What you carry at this position in your DNA and what research says about it.
Cardiac Arrhythmia Risk: 10/10 evidence, 26 publications.
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Sample genotype (not yours): C/C
Typical Risk of Cardiac Arrhythmia
Presence of the reference C allele on both chromosomes means you lack the risk-associated T variant. This genotype is associated with a typical QT interval and standard cardiac electrical stability.
What this genotype means: Typical cardiac electrical activity; Standard response to QT-prolonging drugs.
Sample genotype (not yours): C/T
Increased Risk of Drug-Induced Arrhythmia
One copy of the T allele increases susceptibility to QT prolongation and abnormal heart rhythms. This risk is particularly pronounced when taking certain medications that affect cardiac electrical activity.
What this genotype means: Increased sensitivity to QT-prolonging medications; Slightly elevated risk of cardiac events under stress.
Sample genotype (not yours): T/T
Higher Risk of Drug-Induced Arrhythmia
Two copies of the T allele significantly increase the risk of QT prolongation and cardiac arrhythmias. This susceptibility is highly relevant when taking medications known to prolong the QT interval.
What this genotype means: Elevated risk of drug-induced long QT syndrome; Potential susceptibility to rare hereditary cardiac syndromes.
Gene function and biological role
Gene Function: KCNE1 encodes a potassium channel beta-subunit that is crucial for regulating the electrical activity of the heart [1]. It partners with other channel proteins to control the flow of potassium ions, which helps the heart muscle repolarize and relax after each beat [2]. Mutations or variations in this gene can disrupt these electrical currents, leading to abnormal heart rhythms [3]. This gene is also expressed in the inner ear, where potassium recycling is essential for normal hearing [4].
Variant Impact: Known as p.Asp85Asn or D85N, this missense change replaces aspartate with asparagine at position 85 of the KCNE1 protein. This amino acid substitution alters the regulatory subunit's structure, reducing the potassium currents that help the heart reset between beats [2]. The change makes the cardiac electrical system more vulnerable to delays, especially when challenged by certain medications [5]. While common in some populations, it is widely studied as a genetic modifier that increases susceptibility to cardiac arrhythmias [6].
Key Insight: This variant acts as a silent genetic modifier that often only reveals itself when a person takes common medications like certain antibiotics or antidepressants.
Location: KCNE1. Chromosome 21 · 21q22.12 · 34.4 Mb
Estimated prevalence by population
No frequency data available
This variant is not present in the gnomAD database.
Showing effects for C/C genotype
Cardiovascular & Metabolic
Heart Rhythm & Conduction
Long QT Syndrome. Evidence: 6/10. Source: PMID 32429735. Typical Risk.
QT Interval. Evidence: 10/10. Source: PMID 36050321. Typical.
Pharmacogenomics
Adverse Drug Reactions
Drug-Induced Arrhythmia. Evidence: 6/10. Source: PMID 22100668. Typical Risk.
Organ Systems
Hearing & Balance
Hearing Loss. Evidence: 5/10. Source: PMID 16823764. Typical Risk.
Showing effects for C/T genotype
Long QT Syndrome. Evidence: 6/10. Source: PMID 32429735. Increased Risk.
QT Interval. Evidence: 10/10. Source: PMID 36050321. Slightly Longer.
Drug-Induced Arrhythmia. Evidence: 6/10. Source: PMID 22100668. Increased Risk.
Showing effects for T/T genotype
Long QT Syndrome. Evidence: 6/10. Source: PMID 32429735. Higher Risk.
QT Interval. Evidence: 10/10. Source: PMID 36050321. Longer.
Drug-Induced Arrhythmia. Evidence: 6/10. Source: PMID 22100668. Higher Risk.
Hearing Loss. Evidence: 5/10. Source: PMID 16823764. Slightly Increased.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Possessing two copies of the reference C allele, which encodes the standard aspartate amino acid at position 85, is associated with normal potassium channel function in the heart. This genotype does not carry the susceptibility to drug-induced QT prolongation or hereditary long QT syndrome linked to the T allele [1]. Large-scale genetic studies show that individuals with this genotype have a typical QT interval, representing a stable cardiac repolarization phase [2]. Furthermore, clinical guidelines and pharmacogenomic databases indicate no elevated risk of developing drug-induced arrhythmias when taking common QT-prolonging medications [3]. This baseline status means standard medical care and prescribing practices apply. Regular cardiovascular health maintenance remains the primary focus. No special precautions are typically recommended for this genotype.
Typical cardiac electrical activity; Standard response to QT-prolonging drugs.
Sample genotype: CT (Heterozygous)
A single copy of the T allele (Asn85) acts as a genetic modifier for cardiac repolarization. This single copy is sufficient to reduce potassium currents, making the heart's electrical system more sensitive to external stressors [1]. Clinical studies have shown that carriers have a significantly higher risk of developing drug-induced long QT syndrome and a rare, dangerous arrhythmia called Torsades de Pointes when exposed to certain drugs [2]. These medications include common antibiotics, antiarrhythmics, and antidepressants [3]. While many carriers never experience symptoms, knowing this status can help healthcare providers select safer alternative medications. Electrocardiogram monitoring may be considered when initiating high-risk drugs. This genetic marker serves as an important tool for personalized medicine.
Increased sensitivity to QT-prolonging medications; Slightly elevated risk of cardiac events under stress.
Sample genotype: TT (Homozygous)
Two copies of the T allele (Asn85) lead to a more pronounced reduction in cardiac potassium currents. This genotype is associated with a significantly increased risk of long QT syndrome and drug-induced arrhythmias [1]. When exposed to QT-prolonging drugs like sotalol or amiodarone, individuals with this genotype are at a higher risk of developing Torsades de Pointes [2]. Additionally, in rare cases, carrying two copies of this variant has been linked to recessive forms of hereditary long QT syndromes [3]. Healthcare providers can use this information to avoid high-risk medications and monitor cardiac health more closely. Preventive measures often focus on avoiding known triggers of arrhythmia. This genotype represents a key genetic risk factor for cardiac electrical instability.
Elevated risk of drug-induced long QT syndrome; Potential susceptibility to rare hereditary cardiac syndromes.
Variants with shared genetic architecture
rs1805127 · KCNE1 Gene · Chr 21 · Atrial Fibrillation Risk
rs120074184 · KCNQ1 Gene · Chr 11 · Long QT Syndrome Risk
rs120074186 · KCNQ1 Gene · Chr 11 · Long QT Syndrome Risk
D85N, a KCNE1 polymorphism, is a disease-causing gene variant in long QT syndrome.
Content updated August 2026.
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