cell differentiation Ag found on a subset of CD8 T cells in the periphery. It is involved in target cell killing by CTLs, augments TCR-mediated activation of IL-2 and IFN-gamma production in CD8 T cells, and regulates CD8 T cell homing in vivo. In this study, we show that cross-linking of Ly6C causes clustering of LFA-1 (CD11a/CD18) on the surface of CD8 T cells via a mechanism dependent on reorganization of actin cytoskeleton and intracellular protease, calpain, but not the phosphatidylinositol 3-kinase pathway. In the capillary flow-adhesion assay, Ly6C cross-linking significantly augments lymphocyte adhesion to endothelium, and this is inhibited by an Ab that blocks LFA-1 function. Furthermore, upon in vitro cross-linking and during in vivo homing into lymph nodes, Ly6C is transiently lost from cell surface but becomes re-expressed on lymph node-resident CD8 T cells. The abilities of Ly6C to induce LFA-1 clustering and to be re-expressed after signaling-associated down-regulation may be important in regulating the homing of CD8 T cells into lymph nodes and in subsequent steps of CD8 T cell activation and effector function that again involve LFA-1.