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Stanley Nattel
Researcher at Montreal Heart Institute
Publications - 802
Citations - 72437
Stanley Nattel is an academic researcher from Montreal Heart Institute. The author has contributed to research in topics: Atrial fibrillation & Heart failure. The author has an hindex of 132, co-authored 778 publications receiving 65700 citations. Previous affiliations of Stanley Nattel include Mayo Clinic & Brigham and Women's Hospital.
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Journal ArticleDOI
Electrophysiological effects of alpha-adrenergic stimulation.
TL;DR: Conduction and refractoriness of normal cardiac tissue (other than the sinus node) are unaffected by direct α‐receptor stimulation, which justifies the use of combined beta and muscarinic blockers to achieve autonomic blockade under most circumstances.
Journal Article
Prognostic implications of transient left ventricular cavitary dilation during exercise and dipyridamole-thallium imaging.
Veilleux M,Jean Lette,Antonio de Pádua Mansur,Bertrand C,Cerino M,Picard M,McNamara D,M C Eybalin,A Levasseur,Stanley Nattel +9 more
TL;DR: Patients with dipyridamole-inducedTLVD are at greater risk than those with exercise-induced TLVD at the authors' institution, and both fatal and nonfatal cardiac events were more frequent in the dipyrinole group.
Journal ArticleDOI
Close connections between contraction and rhythm: a new genetic cause of atrial fibrillation/cardiomyopathy and what it can teach us
TL;DR: This editorial refers to ‘A frameshift deletion in the sarcomere gene MYL4 causes early-onset familial atrial fibrillation’, by D.F. Gudbjartsson et al.
Journal ArticleDOI
Nuclear factor of activated T cells mediates RhoA-induced fibronectin upregulation in glomerular podocytes
Lei Zhu,Xiao-Yan Qi,Lamine Aoudjit,Flaviana Mouawad,Cindy Baldwin,Stanley Nattel,Tomoko Takano +6 more
TL;DR: The results indicate that RhoA activates NFAT by inducing a rise of [Ca(2+)]i in podocytes, which in turn contributes to fibronectin upregulation, which may be responsible for the pathogenesis of certain glomerular diseases such as hypertension-mediated glomerulosclerosis.
Journal ArticleDOI
Cardiac pathways distinguish two epistatic modules enacting BP quantitative trait loci and candidate gene analysis
Cristina Chauvet,Annie Ménard,Johanne Tremblay,Chunjie Xiao,Yanfen Shi,Nathalie L'Heureux,Sophie Cardin,Jean-Claude Tardif,Stanley Nattel,Alan Y. Deng +9 more
TL;DR: The lack of an amino-acid alteration, coupled with a lack of difference in the α1-Na-K-ATPase activity, excluded ATPase, Na+/K+-transporting, α-1 polypeptide as a candidate gene for C2QTL6, a novel diagnostic and/or therapeutic target for essential hypertension and hypertension-associated diseases.