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10.1093/eurheartj/ehaa1051 http://scihub22266oqcxt.onion/10.1093/eurheartj/ehaa1051 33421051!?!33421051 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33421051&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Eur+Heart+J 2021 ; 42 (11): 1073-1081 Nephropedia Template TP {{tp|p=33421051|t=2021. Brugada syndrome and reduced right ventricular outflow tract conduction reserve: a final common pathway?|pdf=|usr=}}{{33421051}} gab.com Text Brugada syndrome and reduced right ventricular outflow tract conduction reserve: a final common pathway JO: Eur Heart J http://www.kidney.de/pget.php?&tw=1&pmid=33421051 #FOAvip Brugada syndrome (BrS) was first described as a primary electrical disorder predisposing to the risk of sudden cardiac death and characterized by right precordial lead ST elevation. Early description of right ventricular structural abnormalities and of right ventricular outflow tract (RVOT) conduction delay in BrS patients set the stage for the current controversy over the pathophysiology underlying the syndrome: channelopathy or cardiomyopathy; repolarization or depolarization. This review examines the current understanding of the BrS substrate, its genetic and non-genetic basis, theories of pathophysiology, and the clinical implications thereof. We propose that the final common pathway for BrS could be viewed as a disease of 'reduced RVOT conduction reserve'. Twit Text FOAVip Brugada syndrome and reduced right ventricular outflow tract conduction reserve: a final common pathway ????Eur Heart J http://www.kidney.de/pget.php?&tw=1&pmid=33421051 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33421051 #FOAvip English Wikipedia <ref>{{Cite pmid|33421051}}</ref> Brugada syndrome and reduced right ventricular outflow tract conduction reserve: a final common pathway? #MMPMID33421051 Behr ER; Ben-Haim Y; Ackerman MJ; Krahn AD; Wilde AAM Eur Heart J 2021[Mar]; 42 (11): 1073-1081 PMID33421051show ga Brugada syndrome (BrS) was first described as a primary electrical disorder predisposing to the risk of sudden cardiac death and characterized by right precordial lead ST elevation. Early description of right ventricular structural abnormalities and of right ventricular outflow tract (RVOT) conduction delay in BrS patients set the stage for the current controversy over the pathophysiology underlying the syndrome: channelopathy or cardiomyopathy; repolarization or depolarization. This review examines the current understanding of the BrS substrate, its genetic and non-genetic basis, theories of pathophysiology, and the clinical implications thereof. We propose that the final common pathway for BrS could be viewed as a disease of 'reduced RVOT conduction reserve'. |*Brugada Syndrome[MESH] |*COVID-19[MESH] |Angiotensin Receptor Antagonists[MESH] |Angiotensin-Converting Enzyme Inhibitors[MESH] |Electrocardiography[MESH] |Hospitals[MESH] |Humans[MESH]Brugada syndrome and reduced right ventricular outflow tract conductio(epmc).pdf DeepDyve Pubget Overpricing