What you carry at this position in your DNA and what research says about it.
Cardiac QT Interval: 7/10 evidence, 29 publications.
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Sample genotype (not yours): G/G
Longer QT Interval and Drug Sensitivity
This genotype is associated with a prolonged cardiac QT interval and altered sensitivity to several common medications.
What this genotype means: Prolonged baseline QT interval; Increased mortality risk on glibenclamide; Altered response to calcium channel blockers.
Sample genotype (not yours): G/T
Typical QT Interval with Drug Sensitivity
This genotype is associated with an average cardiac QT interval but carries specific drug-response variations.
What this genotype means: Average baseline QT interval; Altered sensitivity to sulfonylureas; Increased QT prolongation risk with certain anti-nausea drugs.
Sample genotype (not yours): T/T
Shorter QT Interval and Typical Drug Response
This genotype is associated with a shorter baseline QT interval and standard safety profiles for several common medications.
What this genotype means: Shorter baseline QT interval; Standard response to sulfonylureas; Typical safety profile for calcium channel blockers.
Gene function and biological role
Gene Function: The NOS1AP gene encodes the nitric oxide synthase 1 adaptor protein, which plays a critical role in regulating cardiac repolarization [1]. It modulates the activity of key ion channels in the heart, thereby influencing the duration of the cardiac action potential [2]. Variations in this gene are among the most significant genetic determinants of the QT interval in the general population [1]. By affecting intracellular calcium handling and nitric oxide signaling, NOS1AP helps maintain stable electrical activity in cardiac tissue [2]. Alterations in its expression or function can predispose individuals to cardiac arrhythmias under physiological stress or drug exposure [2].
Variant Impact: The rs10494366 variant is an intronic single nucleotide polymorphism located within the NOS1AP gene. The G allele of this variant is strongly associated with a prolonged QT interval, representing delayed cardiac repolarization [1]. This genetic change alters the regulatory dynamics of cardiac electrical recovery, making carriers more sensitive to certain medications [3]. Specifically, the variant modifies how the heart responds to drugs that affect calcium and potassium currents [3]. Consequently, it serves as a key marker for both baseline electrocardiographic traits and drug-induced cardiac side effects [1] [3].
Key Insight: A single letter change in this gene can alter the heart's electrical recovery time by several milliseconds, a magnitude comparable to the effect of some clinical medications.
Location: NOS1AP. Chromosome 1 · 1q23.3 · 162.1 Mb
Estimated prevalence by population
Global 22.6%; European 13.0%; African 38.2%; East Asian 46.3%; South Asian 41.3%; Americas 16.7%; Ashkenazi 17.6%; Finnish 13.5%; Middle Eastern 17.5%; Amish 20.4%.
Estimated GG genotype frequency.
Global 46.7%; European 46.1%; African 47.2%; East Asian 43.5%; South Asian 45.9%; Americas 48.3%; Ashkenazi 48.7%; Finnish 46.5%; Middle Eastern 48.6%; Amish 49.5%.
Estimated GT genotype frequency.
Global 30.7%; European 40.8%; African 14.6%; East Asian 10.2%; South Asian 12.8%; Americas 35.0%; Ashkenazi 33.7%; Finnish 40.1%; Middle Eastern 33.9%; Amish 30.1%.
Estimated TT genotype frequency.
Showing effects for G/G genotype
Cardiovascular & Metabolic
Heart Rhythm & Conduction
QT Interval. Evidence: 7/10. Source: PMID 16648850. Prolonged QT.
Pharmacogenomics
Diabetes Medication Response
Sulfonylurea Response. Evidence: 5/10. Source: PMID 18551039. Reduced Efficacy.
Cardiovascular Drug Response
Calcium Channel Blocker Safety. Evidence: 5/10. Source: PMID 19076153. Higher Risk.
Adverse Drug Reactions
Anti-Nausea Drug Safety. Evidence: 5/10. Source: PMID 21663814. Typical Risk.
