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BACKGROUND.: Donor-specific anti-HLA antibodies (DSA) are a major cause of alloimmune injury. Transplant recipients with negative complement-dependent cytotoxic crossmatch (CDC-XM) and donor cell-based flow cytometric crossmatch (flow-XM) but low level DSA (i.e., by Luminex) have worse outcomes compared with nonsensitized patients. The aim of this study was to establish whether complement-activating ability in this low-level DSA, present before transplantation, as determined by this technique is important in dictating pathogenicity. METHODS.: We retrospectively studied 52 patients with preformed DSA detected by single-antigen flow cytometric fluorescent beads (SAFBs). Patients were transplanted using a steroid-sparing regimen consisting of alemtuzumab induction, 1 week of corticosteroids and tacrolimus monotherapy.Fifteen (29%) of 52 patients experienced antibody-mediated rejection (AMR), whereas 37 (71%) patients did not. There were no demographic differences between patients with AMR and those without. Pretransplant sera were retested using a modified (SAFB) assay, which detects the presence of the complement fragment C4d as a result of DSA-induced complement activation. RESULTS.: C4d+DSA were detected in 10 (19%) of 52 patients. Biopsy-proven AMR occurred in 7 (70%) of the 10 patients with C4d+DSA and in 8 (19%) of 42 patients with C4d-DSA. AMR-free survival was worse in patients with C4d+DSA (P<0.001). CONCLUSIONS.: The ability of preformed, low-level, DSA to trigger C4d fixation in vitro in patients with negative conventional crossmatch tests is predictive for AMR. C4d SAFB is potentially a powerful tool for risk stratification prior to transplantation and may allow identification of unacceptable donor antigens, or patients who may require enhanced immunosuppression.

Objective We sought to describe the prevalence, management strategies and evaluate the prognosis of patients with iatrogenic catheter‐induced ostial coronary artery dissection (ICOCAD). Background ICOCAD is a rare but potentially devastating complication of cardiac catheterisation. The clinical manifestations of ICOCAD vary from asymptomatic angiographic findings to abrupt vessel closure leading to myocardial infarction and death. Methods 55,968 patients who underwent coronary angiography over a 10‐year period were screened for ICOCAD as defined by the National Heart, Lung, and Blood Institute. The management and all‐cause mortality were retrieved from local and national databases. Results The overall prevalence of ICOCAD was 0.09% (51/55,968 patients). Guide catheters accounted for 75% (n = 37) of cases. Half of the ICOCAD cases involved the right coronary artery while the remaining were related to left main stem (23/51; 45%) and left internal mammary artery (2/51; 4%). Two‐thirds of ICOCAD were high grade (type D, E, and F). The majority of cases were type F dissections (n = 18; 66%), of which two third occurred in females in their 60s. The majority of ICOCAD patients (42/51; 82%) were treated with percutaneous coronary intervention while the remaining underwent coronary artery bypass grafting (3/51; 6%) or managed conservatively (6/51; 12%). Three deaths occurred during the index admission while 48/51 patients (94.1%) were safely discharged without further mortality over a median follow‐up of 3.6 years. Conclusions ICOCAD is a rare but life‐threatening complication of coronary angiography. Timely recognition and prompt bailout PCI is a safe option for majority of patients with good clinical outcomes.