Expression of the leptin receptor in different types of vascular lesions.

Clinical and experimental evidence suggests that the adipokine leptin may be important for the development of cardiovascular complications associated with obesity, possibly through interaction with its receptor on vascular cells. In the present study, we systematically analysed expression of the leptin receptor in normal and diseased vascular specimens using immunohistochemistry, immunofluorescence and quantitative real time-PCR. In particular, human atherosclerotic plaques as well as experimental vascular lesions induced in hypercholesterolemic mice and minipigs, respectively, were examined.

Transfection of the DNA for the receptor KDR/flk-1 attenuates neointimal proliferation and luminal narrowing in a coronary stent angioplasty model.

Background: Neointimal proliferation resulting in luminal renarrowing is the major cause of restenosis limiting the long-term success of coronary angioplasty in 20 to 30% of patients. Local transfection of the DNA encoding for VEGF has been shown to enhance re-endothelialization and reduce neointimal proliferation in an experimental model. We tested the hypothesis that transfection of the DNA for the receptor of vascular endothelial growth factor VEGF, KDR-flk-1, reduces neointimal proliferation after angioplasty.

Shear stress insensitivity of endothelial nitric oxide synthase expression as a genetic risk factor for coronary heart disease.

Coronary heart disease (CHD) is based on the development of atherosclerosis in coronary arteries. Shear stress-induced endothelial nitric oxide (NO) release not only contributes to local blood pressure control but also effectively helps to retard atherosclerosis. Therefore, functionally relevant polymorphisms in the endothelial NO synthase (NOS-3) gene may contribute to the development of CHD.

[Gene therapy in interventional coronary interventions].

Background: 30-50% of patients develop restenosis after PTCA. While most pharmacologic strategies fail to reduce restenosis rate, only implantation of stents and brachytherapy have shown to improve long-term outcome of coronary angioplasty significantly.

Gene Therapy: With expanding knowledge of the process resulting in activation and inhibition of gene expression after angioplasty, a number of studies showed by inhibiting overexpression of some genes or overexpressing down-regulated other genes significant and extensive reduction of neointimal hyperplasia in different angioplasty models.

Decoy oligodeoxynucleotide against activator protein-1 reduces neointimal proliferation after coronary angioplasty in hypercholesterolemic minipigs.

Objectives: We sought to demonstrate, in an appropriate animal model, that co-medication with a transcription factor-blocking agent limits restenosis after percutaneous transluminal coronary angioplasty (PTCA).

Background: Enhanced synthesis in the vessel wall of endothelin-1 (ET-1), a powerful co-mitogen for vascular smooth muscle cells, appears to be one mechanism that promotes restenosis after PTCA. Deformation-induced expression of prepro-ET-1 is governed by the transcription factor, activator protein-1 (AP-1).

Closure of an iatrogenic aortocoronary arteriovenous fistula: transcatheter balloon embolization following failed coil embolization and salvage of coils that migrated into the coronary venous system.

We report a 50-year-old patient with successful percutaneous closure of a large inadvertent surgical aortocoronary arteriovenous fistula (shunt flow: 1.8 L/min). With initial embolization of multiple coils, no lasting occlusion of the large fistula could be achieved.