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GWAS Study

Shared genetic pathways contribute to risk of hypertrophic and dilated cardiomyopathies with opposite directions of effect.

Tadros R, Francis C, Xu X et al.

33495596 PubMed ID
GWAS Study Type
402844 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

TR
Tadros R
FC
Francis C
XX
Xu X
VA
Vermeer AMC
HA
Harper AR
HR
Huurman R
KB
Kelu Bisabu K
WR
Walsh R
HE
Hoorntje ET
TR
Te Rijdt WP
BR
Buchan RJ
VV
van Velzen HG
VS
van Slegtenhorst MA
VJ
Vermeulen JM
OJ
Offerhaus JA
BW
Bai W
DM
de Marvao A
LN
Lahrouchi N
BL
Beekman L
KJ
Karper JC
VJ
Veldink JH
KE
Kayvanpour E
PA
Pantazis A
BA
Baksi AJ
WN
Whiffin N
MF
Mazzarotto F
SG
Sloane G
SH
Suzuki H
SD
Schneider-Luftman D
EP
Elliott P
RP
Richard P
AF
Ader F
VE
Villard E
LP
Lichtner P
MT
Meitinger T
TM
Tanck MWT
VT
van Tintelen JP
TA
Thain A
MD
McCarty D
HR
Hegele RA
RJ
Roberts JD
AJ
Amyot J
DM
Dubé MP
CJ
Cadrin-Tourigny J
GG
Giraldeau G
LP
L'Allier PL
GP
Garceau P
TJ
Tardif JC
BS
Boekholdt SM
LR
Lumbers RT
AF
Asselbergs FW
BP
Barton PJR
CS
Cook SA
PS
Prasad SK
OD
O'Regan DP
VD
van der Velden J
VK
Verweij KJH
TM
Talajic M
LG
Lettre G
PY
Pinto YM
MB
Meder B
CP
Charron P
DB
de Boer RA
CI
Christiaans I
MM
Michels M
WA
Wilde AAM
WH
Watkins H
MP
Matthews PM
WJ
Ware JS
BC
Bezzina CR
Chapter II

Abstract

Summary of the research findings

The heart muscle diseases hypertrophic (HCM) and dilated (DCM) cardiomyopathies are leading causes of sudden death and heart failure in young, otherwise healthy, individuals. We conducted genome-wide association studies and multi-trait analyses in HCM (1,733 cases), DCM (5,521 cases) and nine left ventricular (LV) traits (19,260 UK Biobank participants with structurally normal hearts). We identified 16 loci associated with HCM, 13 with DCM and 23 with LV traits. We show strong genetic correlations between LV traits and cardiomyopathies, with opposing effects in HCM and DCM. Two-sample Mendelian randomization supports a causal association linking increased LV contractility with HCM risk. A polygenic risk score explains a significant portion of phenotypic variability in carriers of HCM-causing rare variants. Our findings thus provide evidence that polygenic risk score may account for variability in Mendelian diseases. More broadly, we provide insights into how genetic pathways may lead to distinct disorders through opposing genetic effects.

5,521 cases, 397,323 controls

Chapter III

Study Statistics

Key metrics and study information

402844
Total Participants
GWAS
Study Type
Yes
Replicated
2,694 European ancestry cases, 47,486 European ancestry controls
Replication Participants
European
Ancestry
U.K., Netherlands, Canada
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

Important Disclaimer: This review has been performed semi-automatically and is provided for informational purposes only. While we strive for accuracy, this analysis may contain errors, omissions, or misinterpretations of the original research. DNA Genics disclaims all liability for any inaccuracies, errors, or consequences arising from the use of this information. Users should independently verify all information and consult original research publications before making any decisions based on this content. This analysis is not intended as a substitute for professional scientific review or medical advice.

Analysis In Progress

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