Lipids, Blood Pressure, and Diabetes Mellitus on Risk of
Cardiovascular Diseases in East Asians: A Mendelian
Randomization Study
Jonathan L. Ciofani, MDa,b,c,*, Daniel Han, PhDd,e,f, Usaid K. Allahwala, PhDb,c,
Benjamin Woolf, MScg,h,i, Dipender Gill, PhDa,j, and Ravinay Bhindi, PhDb,c
Elevated blood pressure, dyslipidemia, and impaired glycemic control are well-established
cardiovascular risk factors in Europeans, but there are comparatively few studies focused
on East Asian populations. This study evaluated the potential causal relations between traditional cardiovascular risk factors and disease risk in East Asians through a 2-sample
Mendelian randomization approach. We collected summary statistics for blood pressure
parameters, lipid subsets, and type 2 diabetes mellitus liability from large genome-wide
association study meta-analyses conducted in East Asians and Europeans. These were
paired with summary statistics for ischemic heart disease (IHD), ischemic stroke (IS),
peripheral vascular disease, heart failure (HF) and atrial fibrillation (AF). We performed
univariable Mendelian randomization analyses for each exposure-outcome pair, followed
by multivariable analyses for the available lipid subsets. The genetically predicted risk factors associated with IHD and AF were similar between East Asians and Europeans. However, in East Asians only genetically predicted elevated blood pressure was significantly
associated with IS (odds ratio 1.05, 95% confidence interval 1.04 to 1.06, p <0.0001) and
HF (odds ratio 1.05, 95% confidence interval 1.04 to 1.06, p <0.0001), whereas nearly all
genetically predicted risk factors were significantly associated with IS and HF in Europeans. In conclusion, this study provides supportive evidence for similar causal relations
between traditional cardiovascular risk factors and IHD and AF in both East Asian and
European ancestry populations. However, the identified risk factors for IS and HF differed between East Asians and Europeans, potentially highlighting distinct disease etiologies between these populations. © 2023 The Author(s). Published by Elsevier Inc. This is
an open access article under the CC BY license (http://creativecommons.org/licenses/by/
4.0/) (Am J Cardiol 2023;205:329−337)
Keywords: lipids, blood pressure, diabetes mellitus, ischemic heart disease, atrial fibrillation,
heart failure, peripheral vascular disease, stroke, mendelian randomisation, genetics
Dyslipidemia, hypertension, and type 2 diabetes mellitus
(T2DM) have consistently been identified as common modifiable risk factors for cardiovascular diseases. However, most
evidence comes from European ancestry populations,1−3 with
comparatively little evidence from subjects of East Asian
a
Department of Epidemiology and Biostatistics, School of Public
Health, Imperial College London, London, United Kingdom; bDepartment
of Cardiology, Royal North Shore Hospital, Sydney, New South Wales,
Australia; cFaculty of Medicine and Health, The University of Sydney,
Sydney, New South Wales, Australia; dMedical Research Council Laboratory of Molecular Biology, Cambridge, United Kingdom; eDepartment of
Physiology, Development and Neuroscience, University of Cambridge,
Cambridge, United Kingdom; fSchool of Mathematics and Statistics, University of New South Wales, Sydney, New South Wales, Australia; gMedical Research Council Integrative Epidemiology Unit, University of
Bristol, Bristol, United Kingdom; hSchool of Psychological Science, University of Bristol, Bristol, United Kingdom; iFaculty of Epidemiology and
Population Health, London School of Hygiene and Tropical Medicine,
London, United Kingdom; and jChief Scientific Advisor Office, Novo Nordisk, Copenhagen, Denmark. Manuscript received June 20, 2023; revised
manuscript received and accepted August 3, 2023.
Funding: none.
See page 334 for Declaration of Competing Interest.
*Corresponding author: Tel: (02) 9926 7111.
E-mail address: jonathan.ciofani20@imperial.ac.uk (J.L. Ciofani).
ancestry despite comprising at least one-fifth of the world
population. Several observational studies have demonstrated notable epidemiologic differences in the burden of
cardiovascular diseases for East Asians compared with
Europeans and North Americans.4−6 However there
remains a relative scarcity of randomized trials performed
in East Asian populations to investigate these observational
findings. Mendelian randomization (MR) is a research
methodology that can test potentially causal relations
between cardiovascular risk factors and diseases. A proportion of the phenotype of an individual is determined by
genetic polymorphisms that are randomly inherited at birth.
