Relations between circulating microRNAs and atrial fibrillation: data from the Framingham Offspring Study
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AuthorsMcManus, David D.
Larson, Martin G.
Ellinor, Patrick T.
Freedman, Jane E.
Benjamin, Emelia J.
UMass Chan AffiliationsDepartment of Quantitative Health Sciences
Meyers Primary Care Institute
Department of Medicine, Division of Cardiology
Document TypeJournal Article
MetadataShow full item record
AbstractBACKGROUND: MicroRNA (miRNA) expression in atrial tissue has been implicated in pathologic susceptibility to atrial fibrillation (AF). Nevertheless, data on how circulating levels relate to AF are limited. OBJECTIVE: The purpose of this study was to test the hypothesis that circulating miRNAs are associated with AF. METHODS: Among 2445 Framingham Heart Study Offspring participants, we measured the expression of 385 circulating whole blood miRNAs by high-throughput quantitative reverse transcriptase polymerase chain reaction. We related miRNA levels with prevalent and new-onset AF. RESULTS: Mean age of the cohort was 66.3 +/- 8.9 years, and 56% were women; 153 participants had clinically apparent AF at baseline, and 107 developed AF during median follow-up of 5.4 years. miRNA-328 (miR-328) expression was lower among participants with prevalent AF (8.76 cycle threshold) compared to individuals with no AF (7.75 cycle threshold, P < .001). The association between miR-328 and prevalent AF persisted after adjustment for age, sex, and technical covariates (odds ratio 1.21, P = 1.8 x 10(-4)) but was attenuated in analyses adjusting for clinical AF risk factors (odds ratio 1.14, P = .017). In contrast to the associations between miR-328 and prevalent AF, none of the circulating miRNAs were associated with incident AF. CONCLUSION: Circulating levels of miR-328, a miRNA known to promote atrial electrical remodeling by reducing L-type Ca(2+) channel density, were associated with prevalent AF. Adjustment for risk factors that promote atrial remodeling, including hypertension, attenuated the association between miR-328 and AF, potentially implicating miR-328 as a potential mediator of atrial remodeling and AF vulnerability. reserved.
Heart Rhythm. 2014 Apr;11(4):663-9. doi: 10.1016/j.hrthm.2014.01.018. Link to article on publisher's site
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/37280