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May warrant autoimmune evaluation in unexplained QT prolongation; extends mechanistic understanding but leaves clinical translation open.
Anti-Ro/SSA indicates anti-Ro/Sjogren's syndrome-related antigen A; hERG, human ether-a-go-go-related gene K + -channel; I CaL , L-type calcium current; I K1 , inward rectifier K + -current; I KAch , acetylcholine-activated current; I Kr , rapid component of the delayed rectifier potassium current; I Ks , slow component of the delayed rectifier potassium current; I Na , sodium current; I to , transient outward potassium current; LQTS, long-QT syndrome; MiRP, MinK related protein 1; TNF-a, tumor necrosis factor-a.*Proposed, because no direct evidence is currently available.† A more comprehensive, detailed, and frequently updated list of QT-prolonging drugs is available at the website (https://www.crediblemeds.org).‡ Although hERG inhibition with I Kr decrease is the mechanism involved in most cases, some drugs can inhibit other potassium currents (I to , I Ks , or I K1 ) or augment sodium or calcium currents (I Na or I CaL ).
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Lazzerini et al. (2018) studied this question.
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