PubMed · 13834455
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L STERN, J LIND. 1960. Neonatal T wave patterns.. https://doi.org/10.1111/j.1651-2227.1960.tb07746.x
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The Food and Drug Administration (FDA) is reclassifying arrhythmia detector and alarm devices from class III to class II (special controls). This device is used to monitor an electrocardiogram (ECG) and to produce a visible or audible signal or alarm when an atrial or ventricular arrhythmia occurs. An atrial or ventricular arrhythmia occurs during a premature contraction or ventricular fibrillation. FDA is reclassifying this device based on new information contained in reclassification petitions regarding the device submitted by the Health Industry Manufacturers Association (HIMA) (now known as Advamed), Quinton Instrument Co., and Zymed Medical Instrumentation. Elsewhere in this issue of the Federal Register, FDA is announcing the availability of the guidance document that will serve as the special control for this device. FDA is taking this action under the Federal Food, Drug, and Cosmetic Act (the act), as amended by the Medical Device Amendments of 1976 (the 1976 amendments), the Safe Medical Devices Act of 1990 (the SMDA), the Food and Drug Administration Modernization Act of 1997 (the FDAMA), and the Medical Device User Fee and Modernization Act of 2002 (MDUFMA).
Voltage-gated potassium channels formed with the cardiac subunit HERG and a polymorphic variant of MinK-related peptide 1 (MiRP1) exhibit increased susceptibility to the antibiotic sulfamethoxazole (SMX) compared with channels formed with wild-type (WT) subunits. Here the molecular bases for SMX high-affinity block are investigated. The polymorphism causes a benign T to A amino acid mutation at position 8 (T8A) that destroys an N-glycosylation site of MiRP1. In vitro disruption of glycosylation by mutagenesis or in vivo by treatment with neuraminidase is associated with increased susceptibility to SMX and to other elementary agents such as divalent cations. Defective glycosylation does not affect the ability of T8A to form stable complexes with HERG, but rather it increases drug susceptibility through structural modifications in the channel complex. We conclude that N-glycosylation may play a key role in the etiology of life-threatening arrhythmia.
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