Delayed endovascular treatment of descending aorta stent graft collapse in a patient treated for post- traumatic aortic rupture: a case report

Background: We report a case of delayed endovascular correction of graft collapse occurred after emergent Thoracic Endovascular Aortic Repair (TEVAR) for traumatic aortic isthmus rupture.Case presentation: In 7 th post-operative day after emergent TEVAR for traumatic aortic isthmus rupture (Gore TAG \uae 28-150), a partial collapse of the endoprosthesis at the descending tract occurred, with no signs of visceral ischemia. Considering patient's clinical conditions, the graft collapse wasn't treated at that time. When general conditions allowed reintervention, the patient refused any new treatment, so he was discharged.Four months later the patient complainted for severe gluteal and sural claudication, erectile disfunction and abdominal angina; endovascular correction was performed. At 18 months the graft was still patent.Discussion and Conclusion: Graft collapse after TEVAR is a rare event, which should be detected and treated as soon as possible. Delayed correction of this complication can be lethal due to the risk of visceral ischemia and limbs loss

Clonal evolution of CD8+ T cell responses against latent viruses: relationship among phenotype, localization, and function

Human cytomegalovirus (hCMV) infection is characterized by a vast expansion of resting effector-type virus-specific T cells in the circulation. In mice, interleukin-7 receptor α (IL-7Rα)-expressing cells contain the precursors for long-lived antigen-experienced CD8(+) T cells, but it is unclear if similar mechanisms operate to maintain these pools in humans. Here, we studied whether IL-7Rα-expressing cells obtained from peripheral blood (PB) or lymph nodes (LNs) sustain the circulating effector-type hCMV-specific pool. Using flow cytometry and functional assays, we found that the IL-7Rα(+) hCMV-specific T cell population comprises cells that have a memory phenotype and lack effector features. We used next-generation sequencing of the T cell receptor to compare the clonal repertoires of IL-7Rα(+) and IL-7Rα(-) subsets. We observed limited overlap of clones between these subsets during acute infection and after 1 year. When we compared the hCMV-specific repertoire between PB and paired LNs, we found many identical clones but also clones that were exclusively found in either compartment. New clones that were found in PB during antigenic recall were only rarely identical to the unique LN clones. Thus, although PB IL-7Rα-expressing and LN hCMV-specific CD8(+) T cells show typical traits of memory-type cells, these populations do not seem to contain the precursors for the novel hCMV-specific CD8(+) T cell pool during latency or upon antigen recall. IL-7Rα(+) PB and LN hCMV-specific memory cells form separate virus-specific compartments, and precursors for these novel PB hCMV-specific CD8(+) effector-type T cells are possibly located in other secondary lymphoid tissues or are being recruited from the naive CD8(+) T cell pool. IMPORTANCE: Insight into the self-renewal properties of long-lived memory CD8(+) T cells and their location is crucial for the development of both passive and active vaccination strategies. Human CMV infection is characterized by a vast expansion of resting effector-type cells. It is, however, not known how this population is maintained. We here investigated two possible compartments for effector-type cell precursors: circulating acute-phase IL-7Rα-expressing hCMV-specific CD8(+) T cells and lymph node (LN)-residing hCMV-specific (central) memory cells. We show that new clones that appear after primary hCMV infection or during hCMV reactivation seldom originate from either compartment. Thus, although identical clones may be maintained by either memory population, the precursors of the novel clones are probably located in other (secondary) lymphoid tissues or are recruited from the naive CD8(+) T cell pool

Value of risk scores in the decision to palliate patients with ruptured abdominal aortic aneurysm

