Background-Considering experimental evidence that stem cells enhance myocardial regeneration and granulocyte colony-stimulating factor (G-CSF) mediates mobilization of CD34ϩ mononuclear blood stem cells (MNC CD34ϩ ), we tested the impact of G-CSF integrated into primary percutaneous coronary intervention (PCI) management of acute myocardial infarction in man. Methods and Results-Fifty consecutive patients with ST-segment elevation myocardial infarction were subjected to primary PCI stenting with abciximab and followed up for 6 months; 89Ϯ35 minutes after successful PCI, 25 patients were randomly assigned in this pilot study (PROBE design) to receive subcutaneous G-CSF at 10 g/kg body weight for 6 days in addition to standard care, including aspirin, clopidogrel, an ACE inhibitor, ␤-blocking agents, and statins. By use of CellQuest software on peripheral blood samples incubated with CD45 and CD34, mobilized MNC CD34ϩ were quantified on a daily basis. With homogeneous demographics and clinical and infarct-related characteristics, G-CSF stimulation led to mobilization of MNC CD34ϩ to between 3.17Ϯ2.93 MNC CD34ϩ /L at baseline and 64.55Ϯ37.11 MNC CD34ϩ /L on day 6 (PϽ0.001 versus control); there was no indication of leukocytoclastic effects, significant pain, impaired rheology, inflammatory reactions, or accelerated restenosis at 6 months. Within 35 days, G-CSF and MNC

Cardiac manifestation is the major cause of morbidity in patients with hypereosinophilic syndrome (HES). Clinical features range from heart failure to arterial embolism, which are caused by thickening of the endocardium and mural left ventricular thrombosis. Modern magnetic resonance imaging and echocardiography are able to detect fibrosis, eosinophilic infiltrate and thrombi to stage the fibrotic evolution of the disease. Treatment of HES involves standard medication for heart failure, anticoagulant therapy, immunosuppressive therapy and potentially surgical resection. The outcome of HES depends on both the progression of endocardial fibrosis and associated complications and the 5-year mortality is estimated at 30%.

Stent-graft-induced occlusion of the ostial LSA was tolerated by all patients without chronic functional deficit. In the absence of stenotic vertebral and/or carotid arteries and with a documented intact vertebrobasilar system, prophylactic transposition of the LSA is not required prior to intentional stent-graft occlusion of the LSA.

Background-Formation of aortic aneurysm late after surgical repair of coarctation carries a significant risk of rupture and lethal outcome, and repeat surgery is associated with a 14% in-hospital mortality rate and morbidity from paraplegia, injury to the central nervous system, or from bleeding. The potential of nonsurgical endovascular repair by the use of stent-grafts in lieu of repeat surgery for postcoarctation aneurysm is unknown. Methods and Results-The concept of postsurgical endovascular stent-graft placement was evaluated with respect to feasibility and safety in 6 consecutive patients with late aneurysm formation after coarctation repair. All patients had aneurysm formation late after patch aortoplasty; placement of an elephant trunk during surgical repair of secondary type I dissection preceded formation of a local aneurysm in 2 cases. Patient age was 49Ϯ12 years, ranging from 31 to 68 years. Transluminal placement of customized stent-grafts was successful, with no 30-day or 1-year intervention-related mortality or morbidity. Follow-up survey of 11 to 47 months revealed optimal reconstruction of the thoracic aorta; 1 patient died 11 months after endovascular repair from cancer. Conclusions-Nonsurgical

In consideration of the findings of the studies performed to date, the rate-adaptive AV delay should be deactivated.