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Kommerell diverticulum (KD) is an uncommon congenital vascular anomaly. This study assessed outcomes of open and endovascular repair of this disorder.Between 1997 and 2016, 152 adult patients presented with KD at Cleveland Clinic (Cleveland, OH), 87 had no intervention, and 65 underwent open repair (n = 55; 19 elephant trunk [ET] procedures [9 with aortic dissection], including 7 frozen ET, and completions with 5 thoracic endovascular aortic repairs, 2 open, and 5 lost to follow-up) or endovascular procedures (n = 10). Non-ET open KD repairs consisted of resection (n = 15), interposition graft (n = 16), patch (n = 4), or aortopexy (n = 1). Maximum KD diameter was 2.1 cm for nonsurgical patients and 3.2 cm for surgical patients. Among surgical patients, 51 of 65 had dysphagia or dyspnea. A total of 608 patient-years of follow-up were available.For patients who underwent open and endovascular procedures, after multivariable adjustment, symptoms of dysphagia and hypertension predicted the likelihood of surgery (P.05, all). There was no operative mortality. Complications included nondisabling stroke (n = 5; 8%), tracheostomy (n = 3; 4.6%), vocal cord paralysis (n = 2; 3%), and reoperation for bleeding (n = 3; 4.6%). During follow-up, 3 of 10 patients treated with hybrid or endovascular procedures required reinterventions for endoleaks. One patient had residual symptoms after aortopexy. Among nonsurgical patients, 2 patients refused surgery, and 1 died of aortic rupture, with a 4.7-cm descending aorta and a 3.4-cm KD. Seven additional patients died of nonaortic comorbidities. The remaining patients were asymptomatic, with an aortic diameter smaller than 4.5 cm.Open and endovascular approaches have a high success rate and low mortality risk. Selection of the specific type of intervention should be based on patient anatomy, additional needed procedures, and comorbid conditions.

Background Anomalous aortic origin of the coronary arteries (AAOCA) is associated with sudden cardiac death and frequently treated with unroofing of an intramural segment. Most reports on AAOCA are of patients less than 30 years of age. We have reviewed our "older" patients who have undergone surgical repair and report a novel unroofing technique. Methods A retrospective review was conducted of 40 adult patients who underwent surgery for AAOCA from June 2005 to June 2016. Our surgical approach changed from traditional sharp excision to electrical fulguration of the shared intramural wall segment. We assessed our population for symptom relief, resolution of ischemia, and reintervention. More than 6 months of follow-up was available for 34 patients. Results Mean age was 47.1 ± 11.6 years (range, 19 to 67); 17 patients were female. The coronary anomaly was right from left in 35 patients, left from right 4, and left coronary from noncoronary sinus in 1 patient. Thirty-nine of 40 patients were symptomatic, with two prior sudden cardiac arrests. Preoperatively, 22 of 31 patients tested positive for ischemia, including the asymptomatic. The operation was unroofing in 37 of 40 patients, 17 by sharp excision and 20 by electrical fulguration. There were no 30-day deaths or complications and no reinterventions. Isolated unroofing by fulguration required shorter cardiopulmonary bypass and cross-clamp times than excision: 39 versus 62 minutes (p = 0.02) and 28 versus 42 minutes (p = 0.02), respectively. At an average follow-up of 5.0 years, 28 of 34 patients reported symptomatic improvement. There were two unrelated late deaths. Conclusions Unroofing by sharp excision and by electrical fulguration were equally safe in the short term. Fulguration is technically easier and faster while still equally effective.

Characterization of resistive pulses from the translocation of particles through lipid-coated nanopores has previously been used to determine the size, charge, and ligand affinity of proteins. Here, we coat the nanopores with a lipid bilayer to prevent non-specific adsorption, concentrate a protein of interest on the bilayer surface, and slow the translocation times of proteins through the pore so that events may be effectively time-resolved and detected. This study aims to characterize cholera toxin and the binding kinetics of the multivalent interaction with GM1 gangliosides embedded in the lipid coating. Understanding the parameters of the GM1 and cholera toxin interaction on a single molecule basis may provide additional information about the pathophysiology of vibrio cholerae, which is known to attack GM1 dense cells in the intestinal epithelia. By monitoring the frequency of translocation events of the protein-ligand complex as a function of time, it is possible to measure the binding kinetics of the interaction between cholera toxin and the GM1 lipid anchors. Thus far, we have determined the shape, volume, and charge of the membrane-associated protein in addition to the effective on-rate of binding under varying concentrations of the GM1 ligand.