Abstract
Abnormalities in heart rhythm continue to cause high rates of illness and death. Better treatment could be provided by solving two main challenges: the early identification of patients who are at risk, and the characterization of molecular pathways that culminate in arrhythmias. By analysing mechanisms that increase susceptibility to arrhythmia in individuals with genetic syndromes, it might be possible to improve current therapies and to develop new ways to treat and prevent common arrhythmias.
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Acknowledgements
This work was supported in part by grants from the United States Public Health Service.
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D.M.R. accepted fees for one-time consultations on QT prolongation by new non-cardiovascular therapies, on genetic testing for new drugs, and/or on developing new antiarrhythmic drugs from Sapphire Therapeutics, Atlas Venture Advisors, Pfizer, Avanir Pharmaceuticals, Baker Brothers Advisors, CardioKine and Eli Lilly and Company. D.M.R. also is paid royalties on a patent on D85N as a predictive single-nucleotide polymorphism for drug-induced long-QT syndrome. B.C.K. declares no competing interests.
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Correspondence should be addressed to D.M.R. (dan.roden@vanderbilt.edu).
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Knollmann, B., Roden, D. A genetic framework for improving arrhythmia therapy. Nature 451, 929–936 (2008). https://doi.org/10.1038/nature06799
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DOI: https://doi.org/10.1038/nature06799
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