Browsing by Subject "Carotid Stenosis"

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    Geographic variation in carotid revascularization among Medicare beneficiaries, 2003-2006.
    (Archives of internal medicine, 2010-07) Patel, MR; Greiner, MA; DiMartino, LD; Schulman, KA; Duncan, PW; Matchar, DB; Curtis, LH

    Background

    Little is known about patterns in the use of carotid revascularization since a 2004 Medicare national coverage decision supporting carotid artery stenting. We examined geographic variation in and predictors of carotid endarterectomy and carotid stenting.

    Methods

    Analysis of claims from the Centers for Medicare & Medicaid Services from January 1, 2003, through December 31, 2006. Patients were 65 years or older and had undergone carotid endarterectomy or carotid stenting. The main outcome measures were annual age-adjusted rates of carotid endarterectomy and carotid stenting, factors associated with the use of carotid revascularization, and mortality rate at 30 days and 1 year.

    Results

    The rate of endarterectomy decreased from 3.2 per 1000 person-years in 2003 to 2.6 per 1000 person-years in 2006. After adjustment for demographic and clinical characteristics, there was significant geographic variation in the odds of carotid revascularization, with the East North Central region having the greatest odds of endarterectomy (odds ratio, 1.60; 95% confidence interval, 1.55-1.65) and stenting (1.61; 1.46-1.78) compared with New England. Prior endarterectomy (odds ratio, 3.06; 95% confidence interval, 2.65-3.53) and coronary artery disease (2.12; 2.03-2.21) were strong predictors of carotid stenting. In 2005, mortality was 1.2% at 30 days and 6.8% at 1 year for endarterectomy and 2.3% at 30 days and 10.3% at 1 year for stenting.

    Conclusions

    Significant geographic variation exists for carotid endarterectomy and carotid stenting. Prior endarterectomy and coronary disease were associated with greater odds of carotid stenting.
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    Targeting Gbeta gamma signaling in arterial vascular smooth muscle proliferation: a novel strategy to limit restenosis.
    (Proc Natl Acad Sci U S A, 1999-03-30) Iaccarino, G; Smithwick, LA; Lefkowitz, RJ; Koch, WJ
    Restenosis continues to be a major problem limiting the effectiveness of revascularization procedures. To date, the roles of heterotrimeric G proteins in the triggering of pathological vascular smooth muscle (VSM) cell proliferation have not been elucidated. betagamma subunits of heterotrimeric G proteins (Gbetagamma) are known to activate mitogen-activated protein (MAP) kinases after stimulation of certain G protein-coupled receptors; however, their relevance in VSM mitogenesis in vitro or in vivo is not known. Using adenoviral-mediated transfer of a transgene encoding a peptide inhibitor of Gbetagamma signaling (betaARKct), we evaluated the role of Gbetagamma in MAP kinase activation and proliferation in response to several mitogens, including serum, in cultured rat VSM cells. Our results include the striking finding that serum-induced proliferation of VSM cells in vitro is mediated largely via Gbetagamma. Furthermore, we studied the effects of in vivo adenoviral-mediated betaARKct gene transfer on VSM intimal hyperplasia in a rat carotid artery restenosis model. Our in vivo results demonstrated that the presence of the betaARKct in injured rat carotid arteries significantly reduced VSM intimal hyperplasia by 70%. Thus, Gbetagamma plays a critical role in physiological VSM proliferation, and targeted Gbetagamma inhibition represents a novel approach for the treatment of pathological conditions such as restenosis.