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10.1016/j.hrthm.2015.06.042 http://scihub22266oqcxt.onion/10.1016/j.hrthm.2015.06.042 C4624040!4624040 !26142302     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26142302 &cmd=llinks): Failed to open stream: HTTP request failed! 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Electrophysiologic consequences of KATP gain of function in the heart: Conduction abnormalities in Cantu syndrome |pdf=|usr=}}{{26142302 }} gab.com Text Electrophysiologic consequences of KATP gain of function in the heart: Conduction abnormalities in Cantu syndrome JO: Heart Rhythm http://www.kidney.de/pget.php?&tw=1&pmid=26142302 #FOAvip BACKGROUND: Gain-of-function (GOF) mutations in the KATP channel subunits Kir6.1 and SUR2 cause Cantu syndrome (CS), a disease characterized by multiple cardiovascular abnormalities. OBJECTIVE: The purpose of this study was to better determine the electrophysiologic consequences of such GOF mutations in the heart. METHODS: We generated transgenic mice (Kir6.1-GOF) expressing ATP-insensitive Kir6.1[G343D] subunits under ?-myosin heavy chain (?-MHC) promoter control, to target gene expression specifically in cardiomyocytes, and performed patch-clamp experiments on isolated ventricular myocytes and invasive electrophysiology on anesthetized mice. RESULTS: In Kir6.1-GOF ventricular myocytes, KATP channels showed decreased ATP sensitivity but no significant change in current density. Ambulatory ECG recordings on Kir6.1-GOF mice revealed AV nodal conduction abnormalities and junctional rhythm. Invasive electrophysiologic analyses revealed slowing of conduction and conduction failure through the AV node but no increase in susceptibility to atrial or ventricular ectopic activity. Surface ECGs recorded from CS patients also demonstrated first-degree AV block and fascicular block. CONCLUSION: The primary electrophysiologic consequence of cardiac KATP GOF is on the conduction system, particularly the AV node, resulting in conduction abnormalities in CS patients who carry KATP GOF mutations. Twit Text FOAVip Electrophysiologic consequences of KATP gain of function in the heart: Conduction abnormalities in Cantu syndrome ????Heart Rhythm http://www.kidney.de/pget.php?&tw=1&pmid=26142302 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26142302 #FOAvip English Wikipedia <ref>{{Cite pmid|26142302 }}</ref> Electrophysiologic consequences of KATP gain of function in the heart: Conduction abnormalities in Cantu syndrome #MMPMID26142302 Levin MD ; Zhang H ; Uchida K ; Grange DK ; Singh GK ; Nichols CG Heart Rhythm 2015[Nov]; 12 (11 ): 2316-24 PMID26142302 show ga BACKGROUND: Gain-of-function (GOF) mutations in the KATP channel subunits Kir6.1 and SUR2 cause Cantu syndrome (CS), a disease characterized by multiple cardiovascular abnormalities. OBJECTIVE: The purpose of this study was to better determine the electrophysiologic consequences of such GOF mutations in the heart. METHODS: We generated transgenic mice (Kir6.1-GOF) expressing ATP-insensitive Kir6.1[G343D] subunits under ?-myosin heavy chain (?-MHC) promoter control, to target gene expression specifically in cardiomyocytes, and performed patch-clamp experiments on isolated ventricular myocytes and invasive electrophysiology on anesthetized mice. RESULTS: In Kir6.1-GOF ventricular myocytes, KATP channels showed decreased ATP sensitivity but no significant change in current density. Ambulatory ECG recordings on Kir6.1-GOF mice revealed AV nodal conduction abnormalities and junctional rhythm. Invasive electrophysiologic analyses revealed slowing of conduction and conduction failure through the AV node but no increase in susceptibility to atrial or ventricular ectopic activity. Surface ECGs recorded from CS patients also demonstrated first-degree AV block and fascicular block. CONCLUSION: The primary electrophysiologic consequence of cardiac KATP GOF is on the conduction system, particularly the AV node, resulting in conduction abnormalities in CS patients who carry KATP GOF mutations. |*Gene Expression Regulation, Developmental [MESH] |Animals [MESH] |Atrioventricular Block/*genetics [MESH] |Brugada Syndrome/genetics [MESH] |Cardiac Conduction System Disease [MESH] |Cardiomegaly/diagnostic imaging/*genetics [MESH] |Cells, Cultured [MESH] |Child, Preschool [MESH] |Disease Models, Animal [MESH] |Echocardiography, Doppler [MESH] |Electrocardiography [MESH] |Electrophysiological Phenomena/genetics [MESH] |G Protein-Coupled Inwardly-Rectifying Potassium Channels/*genetics [MESH] |Humans [MESH] |Hypertrichosis/diagnostic imaging/*genetics [MESH] |KATP Channels/*genetics [MESH] |Male [MESH] |Mice [MESH] |Mice, Transgenic [MESH] |Mutation [MESH] |Myocytes, Cardiac/cytology/physiology [MESH] |Osteochondrodysplasias/diagnostic imaging/*genetics [MESH] |Random Allocation [MESH] |Rare Diseases [MESH]Electrophysiologic consequences of KATP gain of function in the heart:(epmc).pdf DeepDyve Pubget Overpricing