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pubmed-article:7634458pubmed:abstractTextThe most common form of idiopathic ventricular tachycardia (VT) is repetitive monomorphic VT (RMVT), which is characterized by frequent ventricular ectopy and salvos of nonsustained VT with intervening sinus rhythm. Unlike most other forms of idiopathic VT, this tachycardia typically occurs at rest and is nonsustained. The mechanism of RMVT is undefined. Because of a common site of origin, the right ventricular outflow tract (RVOT), we hypothesized that RMVT is mechanistically related to paroxysmal sustained, exercise-induced VT, which has been shown to be consistent with cAMP-mediated triggered activity. Therefore, in this study, we sought to identify (1) the mechanism of RMVT at the cellular level by using electropharmacological probes known to activate either stimulatory or inhibitory G proteins and thereby modify intracellular cAMP levels, (2) potential autonomic triggers of RMVT through analysis of heart rate variability, and (3) whether well-characterized somatic activating mutations in the stimulatory G protein, G alpha s, underlie RMVT.lld:pubmed
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pubmed-article:7634458pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:7634458pubmed:articleTitleMechanism of repetitive monomorphic ventricular tachycardia.lld:pubmed
pubmed-article:7634458pubmed:affiliationDepartment of Medicine, New York Hospital-Cornell Medical Center, NY 10021, USA.lld:pubmed
pubmed-article:7634458pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:7634458pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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