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GWAS Study

Large-scale genome-wide association analyses identify novel genetic loci and mechanisms in hypertrophic cardiomyopathy.

Tadros R, Zheng SL, Grace C et al.

39966646 PubMed ID
GWAS Study Type
74259 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

TR
Tadros R
ZS
Zheng SL
GC
Grace C
JP
Jordà P
FC
Francis C
WD
West DM
JS
Jurgens SJ
TK
Thomson KL
HA
Harper AR
OE
Ormondroyd E
XX
Xu X
TP
Theotokis PI
BR
Buchan RJ
MK
McGurk KA
MF
Mazzarotto F
BB
Boschi B
PE
Pelo E
LM
Lee M
NM
Noseda M
VA
Varnava A
VA
Vermeer AMC
WR
Walsh R
AA
Amin AS
VS
van Slegtenhorst MA
RN
Roslin NM
SL
Strug LJ
SE
Salvi E
LC
Lanzani C
DM
de Marvao A
RJ
Roberts JD
TM
Tremblay-Gravel M
GG
Giraldeau G
CJ
Cadrin-Tourigny J
LP
L'Allier PL
GP
Garceau P
TM
Talajic M
GT
Gagliano Taliun SA
PY
Pinto YM
RH
Rakowski H
PA
Pantazis A
BW
Bai W
BJ
Baksi J
HB
Halliday BP
PS
Prasad SK
BP
Barton PJR
OD
O'Regan DP
CS
Cook SA
DB
de Boer RA
CI
Christiaans I
MM
Michels M
KC
Kramer CM
HC
Ho CY
NS
Neubauer S
MP
Matthews PM
WA
Wilde AAM
TJ
Tardif JC
OI
Olivotto I
AA
Adler A
GA
Goel A
WJ
Ware JS
BC
Bezzina CR
WH
Watkins H
Chapter II

Abstract

Summary of the research findings

Hypertrophic cardiomyopathy (HCM) is an important cause of morbidity and mortality with both monogenic and polygenic components. Here, we report results from a large genome-wide association study and multitrait analysis including 5,900 HCM cases, 68,359 controls and 36,083 UK Biobank participants with cardiac magnetic resonance imaging. We identified 70 loci (50 novel) associated with HCM and 62 loci (20 novel) associated with relevant left ventricular traits. Among the prioritized genes in the HCM loci, we identify a novel HCM disease gene, SVIL, which encodes the actin-binding protein supervillin, showing that rare truncating SVIL variants confer a roughly tenfold increased risk of HCM. Mendelian randomization analyses support a causal role of increased left ventricular contractility in both obstructive and nonobstructive forms of HCM, suggesting common disease mechanisms and anticipating shared response to therapy. Taken together, these findings increase our understanding of the genetic basis of HCM, with potential implications for disease management.

252 African ancestry cases, 1,363 African ancestry controls, 123 Admixed American ancestry cases, 175 Admixed American ancestry controls, 72 East Asian ancestry cases, 346 East Asian ancestry controls, 5,222 European ancestry cases, 63,447 European ancestry controls, 189 South Asian ancestry cases, 1,903 South Asian ancestry controls, 42 cases, 1,125 controls

Chapter III

Study Statistics

Key metrics and study information

74259
Total Participants
GWAS
Study Type
No
Replicated
African unspecified, Hispanic or Latin American, East Asian, European, South Asian, NR
Ancestry
Canada, Netherlands, U.S., Italy, U.K.
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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Analysis In Progress

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