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Research Article Free access | 10.1172/JCI1582

Right ventricular outflow tract tachycardia due to a somatic cell mutation in G protein subunitalphai2.

B B Lerman, B Dong, K M Stein, S M Markowitz, J Linden, and D F Catanzaro

Department of Medicine, Division of Cardiology, The New York Hospital-Cornell Medical Center, New York, 10021, USA. blerman@mail.med.cornell.edu

Find articles by Lerman, B. in: JCI | PubMed | Google Scholar

Department of Medicine, Division of Cardiology, The New York Hospital-Cornell Medical Center, New York, 10021, USA. blerman@mail.med.cornell.edu

Find articles by Dong, B. in: JCI | PubMed | Google Scholar

Department of Medicine, Division of Cardiology, The New York Hospital-Cornell Medical Center, New York, 10021, USA. blerman@mail.med.cornell.edu

Find articles by Stein, K. in: JCI | PubMed | Google Scholar

Department of Medicine, Division of Cardiology, The New York Hospital-Cornell Medical Center, New York, 10021, USA. blerman@mail.med.cornell.edu

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Department of Medicine, Division of Cardiology, The New York Hospital-Cornell Medical Center, New York, 10021, USA. blerman@mail.med.cornell.edu

Find articles by Linden, J. in: JCI | PubMed | Google Scholar

Department of Medicine, Division of Cardiology, The New York Hospital-Cornell Medical Center, New York, 10021, USA. blerman@mail.med.cornell.edu

Find articles by Catanzaro, D. in: JCI | PubMed | Google Scholar

Published June 15, 1998 - More info

Published in Volume 101, Issue 12 on June 15, 1998
J Clin Invest. 1998;101(12):2862–2868. https://doi.org/10.1172/JCI1582.
© 1998 The American Society for Clinical Investigation
Published June 15, 1998 - Version history
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Abstract

Idiopathic ventricular tachycardia is a generic term that describes the various forms of ventricular arrhythmias that occur in patients without structural heart disease and in the absence of the long QT syndrome. Many of these tachycardias are focal in origin, localize to the right ventricular outflow tract (RVOT), terminate in response to beta blockers, verapamil, vagal maneuvers, and adenosine, and are thought to result from cAMP-mediated triggered activity. DNA was prepared from biopsy samples obtained from myocardial tissue from a patient with adenosine-insensitive idiopathic ventricular tachycardia arising from the RVOT. Genomic sequences of the inhibitory G protein Galphai2 were determined after amplification by PCR and subcloning. A point mutation (F200L) in the GTP binding domain of the inhibitory G protein Galphai2 was identified in a biopsy sample from the arrhythmogenic focus. This mutation was shown to increase intracellular cAMP concentration and inhibit suppression of cAMP by adenosine. No mutations were detected in Galphai2 sequences from myocardial tissue sampled from regions remote from the origin of tachycardia, or from peripheral lymphocytes. These findings suggest that somatic cell mutations in the cAMP-dependent signal transduction pathway occurring during myocardial development may be responsible for some forms of idiopathic ventricular tachycardia.

Version history
  • Version 1 (June 15, 1998): No description

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