<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Christophersen IE</submitter><funding>NCATS NIH HHS</funding><funding>NIDDK NIH HHS</funding><funding>NHLBI NIH HHS</funding><pagination>e001667</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5567993</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(4)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>The P wave on an ECG is a measure of atrial electric function, and its characteristics may serve as predictors for atrial arrhythmias. Increased mean P-wave duration and P-wave terminal force traditionally have been used as markers for left atrial enlargement, and both have been associated with increased risk of atrial fibrillation. Here, we explore the genetic basis of P-wave morphology through meta-analysis of genome-wide association study results for P-wave duration and P-wave terminal force from 12 cohort studies.&lt;h4>Methods and results&lt;/h4>We included 44 456 individuals, of which 6778 (16%) were of African ancestry. Genotyping, imputation, and genome-wide association study were performed at each study site. Summary-level results were meta-analyzed centrally using in</pubmed_abstract><journal>Circulation. Cardiovascular genetics</journal><pubmed_title>Fifteen Genetic Loci Associated With the Electrocardiographic P Wave.</pubmed_title><pmcid>PMC5567993</pmcid><funding_grant_id>K23 HL114724</funding_grant_id><funding_grant_id>UL1 TR000124</funding_grant_id><funding_grant_id>UL1 TR001881</funding_grant_id><funding_grant_id>K24 HL105780</funding_grant_id><funding_grant_id>R01 HL120393</funding_grant_id><funding_grant_id>R01 HL116747</funding_grant_id><funding_grant_id>R01 HL090620</funding_grant_id><funding_grant_id>R01 HL092577</funding_grant_id><funding_grant_id>R01 HL111314</funding_grant_id><funding_grant_id>U01 HL120393</funding_grant_id><funding_grant_id>P30 DK063491</funding_grant_id><funding_grant_id>R01 HL105756</funding_grant_id><funding_grant_id>R01 HL128914</funding_grant_id><funding_grant_id>U01 HL130114</funding_grant_id><pubmed_authors>Peters A</pubmed_authors><pubmed_authors>Psaty BM</pubmed_authors><pubmed_authors>Rotter JI</pubmed_authors><pubmed_authors>Soliman EZ</pubmed_authors><pubmed_authors>Sinner MF</pubmed_authors><pubmed_authors>Chung MK</pubmed_authors><pubmed_authors>Whitsel EA</pubmed_authors><pubmed_authors>Avery CL</pubmed_authors><pubmed_authors>Buzkova P</pubmed_authors><pubmed_authors>Van Wagoner DR</pubmed_authors><pubmed_authors>Uitterlinden A</pubmed_authors><pubmed_authors>Meitinger T</pubmed_authors><pubmed_authors>Alonso A</pubmed_authors><pubmed_authors>Stricker BH</pubmed_authors><pubmed_authors>Felix SB</pubmed_authors><pubmed_authors>Kors JA</pubmed_authors><pubmed_authors>Ellinor PT</pubmed_authors><pubmed_authors>Limacher MC</pubmed_authors><pubmed_authors>Wilhelmsen KC</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Muller C</pubmed_authors><pubmed_authors>Muller-Nurasyid M</pubmed_authors><pubmed_authors>Magnani JW</pubmed_authors><pubmed_authors>Schnabel RB</pubmed_authors><pubmed_authors>Krijthe BP</pubmed_authors><pubmed_authors>Dorr M</pubmed_authors><pubmed_authors>Christophersen IE</pubmed_authors><pubmed_authors>Waldenberger M</pubmed_authors><pubmed_authors>Weng LC</pubmed_authors><pubmed_authors>Niemeijer MN</pubmed_authors><pubmed_authors>Kerr KF</pubmed_authors><pubmed_authors>Sotoodehnia N</pubmed_authors><pubmed_authors>van Duijn C</pubmed_authors><pubmed_authors>Isaacs A</pubmed_authors><pubmed_authors>Hofman A</pubmed_authors><pubmed_authors>Lubitz SA</pubmed_authors><pubmed_authors>Smith JD</pubmed_authors><pubmed_authors>Benjamin EJ</pubmed_authors><pubmed_authors>Yin X</pubmed_authors><pubmed_authors>Reiner AP</pubmed_authors><pubmed_authors>Duan Q</pubmed_authors><pubmed_authors>Tinker LF</pubmed_authors><pubmed_authors>Volker U</pubmed_authors><pubmed_authors>Heckbert SR</pubmed_authors><pubmed_authors>Bis JC</pubmed_authors><pubmed_authors>Arking DE</pubmed_authors><pubmed_authors>Zhang ZM</pubmed_authors><pubmed_authors>Kaab S</pubmed_authors><pubmed_authors>Teumer A</pubmed_authors><pubmed_authors>Barnard J</pubmed_authors><pubmed_authors>Petersmann A</pubmed_authors><pubmed_authors>North KE</pubmed_authors></additional><is_claimable>false</is_claimable><name>Fifteen Genetic Loci Associated With the Electrocardiographic P Wave.</name><description>&lt;h4>Background&lt;/h4>The P wave on an ECG is a measure of atrial electric function, and its characteristics may serve as predictors for atrial arrhythmias. Increased mean P-wave duration and P-wave terminal force traditionally have been used as markers for left atrial enlargement, and both have been associated with increased risk of atrial fibrillation. Here, we explore the genetic basis of P-wave morphology through meta-analysis of genome-wide association study results for P-wave duration and P-wave terminal force from 12 cohort studies.&lt;h4>Methods and results&lt;/h4>We included 44 456 individuals, of which 6778 (16%) were of African ancestry. Genotyping, imputation, and genome-wide association study were performed at each study site. Summary-level results were meta-analyzed centrally using in</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Aug</publication><modification>2026-05-03T21:06:10.231Z</modification><creation>2019-03-26T23:48:43Z</creation></dates><accession>S-EPMC5567993</accession><cross_references><pubmed>28794112</pubmed><doi>10.1161/CIRCGENETICS.116.001667</doi><doi>10.1161/circgenetics.116.001667</doi></cross_references></HashMap>