Our goal was to assess the results after orthotopic branched endovascular aortic arch repair using a new double-branch endoprosthesis in patients with thoracic aortic disease affecting the aortic arch who cannot undergo classical surgery. Within a 4-year period, 15 patients with thoracic aortic disease affecting the aortic arch were treated with the Bolton Relay plus double-branch endoprosthesis (Bolton Medical, Sunrise, FL, USA). We assessed clinical outcome, occurrence of endoleaks and the need for secondary interventions. The median logistic EuroSCORE I level was 13.6 (4.2; 22.8). The in-hospital mortality rate was 6.7%. A disabling stroke was observed in 1 (6.7%) patient, whereas non-disabling strokes occurred in 2 (13.3%) patients. Type I and III endoleaks occurred in 6.7%. The median follow-up period was 263 (1st quartile 84; 2nd quartile 564) days. Four patients died during the follow-up period. Aortic-related survival was 100%. Orthotopic branched endovascular aortic arch repair using the Bolton Relay Plus double-branch endoprosthesis is a safe and feasible technique enriching the armamentarium to treat patients with thoracic aortic disease who cannot undergo classical surgery. Aortic-related survival is excellent, and the occurrence of disabling stroke and endoleaks warranting treatment is low. Further studies are needed to assess the long-term durability of this new method.

After tissue injury, both wound sealing and apoptosis contribute to restoration of tissue integrity and functionality. Although the role of platelets (PLTs) for wound closure and induction of regenerative processes is well established, the knowledge about their contribution to apoptosis is incomplete. Here, we show that PLTs present the death receptor Fas ligand (FasL) on their surface after activation. Activated PLTs as well as the isolated membrane fraction of activated PLTs but not of resting PLTs induced apoptosis in a dose-dependent manner in primary murine neuronal cells, human neuroblastoma cells, and mouse embryonic fibroblasts. Membrane protein from PLTs lacking membrane-bound FasL (FasL^△m/△m) failed to induce apoptosis. Bax/Bak-mediated mitochondrial apoptosis signaling in target cells was not required for PLT-induced cell death, but increased the apoptotic response to PLT-induced Fas signaling. In vivo, PLT depletion significantly reduced apoptosis in a stroke model and an inflammation-independent model of N-methyl-d-aspartic acid-induced retinal apoptosis. Furthermore, experiments using PLT-specific PF4Cre⁺ FasL^fl/fl mice demonstrated a role of PLT-derived FasL for tissue apoptosis. Because apoptosis secondary to injury prevents inflammation, our findings describe a novel mechanism on how PLTs contribute to tissue homeostasis. Key Points PLTs contribute to apoptosis in vivo and express the death receptor ligand FasL upon activation. Membrane-bound FasL mediates PLT-induced apoptosis, whereas Bax/Bak signaling is not required but reinforces PLT-induced apoptosis.

OBJECTIVES: Thoracic endovascular aortic repair is the treatment of choice in complicated acute type B aortic dissection. How to infer predissection aortic diameter is not well understood. Our aim was to delineate changes in descending aortic geometry due to dissection. METHODS: Five tertiary centres reviewed their acute aortic dissection type B databases containing 802 patients. All patients who had undergone computed tomography angiography less than 2 years before and immediately after aortic dissection onset were included. We compared the aortic geometry before and after the dissection onset. RESULTS: Altogether 25 patients were included [median age 60 (first quartile 52, third quartile 72) years; 60% men]. In all except 1 patient, the maximum descending aortic diameter was less than 45 mm before aortic dissection onset. The largest increase in diameter induced by the dissection was observed in the proximal descending aorta 28.2 (25.1, 32.1) vs 34.6 (31.3, 39.1) mm (+6.4 mm; +23%; P < 0.001). The thoracic descending aortic length increased after the dissection onset [253.3 (229.3, 271.9) vs 261.3 (247.9, 285.4) mm; P = 0.003]. The predissection aortic diameter of the proximal thoracic descending aorta was 7.9 (5.2, 10.7) mm larger (P < 0.001) than the post-dissection area-derived true-lumen diameter and 2.5 (1.3, 6.1) mm larger than the maximum true-lumen diameter (P < 0.001). CONCLUSIONS: Type B aortic dissection increases the diameter, length and volume of the descending thoracic aorta. The predissection aortic diameter most closely resembles the post-dissection maximum diameter of the true lumen.

OBJECTIVES: We measured aortic dimensions, particularly length parameters, using 3D imaging with the aim of refining the risk-morphology for Stanford type A aortic dissection (TAD). METHODS: Computer tomography angiography studies were analysed using the curved multiplanar reformats. At defined landmarks, the diameters and lengths of aortic segments were recorded. Three groups were compared retrospectively: patients actually suffering from a TAD (TAD-group; n = 150), patients before suffering a TAD (preTAD-group n = 15) and a healthy control group (n = 215). Receiver operating characteristic curves (ROCs) were analysed (control versus preTAD) to study the diagnostic value of the individual variables. RESULTS: Median diameters of preTAD (43 mm) and TAD (50 mm) aortas were significantly (P < 0.001) larger than those of the control group (35 mm). Ninety-three percent of preTAD and 68% of TAD aortas were less than 55 mm in the mid-ascending aorta. The ascending aorta and the aortic arch were significantly longer in both preTAD and TAD aortas compared to control aortas (P < 0.001); in the control aortas the central line distance from the aortic valve to the brachiocephalic trunk was 93 mm. In preTAD aortas, it was 111 mm, and it was 117 mm in TAD aortas (P < 0.001). In ROC analysis, the area under the curve was 0.912 for the ascending diameter and 0.787 for the ascending and arch lengths. CONCLUSIONS: TAD-prediction based on the aortic diameter is ineffective. Besides circumferential dilatation, ascending aorta elongation precedes TAD and appears to be a useful additional parameter for prognostication. We propose a diagnostic score involving ascending aorta diameter and length.

To study the lengths and diameters of aortic segments in healthy and diseased aortas and to assess the role of aortic elongation in Type A aortic dissection (TAD) prediction. Ectasia and aneurysm were defined by ascending aorta diameters of 45–54 mm and ≥55 mm, respectively. Computed tomography angiography studies of 256 healthy, 102 ectasia, 38 aneurysm, 17 pre-TAD and 166 TAD aortas were analysed using curved multiplanar reformats. The study groups were structurally equal. The diameter of the ascending aorta was 35 mm in the control group and was larger (P < 0.001) in the pre-TAD (43 mm) and TAD (56 mm) groups. The length of the ascending aorta from the aortic annulus to the brachiocephalic trunk was 92 mm in the control group, 113 mm in the ectasia group, 120 mm in the aneurysm group and 111 mm and 118 mm in the pre-TAD and TAD groups (all P < 0.001 compared with the control group). An ascending aorta length of 120 mm was exceeded in 2% of the control group, 31% of the ectasia group, 50% of the aneurysm group, 24% of the pre-TAD group and 48% of the TAD group. The correlation between the diameter and the length of the ascending aorta was r = 0.752; therefore, both parameters must be examined separately. A score considering both parameters identified 23.5% of pre-TAD patients, significantly more than the diameter alone, and 31.4% of ectasia aortas were elongated. Patients with ectatic (45–54 mm diameter) and elongated (≥120 mm) ascending aortas represent a high-risk subpopulation for TAD.