Showing effects for G/T genotype
QT Interval. Evidence: 7/10. Source: PMID 16648850. Typical QT.
Anti-Nausea Drug Safety. Evidence: 5/10. Source: PMID 21663814. Higher Risk.
Showing effects for T/T genotype
QT Interval. Evidence: 7/10. Source: PMID 16648850. Shorter QT.
Sulfonylurea Response. Evidence: 5/10. Source: PMID 18551039. Typical Response.
Calcium Channel Blocker Safety. Evidence: 5/10. Source: PMID 19076153. Typical Risk.
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Carrying two copies of the G allele is linked to a prolonged heart-rate-corrected QT interval, which represents a longer time for the heart ventricles to recharge electrically [1]. Studies indicate that each G allele adds approximately 3.8 milliseconds to the QT duration, meaning homozygotes experience a cumulative prolongation [1]. While this baseline increase does not automatically translate to sudden cardiac arrest in healthy individuals, it can interact unfavorably with certain drugs [2]. For instance, users of dihydropyridine calcium channel blockers or the sulfonylurea glibenclamide with this genotype have shown higher cardiovascular mortality rates in clinical cohorts [3] [4]. Conversely, when taking digoxin, this genotype is associated with a more pronounced shortening of the QT interval [5]. Understanding these interactions is highly valuable for personalizing cardiovascular and diabetes therapies.
Prolonged baseline QT interval; Increased mortality risk on glibenclamide; Altered response to calcium channel blockers.
Sample genotype: GT (Heterozygous)
Carrying one G allele and one T allele generally results in an average baseline QT interval, balancing the opposing genetic influences [1]. However, this intermediate genetic profile still carries important pharmacogenomic implications that can affect medication safety [2]. Individuals with this genotype may experience reduced glucose-lowering efficacy and higher mortality risks when treated with the sulfonylurea glibenclamide [3]. Additionally, there is an increased risk of all-cause and cardiovascular mortality when starting dihydropyridine calcium channel blockers [4]. On the other hand, this genotype is associated with an increased risk of QT prolongation when using 5-HT3 receptor antagonists like dolasetron or granisetron for nausea [2]. These findings highlight the importance of genetic screening prior to prescribing common cardiac and metabolic drugs.
Average baseline QT interval; Altered sensitivity to sulfonylureas; Increased QT prolongation risk with certain anti-nausea drugs.
Sample genotype: TT (Homozygous)
Carrying two copies of the T allele is associated with a shorter baseline heart-rate-corrected QT interval, representing efficient electrical recovery of the heart ventricles [1]. This shorter duration is generally considered protective against drug-induced arrhythmias that result from QT prolongation [2]. Clinical studies show that patients with this genotype experience optimal glucose-lowering effects and lower mortality rates when treated with sulfonylureas like glibenclamide compared to G allele carriers [3]. Furthermore, starting dihydropyridine calcium channel blockers does not carry the elevated cardiovascular mortality risks observed in those with the G allele [4]. While there is a documented risk of QT prolongation when taking specific anti-nausea medications like dolasetron, the baseline shorter QT interval provides a favorable physiological starting point [5]. Overall, this genotype represents a highly stable cardiac electrical profile.
Shorter baseline QT interval; Standard response to sulfonylureas; Typical safety profile for calcium channel blockers.
Variants with shared genetic architecture
rs12143842 · NOS1AP Gene · Chr 1 · QT Interval Duration
rs11153730 · PLN Gene · Chr 6 · QT Interval Duration
rs1805123 · KCNH2 Gene · Chr 7 · Heart Rhythm
A common genetic variant in the NOS1 regulator NOS1AP modulates cardiac repolarization.
Cardiac levels of NOS1AP RNA from right ventricular tissue recovered during lead extraction.
Common NOS1AP variants are associated with a prolonged QTc interval in the Rotterdam Study.
Content updated August 2026.
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