The random allocation of phenotype-determining genetic
polymorphisms is analogous to assignment to a treatment
group in a randomized control trial (Figure 1). MR leverages
this random and non-modifiable allocation of genetic variants to help eliminate the risk of bias because of reverse causality and minimize bias from confounding, both of which
typically hinder interpretation of nonrandomized observational studies. The present study therefore investigates the
potentially causal relations between traditional cardiovascular risk factors and common cardiovascular diseases in East
Asian ancestry individuals and compares results with those
obtained in European ancestry individuals.
0002-9149/© 2023 The Author(s). Published by Elsevier Inc. This is an open access article under the CC BY license
(http://creativecommons.org/licenses/by/4.0/)
https://doi.org/10.1016/j.amjcard.2023.08.007
www.ajconline.org
330
The American Journal of Cardiology (www.ajconline.org)
Figure 1. Overview of comparison between a Mendelian randomization study and a randomized controlled trial.
Methods
The present study uses a 2-sample MR approach. The
exposure variables included low-density lipoprotein cholesterol (LDL-c), triglycerides (TGs), high-density lipoprotein
cholesterol (HDL-c), systolic blood pressure (SBP), diastolic blood pressure (DBP) and T2DM liability. Ischemic
heart disease (IHD), ischemic stroke (IS), peripheral vascular disease (PVD), heart failure (HF), and atrial fibrillation
(AF) were used as the outcome variables. Population homogeneity is a requirement for the samples used in a 2-sample
MR analysis, and thus both exposure and outcome data
were sourced from either East Asian or European ancestry
populations, according to the specified ancestry in the analysis. MR makes 3 further core assumptions which are that
the genetic variants should be: (1) strongly associated with
the exposure; (2) exclusively associated with the outcome
through the exposure; and (3) independent of potential
confounders. To address the first criterion, uncorrelated
genetic variants were selected that were significantly associated with the exposure subsets at p <5 £ 10 8; and to
evaluate the latter 2 criteria, sensitivity analyses were performed as described later.
Data for the present study are publicly available. Ethical
approval and consent were obtained by the original studies.
Preparation of this manuscript was based on the Strengthening the Reporting of Observational Studies in Epidemiology
using Mendelian Randomization Guidelines.7
For the East Asian analyses: the data for lipid subsets
was extracted from a genome-wide association study
(GWAS) meta-analysis performed by the Global Lipids
Genetic Consortium for LDL-c, HDL-c and log TG using
data from 40 cohorts which included 146,492 East Asian
individuals8 (summary statistics available at: http://csg.sph.
umich.edu/willer/public/glgc-lipids2021/); BP data were
Preventive Cardiology/Cardiovascular risk factors in East Asians
extracted from a GWAS meta-analysis of SBP and DBP
from 183,785 East Asian individuals, including 125,778
participants from BioBank Japan (BBJ) (summary statistics
for significant SNPs are available from the Supplementary
Table of the original manuscript)9; and T2DM liability data
were extracted from a GWAS meta-analysis of 433,540
East Asian ancestry individuals from 23 cohorts, including
191,832 individuals from BBJ (summary statistics available
at: https://blog.nus.edu.sg/agen/).10
For the European analyses: the LDL-c, HDL-c, and log TG
data were similarly extracted from a GWAS meta-analysis
performed by the Global Lipids Genetic Consortium using
data from up to 146 cohorts and 1,320,016 participants8 (summary statistics available at: http://csg.sph.umich.edu/willer/
public/glgc-lipids2021/); BP data were extracted from a
GWAS meta-analysis of SBP and DBP including up to
1,006,863 European participants (summary statistics for significant SNPs available from the Supplementary Table of the
original manuscript)11; and T2DM liability data were
extracted from a GWAS meta-analysis of DIAGRAM, GERA
and UK Biobank including up to 659,316 European ancestry
individuals (summary statistics available at: https://www.ebi.
ac.uk/gwas/studies/GCST006867).12
Single-nucleotide polymorphisms (SNPs) that were
associated with each exposure variable at p <5 £ 10 8
were extracted. Linkage disequilibrium (LD) clumping was
performed (r2 <0.001, 10 megabase distance cutoff, East
Asian or European ancestry participants of the 1000
genomes project) and the variants with the smallest
p values were selected for further analysis.
