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Genetic variants may account for paradoxical racial difference in AF risk
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An atrial fibrillation–associated single nucleotide polymorphism, rs10824026, may partially be the cause of the paradoxical racial difference in risk for atrial fibrillation between white and black individuals, researchers reported in JAMA Cardiology.
Jason D. Roberts, MD, MAS, from the section of cardiac electrophysiology, division of cardiology, department of medicine at the University of California, San Francisco, and colleagues sought to investigate why black individuals have greater risk factors for AF than white individuals, but are less likely to develop AF. The researchers conducted a genome-wide admixture analysis and candidate single nucleotide polymorphism (SNP) study using data from three cohort studies: the Cardiovascular Health Study, the Atherosclerosis Risk in Communities (ARIC) Study, and the Health, Aging and Body Composition Study.
According to the analysis, SNP rs10824026 (chromosome 10: position 73661450) was a mediator in the higher risk for AF in white individuals compared with their black counterparts in the Cardiovascular Health Study (11.4%; 95% CI, 2.9-29.9) and the ARIC Study (31.7%; 95% CI, 16-53). During admixture mapping of black individuals in the Cardiovascular Health Study, the ARIC Study and the Health, Aging and Body Composition Study, no novel genetic loci associated with the arrhythmia were identified.
“No additional genetic variants accounting for a significant portion of the differential racial risk of AF were identified with genome-wide admixture mapping, suggesting that additional genetic or environmental influences beyond single SNPs in isolation may account for the paradoxical racial risk of AF among white individuals and black individuals,” the researchers wrote.
In a related editorial, Thomas D. Stamos, MD, and Dawood Darbar, MD, from the division of cardiology at the University of Illinois, acknowledged that these findings “provide some insight into the role of common genetic variants in mediating the AF paradox in black individuals. However, it also highlights some of the challenges associated with defining the etiologic basis for the differential racial risk of AF.”
Stamos and Darbar suggested that possible reasons for the study’s failure to identify any AF-associated alleles with admixture mapping may be due to inadequate power or to the fact that currently less than 10% of the heritability of the arrhythmia is known.
The missing heritability, Stamos and Darbar wrote, may be partially due to “multiple low-level genetic variants that cannot be uncovered by current approaches or by gene-gene and/or gene-environment interactions.” – by Tracey Romero
Disclosure: The researchers, Darbar and Stamos report no relevant financial disclosures.
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