Background This study sought to evaluate safety and radiation exposure when using intracardiac echocardiography (ICE) in comparison to transesophageal echocardiography (TEE) in order to guide transcatheter closure of interatrial communications. Methods Eighty patients (44 males, 36 females, mean age 46, SD 13 years) undergoing device closure of atrial septal defect (n Z 12) or patent foramen ovale (n Z 68) had the procedure guided by ICE (n Z 50, group 1) or TEE (n Z 30, group 2). In group 1, all procedural stages were completely guided by ICE, including imaging of the interatrial communication during balloon sizing, device unfolding and release, and during the final check for adequate positioning. In group 2, exclusive implantation of devices was guided by use of TEE. Results Especially, the spatial relationship between device and cardiac structures (e.g. the ascending aorta, the interatrial septum and the superior vena cava) was accurately demonstrated in group 1. Image resolution provided by ICE was superior to that of TEE. No severe complications, including any related to ICE, were seen. Fluoroscopy time (FT) and procedure time (PT) were shorter in group 1 than in group 2 (FT: 5.5 G 1.5 min vs. 9.3 G 1.6 min, P ! 0.0001; PT: 31.9 G 4.6 min vs. 38.8 G 5.8 min, P ! 0.01). Neither sedation nor anesthesia was required in group 1. Conclusions ICE is a safe tool to guide device closure of interatrial communications. For the patient, procedural stress and radiation exposure are negligible.
Bone marrow-derived stem cells may contribute to the regeneration of non-haematopoietic organs. In order to test whether an increase in circulating stem cell numbers improves impaired myocardial function we treated 16 male patients with chronic heart failure due to dilated (DCM; n = 7) or ischaemic cardiomyopathy (ICM; n = 9) with the stem cell mobilising cytokine granulocyte colony-stimulating factor (G-CSF; four 10-day treatment periods interrupted by treatment-free intervals of equal length). Safety and efficacy analyses were performed at regular intervals. Peak CD34+ cell counts remained constant from cycle to cycle. Cardiac side effects in ICM patients included occasional episodes of dyspnea or angina and one episode of fatal ventricular fibrillation. Nine (4 DCM, 5 ICM) of 12 patients receiving four full G-CSF cycles experienced an improvement by one New York Heart Association (NYHA) class and a statistically significant increase in six-minute walking distance. By contrast, none of 8 ICM historical controls had a change in NYHA class during a similar time period. Statistically significant changes in echocardiographic parameters were not recorded. Sequential administration of G-CSF is feasible and possibly effective in improving physical performance in patients with chronic heart failure. Patients with ICM may be at risk of increased angina and arrhythmias.
Background: Cardio shock wave therapy (CSWT) treated patients show a significant improvement in symptoms has a beneficial affect in patients with heart failure and endstage coronary artery disease. The underlying mechanism is still not known. Vascular endothelial growth factor (VEGF) is a strong mitogen which induces angiogenesis. We invastigated whether VEGF is elevated after shock wave treatment in Human umbilical vascular endothelial cells (HUVEC).Methods: For CSW treatment HUVEC cells were put into a 2 ml Cryo tube 5-106 cells/ml. Shock waves were produced by a modified lithotrypter. The cell containing tubes were installed in a water bath at 37°C directly into the focus of the shock waves. Different energy tlux densities 0.02, 0.05, 0.1, 0.3 mJ/mm2 were used. After shock wave treatment cells were grown for 24-36 h. Cells were centrifuged and m-RNA was isolated using standard methods. Reverse transcriptase -Polymerase chain reaction (RT-PCR) was performed using VEGF165 m-RNA primer. Cell death was measured using MTT-assay.Results: Ceil death increased with increasing energy dosages. RT-PCR revealed a significant increase in cells treated with CSW in comparison to untreated controll cells (Figurel).
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