Background: The aim of this study was to develop a 48-h mortality risk score, which included morphology data, for patients with ruptured abdominal aortic aneurysm presenting to an emergency department, and to assess its predictive accuracy and clinical effectiveness in triaging patients to immediate aneurysm repair, transfer or palliative care. Methods: Data from patients in the IMPROVE (Immediate Management of the Patient With Ruptured Aneurysm: Open Versus Endovascular Repair) randomized trial were used to develop the risk score. Variables considered included age, sex, haemodynamic markers and aortic morphology. Backwards selection was used to identify relevant predictors. Predictive performance was assessed using calibration plots and the C-statistic. Validation of the newly developed and other previously published scores was conducted in four external populations. The net benefit of treating patients based on a risk threshold compared with treating none was quantified. Results: Data from 536 patients in the IMPROVE trial were included. The final variables retained were age, sex, haemoglobin level, serum creatinine level, systolic BP, aortic neck length and angle, and acute myocardial ischaemia. The discrimination of the score for 48-h mortality in the IMPROVE data was reasonable (C-statistic 0·710, 95 per cent c.i. 0·659 to 0·760), but varied in external populations (from 0·652 to 0·761). The new score outperformed other published risk scores in some, but not all, populations. An 8 (95 per cent c.i. 5 to 11) per cent improvement in the C-statistic was estimated compared with using age alone. Conclusion: The assessed risk scores did not have sufficient accuracy to enable potentially life-saving decisions to be made regarding intervention. Focus should therefore shift to offering repair to more patients and reducing non-intervention rates, while respecting the wishes of the patient and family

Antegrade Balloon Dilatation as a Treatment Option for Posttransplant Ureteral Strictures: Case Series of 50 Patients

Objectives: The aim of this study was to investigate the effects of antegrade balloon dilatation on ureteral strictures that developed after kidney transplant. Materials and Methods: The hospital databases of the Erasmus Medical Center (Rotterdam, The Netherlands) and the Academic Medical Center (Amsterdam, The Netherlands) were retrospectively screened for patients who underwent balloon dilatation after kidney transplant. Balloon dilatation was technically successful whenever it was able to pass the strictured segment with the guidewire followed by balloon inflation; the procedure was clinically successful if no further interventions (for example, surgical revision of the ureteroneocystostomy or prolonged double J placement) were necessary. Results: Fifty patients (2.4%) of 2075 kidney transplant recipients underwent antegrade balloon dilatation because of urinary outflow obstruction. Median time between transplant and balloon dilatation was 3 months (range, 0-139 mo). In 43 patients (86%), balloon dilatation was technically successful. In the remaining 7 patients (14%), it was impossible to pass the strictured segment with the guidewire. In 20 of 43 patients (47%) having a technically successful procedure, the procedure was also clinically successful, with median follow-up after balloon dilatation of 35.5 months (range, 0-102 mo). We did not identify any patient or stricture characteristic that influenced the outcome of treatment. Conclusions: Balloon dilatation is a good option for ureter stricture treatment after kidney transplant as it is minimal invasive and can prevent surgical exploration in almost 50% of cases

Selective expansion of influenza a virus-specific T cells in symptomatic human carotid artery atherosclerotic plaques

Background and Purpose-Evidence is accumulating that infection with influenza A virus contributes to atherothrombotic disease. Vaccination against influenza decreases the risk of atherosclerotic syndromes, indicating that inflammatory mechanisms may be involved. We tested the hypothesis that influenza A virus-specific T cells contribute to atherosclerotic plaque inflammation, which mediates the onset of plaque rupture. Methods-T-cell cultures were generated from atherosclerotic segments and peripheral blood of 30 patients with symptomatic carotid artery disease. The response of plaque and peripheral blood T cells to influenza A virus was analyzed and expressed as a stimulation index (SI). Selective outgrowth of intraplaque influenza A-specific T cells was calculated by the ratio of plaque T cell SI and peripheral blood T cell SI for each patient. Accordingly, the patients were categorized as high- (SI ratio >= 5), intermediate- (5 < SI ratio <= 2), and non- (SI ratio < 2) responders. The presence of influenza A virus in the vessel fragments was evaluated by reverse transcription-polymerase chain reaction. Results-High proliferative responses of plaque-derived T cells to influenza A virus were frequently observed. Among the 30 patients, 5 were categorized as high responders, 10 were intermediate responders, and 15 were nonresponders. Live influenza A virus could not be detected in the atherosclerotic plaques by polymerase chain reaction. Conclusions-Selective outgrowth of influenza A virus-specific T cells occurs within the microenvironment of human atherosclerotic plaques. Influenza virus-derived antigens or alternatively, mimicry antigens, appear to be potential candidates for triggering or sustaining plaque inflammation, which eventually leads to symptomatic plaque complications