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(Circulation. 2005;111:381.)
© 2005 American Heart Association, Inc.
Issue Highlights
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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FIBROBLASTS CAN BE GENETICALLY MODIFIED TO PRODUCE EXCITABLE CELLS CAPABLE OF ELECTRICAL COUPLING, by Kizana et al. |
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Genetic engineering to restore or create electrically excitable tissue is being developed as a possible treatment for arrhythmias. To attempt creation of electrical excitability in fibroblasts, myogenesis was forced through expression of a skeletal myogenic determination factor. Cells formed myotubes and expressed muscle-specific proteins. Calcium transients were demonstrable in response to electrical stimulation, indicating likely expression of ion channels needed for excitability and calcium release; however, there was no evidence of electrical coupling between myotubes. In cultured cells that were also transduced with a connexion 43–containing vector dye, transfer studies confirmed communication between myotubes, consistent with formation of gap junctions. Electrical coupling was demonstrated in 15% of excitable adjacent myotubes, indicated by an identical stimulus threshold for calcium transients in the two coupled myotubes. These findings support the feasibility of creating genetically engineered cells for conduction of electrical impulses that could lead to cell-based therapy for arrhythmias. See p 394.
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SHORT-TERM TREATMENT WITH ATORVASTATIN REDUCES PLATELET CD40 LIGAND AND THROMBIN GENERATION IN HYPERCHOLESTEROLEMIC PATIENTS, by Sanguigni et al. |
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In patients at risk for coronary heart disease, treatment with HMG-CoA reductase inhibitors (statins) is uniformly associated with a reduction in subsequent cardiovascular events. The magnitude of risk reduction as compared with other lipid-lowering therapies has prompted considerable speculation that statins possess salutory effects distinct from reductions in LDL cholesterol. In this issue of Circulation, Sanguigni and colleagues have found that statin treatment has important implications for thrombosis. In particular, hypercholesterolemic patients treated with HMG-CoA reductase inhibition demonstrated reduced platelet CD40 ligand content and in vivo thrombin generation. This effect was observed before any observed reductions in LDL
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