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Introduction: To evaluate the ultra-structural changes of the chorioretinal vessels in hypercholesterolemic rabbits after treatment with statins. Methods: New Zealand rabbits were divided into four groups: Control (G0; n=10), and fed a standard diet for 8 months; Hypercholesterolemic (G1, n=8), were fed a 0.5% cholesterol-enriched diet for 8 months. Statins group (G2A y B, n=8), were each fed a 0.5% cholesterol-enriched diet for 8 months plus administration of fluvastatin sodium (G2A) or pravastatin sodium (G2B) at a dose of 2 mg/Kg/day. Eyes were processed by transmission electron microscopy. Results: G1 had a buildup of lipids at the suprachoroidea that compressed the vascular layers. G2 had a substantial decrease in the number of foam cells and lipids but more collagen fibres in the suprachoroidea and vascular layers. The lumen of the choroidal vessels was opened more in G2 in comparison with G1, which had a reduction in the capillary lumen to the point of collapse due to compression and hypertrophy of endothelial and vascular smooth muscle cells. The normal appearance of endothelial cells in G2 was in contrast with the endothelial necrosis observed in G1. In G2, the thickness of the Bruch membrane and the basal membrane of the choroidal and retinal vessels were reduced in comparison with G1. Conclusions: Treatment with statins reduces the build up of lipids and the number of macrophages in the choroid. Additionally, they preserve the endothelial cells and open the vascular lumens of choroidal vessels.

Transforming growth factor β (TGF-β1) is a pleiotropic cytokine with many and complex effects in cell and tissue physiology. This is made possible by a very complex and interwoven signaling system, whose regulation continues to be the focus of a growing line of research. This complex regulation translates to a key role in cardiovascular physiology, hemostasis, and the blood-vessel interface. In accordance with this, the TGF-β1 pathway appears to be deregulated in related disorders, such as atherosclerotic vascular disease and myeloproliferative syndromes. It is expected that the growing amount of experimental and clinical research will yield medical advances in the applications of knowledge of the TGF-β1 pathway to diagnosis and therapeutics.

Background Cardiovascular disease has been linked to endothelial progenitor cell (EPC) depletion and functional impairment in atherosclerosis and aortic stenosis. EPCs may play a pivotal role in vascular grafting. However, the EPC depletion in coronary artery bypass grafting (CABG) patients has not been compared to coronary artery disease-free valvular replacement patients with aortic stenosis. Methods We aimed to assess the basal number of CD34+/KDR+ and CD34+/CD144+ cells in CABG patients, compared to aortic stenosis valvular replacement patients. 100 patients (51 CABG and 49 valvular surgery ones) were included in the present study. All CABG or valvular patients had angiographic demonstration of the presence or the absence of coronary artery disease, respectively. Numbers of CD34+/KDR+ and CD34+/CD144+ were assessed by flow cytometry of pre-surgical blood samples. Results We found a lower number of CD34+/CD144+ cells in CABG patients compared to valvular patients (0.21 ± 0.03% vs. 0.47 ± 0.08%), and this difference remained statistically significant after the P was adjusted for multiple comparisons (P = 0.01428). Both groups had more EPCs than healthy controls. Conclusions Pre-surgical CD34+/CD144+ numbers are decreased in CABG patients, compared to valvular patients with absence of coronary disease., This work was supported by FISS (Health Research Fund, PI080920) and Red Tematica de Investigacion Cardiovascular RECAVA (RD06/0014/1007, RD06/0014/1027), both from the Instituto de Salud Carlos III (ISCIII). We are grateful to Fernando Ortego and all the nurses and doctors from the Cardiac Surgery service, Hospital Clinico San Carlos, for their technical assistance. We acknowledge support from Centro de Microscopía y Citometría (Universidad Complutense) and the Regional Blood Transfusion Centre, Madrid.

Dabigatran is an emerging oral anticoagulant which is a direct inhibitor of thrombin activity. It has been approved in the European Union and the United States of America for the prevention of thrombosis after major orthopedic surgery. It has also been approved by the American Food and Drug Administration and the European Medicines Agency for the prevention of stroke in chronic atrial fibrillation. Dabigatran provides a stable anticoagulation effect without any need to perform periodical laboratory controls. Of note, there is a growing amount of clinical evidence which shows its safety and efficacy. For these reasons, dabigatran may suppose a revolution in oral anticoagulation. However, two important limitations remain. First, it is contraindicated in patients with end-stage renal disease. Second, there is no evidence of the prevention of thrombosis in mechanical heart valves.

Background Transforming growth factor beta (TGF-β1) is a pleiotropic cytokine, which is deregulated in atherosclerosis; however the role of age in this process is unknown. We aimed to assess whether TGF-β1 signaling is affected by age. Methods Vascular smooth muscle cells (VSMC) were obtained from patients undergoing abdominal surgery. Levels of TGF-β1 were measured by ELISA in sera from 169 patients undergoing coronary artery bypass grafting (CABG). The p27 expression was determined by Western blot from internal mammary arteries (IMA) obtained from CABG patients (n = 13). In VSMC from these patients undergoing abdominal surgery, secretion of TGF-β1 was determined by ELISA of cell-conditioned media. Results In VSMC from aged patients we observed a lower TGF-β1 secretion, measured as TGF-β1 concentration in cell conditioned medium (p p = 0.0195). Conclusions VSMC from aged patients showed a higher degree of cellular senescence and it was associated to a lower TGF-β1 secretion and signaling.