Genome-wide association studies and resting heart rate

TY - JOUR

T1 - Genome-wide association studies and resting heart rate

AU - Oskari Kilpeläinen, Tuomas

PY - 2016/11/1

Y1 - 2016/11/1

N2 - Genome-wide association studies (GWASs) have revolutionized the search for genetic variants regulating resting heart rate. In the last 10 years, GWASs have led to the identification of at least 21 novel heart rate loci. These discoveries have provided valuable insights into the mechanisms and pathways that regulate heart rate and link heart rate to cardiovascular morbidity and mortality. GWASs capture majority of genetic variation in a population sample by utilizing high-throughput genotyping chips measuring genotypes for up to several millions of SNPs across the genome in thousands of individuals. This allows the identification of the strongest heart rate associated signals at genome-wide level. While GWASs provide robust statistical evidence of the association of a given genetic locus with heart rate, they are only the starting point for detailed follow-up studies to locate the causal variants and genes and gain further insights into the biological mechanisms underlying the observed associations.

AB - Genome-wide association studies (GWASs) have revolutionized the search for genetic variants regulating resting heart rate. In the last 10 years, GWASs have led to the identification of at least 21 novel heart rate loci. These discoveries have provided valuable insights into the mechanisms and pathways that regulate heart rate and link heart rate to cardiovascular morbidity and mortality. GWASs capture majority of genetic variation in a population sample by utilizing high-throughput genotyping chips measuring genotypes for up to several millions of SNPs across the genome in thousands of individuals. This allows the identification of the strongest heart rate associated signals at genome-wide level. While GWASs provide robust statistical evidence of the association of a given genetic locus with heart rate, they are only the starting point for detailed follow-up studies to locate the causal variants and genes and gain further insights into the biological mechanisms underlying the observed associations.

U2 - 10.1016/j.jelectrocard.2016.07.022

DO - 10.1016/j.jelectrocard.2016.07.022

M3 - Journal article

C2 - 27519143

SN - 0022-0736

VL - 49

SP - 860

EP - 863

JO - Journal of Electrocardiology

JF - Journal of Electrocardiology

IS - 6

ER -