Vascular endothelial growth factor (VEGF) can promote angiogenesis but may also exert certain effects to alter the rate of atherosclerotic plaque development. To evaluate this potential impact on plaque progression, we treated cholesterol-fed mice doubly deficient in apolipoprotein E/apolipoprotein B100 with low doses of VEGF (2 microg/kg) or albumin. VEGF significantly increased macrophage levels in bone marrow and peripheral blood and increased plaque area 5-, 14- and 4-fold compared with controls at weeks 1, 2 and 3, respectively. Plaque macrophage and endothelial cell content also increased disproportionately over controls. In order to confirm that the VEGF-mediated plaque progression was not species-specific, the experiment was repeated in cholesterol-fed rabbits at the three-week timepoint, which showed comparable increases in plaque progression.

In the treatment of blunt traumatic thoracic aortic rupture, the immediate outcome in patients who receive endovascular stent grafts appears to be at least as good as observed after conventional surgical repair. Long-term follow-up is necessary to assess long-term effectiveness of such management.

The development of AOF is a rare but lethal complication after TEVAR, being associated with the need for emergency TEVAR as well as mediastinal haematoma formation. The only durable and successful approach to cure the disease is radical oesophagectomy and extensive aortic reconstruction. These findings may serve as a decision-making tool for physicians treating these complex patients.

In our study, length of aortic coverage is the only independent predictive factor of SCI after endovascular treatment with 205mm as a threshold for increased risk. Hence, methods to prevent SCI, especially those aimed at restoration of an adequate spinal cord perfusion pressure, should be offered to patients requiring extensive coverage of the descending thoracic aorta.

Endovascular stent grafting of the dissected DTA is feasible in selected Marfan patients with low mortality and morbidity rates. Nevertheless, the rate of primary and secondary endoleak is high. Close imaging surveillance is crucial to detect secondary aortic complications and to assess long-term results.

ABPF is a rare but highly lethal complication after TEVAR. The leading mechanism behind ABPF seems to be a continuing external compression of either the bronchial tree or left upper lobe parenchyma. In this setting, persisting or newly developing endoleak formation seems to play a crucial role. Prognosis does not differ in patients with central airway or pulmonary parenchymal fistulation. Radical bronchial or pulmonary parenchymal repair in combination with stent graft removal and aortic reconstruction seems to be the most durable treatment strategy.

No abstract

Endovascular US enhanced vascular gene delivery and increased the efficiency of nonviral platforms to levels previously attained only by adenoviral strategies.