Clinical, biomarker, and genetic predictors of specific types of atrial fibrillation in a community-based cohort: data of the PREVEND study.
Atrial fibrillation (AF) may present variously in time, and AF may progress from self-terminating to non-self-terminating AF, and is associated with impaired prognosis. However, predictors of AF types are largely unexplored. We investigate the clinical, biomarker, and genetic predictors of development of specific types of AF in a community-based cohort.



We included 8042 individuals (319 with incident AF) of the PREVEND study. Types of AF were compared, and multivariate multinomial regression analysis determined associations with specific types of AF.



Mean age was 48.5 ± 12.4 years and 50% were men. The types of incident AF were ascertained based on electrocardiograms; 103(32%) were classified as AF without 2-year recurrence, 158(50%) as self-terminating AF, and 58(18%) as non-self-terminating AF. With multivariate multinomial logistic regression analysis, advancing age (P< 0.001 for all three types) was associated with all AF types, male sex was associated with AF without 2-year recurrence and self-terminating AF (P= 0.031 and P= 0.008, respectively). Increasing body mass index and MR-proANP were associated with both self-terminating (P= 0.009 and P< 0.001) and non-self-terminating AF (P= 0.003 and P< 0.001). The only predictor associated with solely self-terminating AF is prescribed anti-hypertensive treatment (P= 0.019). The following predictors were associated with non-self-terminating AF; lower heart rate (P= 0.018), lipid-lowering treatment prescribed (P= 0.009), and eGFR <60 mL/min/1.73 m2 (P= 0.006). Three known AF-genetic variants (rs6666258, rs6817105, and rs10821415) were associated with self-terminating AF.



We found clinical, biomarker and genetic predictors of specific types of incident AF in a community-based cohort. The genetic background seems to play a more important role than modifiable risk factors in self-terminating AF.
Department of Cardiology, University of Groningen, University Medical Center Groningen, PO Box 30.001, 9700 RB Groningen, The Netherlands.
Anne H
AH
Hobbelt
Department of Cardiology, University of Groningen, University Medical Center Groningen, PO Box 30.001, 9700 RB Groningen, The Netherlands.
Joylene E
JE
Siland
Department of Cardiology, University of Groningen, University Medical Center Groningen, PO Box 30.001, 9700 RB Groningen, The Netherlands.
Bastiaan
B
Geelhoed
Department of Cardiology, University of Groningen, University Medical Center Groningen, PO Box 30.001, 9700 RB Groningen, The Netherlands.
Pim
P
Van Der Harst
Department of Cardiology, University of Groningen, University Medical Center Groningen, PO Box 30.001, 9700 RB Groningen, The Netherlands.
Hans L
HL
Hillege
Department of Cardiology, University of Groningen, University Medical Center Groningen, PO Box 30.001, 9700 RB Groningen, The Netherlands.
Isabelle C
IC
Van Gelder
Department of Cardiology, University of Groningen, University Medical Center Groningen, PO Box 30.001, 9700 RB Groningen, The Netherlands.
Michiel
M
Rienstra
D000328:Adult; D000367:Age Factors; D000419:Albuminuria; D000626:Aminopeptidases / Q000235:genetics; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001281:Atrial Fibrillation / Q000097:blood / Q000453:epidemiology* / Q000235:genetics / Q000503:physiopathology; D009320:Atrial Natriuretic Factor / Q000097:blood*; D001786:Blood Glucose / Q000378:metabolism; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000378:metabolism; D015331:Cohort Studies; D003404:Creatinine / Q000097:blood; D055316:Cystatin C / Q000097:blood; D005260:Female; D020022:Genetic Predisposition to Disease; D005919:Glomerular Filtration Rate; D006339:Heart Rate; D018398:Homeodomain Proteins / Q000235:genetics; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000453:epidemiology*; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D020097:Natriuretic Peptide, Brain / Q000097:blood; D009765:Obesity / Q000453:epidemiology*; D010446:Peptide Fragments / Q000097:blood; D017856:Phosphotransferases (Phosphate Group Acceptor) / Q000235:genetics; D020641:Polymorphism, Single Nucleotide; D012307:Risk Factors; D012737:Sex Factors; D051640:Small-Conductance Calcium-Activated Potassium Channels / Q000235:genetics; D014157:Transcription Factors / Q000235:genetics; D000097577:Homeobox Protein PITX2
D000626:Aminopeptidases; D000959:Antihypertensive Agents; D009320:Atrial Natriuretic Factor; D001786:Blood Glucose; D002097:C-Reactive Protein; D003404:Creatinine; D055316:Cystatin C; D018398:Homeodomain Proteins; D000960:Hypolipidemic Agents; D020097:Natriuretic Peptide, Brain; D010446:Peptide Fragments; D017856:Phosphotransferases (Phosphate Group Acceptor); D051640:Small-Conductance Calcium-Activated Potassium Channels; D014157:Transcription Factors; D000097577:Homeobox Protein PITX2; C406328:KCNN3 protein, human; C552580:midregional pro-atrial natriuretic peptide, human; C109794:pro-brain natriuretic peptide (1-76); C022371:phosphomevalonate kinase; C501315:AOPEP protein, human