Successful Thoracic Endovascular Aortic Repair in Ortner's Syndrome.

We present the case of an 89-year-old man with 3-month history of hoarseness and no other significant clinical manifestations. Flexible laryngoscopy revealed a paralyzed left vocal cord, and contrast-enhanced computed tomography showed a thoracic dissecting aortic aneurysm of the distal aortic arch and proximal descending aorta. The aortic aneurysm was repaired through implantation of an endovascular stent graft, and the patient was discharged uneventfully after a week. The false lumen was completely thrombosed, and the patient had a partial resolution of hoarseness at the 1-year follow-up.

Blood Mixing Upregulates Platelet Membrane-Bound CD40 Ligand Expression In Vitro Independent of Abo Compatibility.

Platelets play a central role in the inflammation response via CD40 ligand (CD40L) expression, which may lead to transfusion reactions. The precise role of platelet CD40L-mediated inflammation in transfusion reactions is unclear. Therefore, we assessed the effects of in vitro blood mixing on platelet CD40L expression. In addition, we examined the effect of ABO compatibility on CD40L expression. Donor-packed red blood cells were acquired from a blood bank, and recipient blood was obtained from patients undergoing cardiac surgery and prepared as washed platelets. Donor blood was mixed with suspended, washed recipient platelets to obtain a final mixing ratio of 1%, 5%, or 10% (vol/vol). The blood mixtures were divided into three groups: group M, cross-matched blood-type mixing (n = 20); group S, ABO type-specific uncross-matched blood (n = 20); and group I, ABO incompatibility (not ABO type-specific blood and not process cross-matched) mixing (n = 20). The blood mixtures were used to detect platelet membrane-bound CD40L expression by flow cytometry. Blood mixing resulted in an increase in CD40L expression in group M (P < 0.001), group S (P < 0.001), and group I (P < 0.001). CD40L expression after blood mixing potentially led to a transfusion reaction in each of the groups. There were no differences in CD40L expression among the three groups (P = 0.988) correlated with ABO compatibility or incompatibility. This indicates that the reactions between red blood cell surface antigens and plasma antibodies do not play a role in the induction of CD40L expression.

Impact of Blood Mixing and ABO Compatibility on Platelet-Leukocyte Aggregations and Platelet P-Selectin Expression: An in Vitro Study.

Effects of blood transfusions on platelet- and leukocyte-related inflammation are unclear. We simulated transfusion using in vitro blood mixing to evaluate platelet-leukocyte aggregations (PLA) and platelet P-selectin expression, and the mechanism of PLA. Donor packed red blood cells (pRBCs) were obtained from a blood bank. Recipient whole blood samples were obtained from patients undergoing cardiac surgery. Blood sample mixtures were divided into four groups: group M, cross-matched blood type mixing; group O, donor type O with other blood type mixing (A, B, or AB); group S, ABO type-specific uncross-matched blood mixing; and group I, ABO incompatibility mixing. Donor pRBCs were added to recipient blood to reach 1%, 5%, and 10% (vol/vol) concentrations. Blood sample mixtures were analyzed to determine the PLA; P-selectin expression; and leukocyte CD11a, CD11b, and CD18 subunits of integrin expression. Analysis of variance tests were used to analyze differences. PLA significantly increased only in groups O and I (P = 0.003 and P < 0.001). Subpopulations of leukocytes significantly increased in all groups. There were no significant differences among the four groups (P = 0.578) in PLA increase. Although there was no significant effect on P-selectin expression (P = 1.000) and leukocyte CD11a and CD18 expression (P = 0.999, P = 0.422) within and between the groups, there was an increase in CD11b expression (P = 0.018). Blood mixing can increase PLA, especially in platelet-neutrophil and platelet-monocyte aggregations, possibly through nonhemolytic reactions. The CD11b integrin with CD18 may play a role in the formation of PLA.