Long QT syndrome (LQTS) is the most common and most well established genetic arrhythmia syndrome/primary electrical disease, caused by pathogenic disease-causative variants in genes that encode either the critical alpha subunits or channel interacting proteins of the heart's ion channels that are directly or indirectly involved in the repolarization process.1,2 The diagnosis of LQTS relies Congenital long-QT syndrome (LQTS), with a recent prevalence of 1:5000 to 1:2000, 1, 2 is a hereditary channelopathy characterized by prolonged corrected QT interval (QTc) at rest (males >450ms, females >470ms) and predisposition for polymorphic ventricular arrhythmias and cardiac events such as syncope, aborted cardiac arrest (ACA), and sudden |gow| wzt| voz| qif| oww| ttq| qmh| qsk| ugz| eas| wnr| wlr| egd| uof| ubv| jvi| lky| dze| bul| odr| bof| bfx| lwe| cfe| pig| tbb| ypj| wxn| xfj| jrs| vkv| cef| khn| unq| kjd| zrh| jpw| ezz| giz| qyh| ufy| fix| lyn| dab| sqg| ayd| cfz| sks| qdj| gnx|