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Objective: The objective of this study was to evaluate the outcome of endovascular aortic arch repair for chronic dissection with a custom-made branched endograft. Background: Acute type A aortic dissections are often treated with prosthetic replacement of the ascending aorta. During follow-up, repair of an aneurysmal evolution of the false lumen distal to the ascending prosthesis can be a challenge both for the surgeon and the patient. Methods: We conducted a multicenter, retrospective study of consecutive patients from 14 vascular units treated with a custom-made, inner-branched device (Cook Medical, Bloomington, IN) for chronic aortic arch dissection. Rates of in-hospital mortality and stroke, technical success, early and late complications, reinterventions, and mortality during follow-up were evaluated. Results: Seventy consecutive patients were treated between 2011 and 2018. All patients were considered unfit for conventional surgery. In-hospital combined mortality and stroke rate was 4% (n = 3), including 1 minor stroke, 1 major stroke causing death, and 1 death following multiorgan failure. Technical success rate was 94.3%. Twelve (17.1%) patients required early reinterventions: 8 for vascular access complication, 2 for endoleak correction, and 2 for pericardial effusion drainage. Median follow-up was 301 (138–642) days. During follow-up, 20 (29%) patients underwent secondary interventions: 9 endoleak corrections, 1 open repair for prosthetic kink, and 10 distal extensions of the graft to the thoracic or thoracoabdominal aorta. Eight patients (11%) died during follow-up because of nonaortic-related cause in 7 cases. Conclusions: Endovascular treatment of aortic arch chronic dissections with a branched endograft is associated with low mortality and stroke rates but has a high reintervention rate. Further follow-up is required to confirm the benefits of this novel approach.

BACKGROUND The infant Jarvik 2000 heart is a tiny hermetically-sealed intracorporeal axial-flow ventricular assist device (VAD) designed for circulatory support for neonates and infants. The anatomic fit, acute biocompatibility and hemodynamic performance of the device were evaluated in a neonate piglet model. METHODS The infant Jarvik 2000 heart with two different blade profiles (low-flow blade design and high-flow blade design) was tested in 6 piglets (8.8±0.9 kg). Using a median sternotomy, the pump was placed in the left ventricle through the apex without cardiopulmonary bypass. An outflow graft was anastomosed to the ascending aorta. Hemodynamics and biocompability were studied for 6 hours. RESULTS All six pumps were implanted without complication. Optimal anatomic positioning was found with the pump body inserted 2.4 cm into the left ventricle. Hemodynamics was stable throughout the 6 hours. The pump flow increased from 0.27 L/min to 0.95 L/min at increasing speeds from 18 krpm to 31 krpm for the low-flow blade design, while the pump flow increased from 0.54 L/min to 1.12 L/min at increasing speeds from 16 krpm to 31 krpm for the high-flow blade design. Under higher speeds, over 80% of flow could be supplied by the device. Blood chemistry and final pathology demonstrated no acute organ injury or thrombosis for both the blade designs. CONCLUSIONS The Infant Jarvik 2000 heart is anatomically and biologically compatible with an acute neonate piglet model. This in vivo study demonstrates the future feasibility of this device for clinical use.

Antibodies to pneumococcus are thought to represent the primary mechanism of naturally acquired resistance to colonization. Here, however, we show that, in patients with chronic obstructive pulmonary disease (COPD), resistance to pneumococcal colonization is not associated with higher concentrations of serum anti-capsular or -noncapsular antibodies. We compared preacquisition serum antibody concentrations to capsular antigens 6B, 7F, 14, 19F, and 23F from patients with COPD who did and did not acquire pneumococcal respiratory tree colonization over the course of 2 years. Colonized patients did not have lower anti-capsular antibody concentrations than control subjects who did not acquire pneumococcus. We found no difference in functional antibody concentrations between colonized patients and control subjects. Furthermore, colonized patients had significantly higher preacquisition concentration of antibody directed against the whole cell and pneumococcal surface protein A than control subjects. We thus conclude that, in adult patients with COPD, resistance to pneumococcal colonization is unlikely to be determined by higher serum antibody concentrations to pneumococcal antigens.Streptococcus pneumoniae is an important human pathogen causing asymptomatic carriage as well as important mucosal and systemic infections. Anti-capsular antibodies are thought to represent the single most important protective mechanism against invasive disease [1]. Antibodies to pneumococcal capsular polysaccharides were the basis of serum therapy in which passively transferred, serotype-specific antipneumococcal serum was shown to reduce mortality from pneu- mococcal pneumonia by half [2]. The development of pneumococcal polysaccharide vaccines for adults [3] and the efficacy of pneumococcal polysaccharide-protein conjugate vaccines in infants and children [4,5] have confirmed that antibodies to polysaccharide antigens can provide excellent protection against invasive disease caused by pneumococci of the same serotype as well as that caused by cross-reacting serotypes.Whether these anti-capsular antibodies represent the mechanism whereby unimmunized individuals develop resistance to pneumococcal infection is less clear. We recently presented seroepidemiologic data that suggest otherwise: the risk of invasive pneumococcal disease in childhood decreases in parallel for many different serotypes (which suggests a serotype-transcending mechanism) and before naturally acquired anti-capsular antibodies are detectable [6]. Antibodies to other, noncapsular antigens have also been suggested to mediate acquired resistance to pneumococcal infection [7,8].It has also generally been assumed that resistance