GWAS analyses of BBJ data were used for all East
Asian outcomes: myocardial infarction (MI),13 IS,13 peripheral artery disease (PAD),13 chronic HF (CHF),13 and AF.14
For each outcome, this included: 14,992 MI cases and
146,212 controls; 22,664 IS cases and 152,022 controls;
4,112 PAD cases and 173,601 controls; 10,540 CHF cases
and 169,186 controls; and 8,180 AF cases and 28,612 controls. Cases were defined by past medical history and textmining of electronic medical records. Data for MI, IS,
PAD, and CHF are available from: https://pheweb.jp/
pheno/MI.13 Data for AF is available from: http://jenger.
riken.jp/en/result.14 For the purpose of reporting results
later, MI is reported as IHD, PAD as PVD, and CHF as HF.
For the European ancestry analyses: IHD data were
extracted from a meta-analysis of 48 studies including
60,801 coronary artery disease cases and 123,504 controls,
with 77% of participants of European ancestry (summary
statistics available at: http://www.cardiogramplusc4d.org/
data-downloads/)15; IS data were extracted from a metaanalysis including 34,217 IS cases and 406,111 controls of
European ancestry (summary statistics available at: https://
www.ebi.ac.uk/gwas/studies/GCST006908)16; PVD data
were extracted from the United Kingdom Biobank GWAS
pipeline using the Phenome Scan Analysis Tool, which
included 1,456 cases and 461,554 controls (summary statistics available from: https://gwas.mrcieu.ac.uk/datasets/ukbb-4929/)17; HF data were extracted from a GWAS metaanalysis of 26 studies including 47,309 cases and 930,014
controls of European ancestry (summary statistics available
at:
https://www.ebi.ac.uk/gwas/studies/GCST009541)18;
and AF data were extracted from a GWAS of 6 contributing
331
studies including 60,620 cases and 970,216 controls of
European ancestry (summary statistics available at: https://
www.ebi.ac.uk/gwas/studies/GCST006414).19
Further details about the genotyping methodology and
phenotype definitions can be found in the original GWAS
manuscripts (Supplementary Table 9).
The primary MR analysis was an inverse variance
weighted (IVW) meta-analysis of the Wald ratios for each
genetic variant. Results are expressed as odds of the outcome per SD increase in genetically predicted lipid variables and per mm Hg increase in BP variables. A
Bonferroni-corrected p value threshold was set at
p = 0.0017 for all primary analyses (0.05 / 30, based on 6
exposure and 5 outcome variables) and p = 0.017 for multivariable analyses if significant on univariable analysis (0.05
/ 3, because 3 lipid subsets were included in each model)
(Figures 2 to 6, Supplementary Tables 1 to 4).
To evaluate for violation of the main MR assumptions
because of horizontal pleiotropy, we performed several sensitivity analyses including weighted-median, weightedmode, MR-Egger, and MR-RAPS (Supplementary Figure
1, Supplementary Tables 1 and 3). Each method makes different assumptions and thus concordance between methods
provides confidence in the conclusion. The weightedmedian approach assumes that at least half the instrumental
variables are valid. Weighted-mode assumes that the most
common causal effect is consistent with the true effect.
MR-Egger uses the Instrument Strength Independent of
Direct Effect (InSIDE) assumption, which states that the
strength of pleiotropic effects from the genetic variants to
the outcome is independent of the strength of the association between genetic variants and exposure. Under this
assumption, the intercept from MR-Egger analysis estimates the average pleiotropic effect of the genetic variants
(Supplementary Table 5). MR-Egger typically has lower
power compared with IVW. MR-RAPS is robust to idiosyncratic and systematic pleiotropy, and weak instrument bias.
Cochran’s Q statistic was used to test for genetic variant
heterogeneity (Supplementary Table 6). Leave-one-out
analyses were performed for each exposure-outcome pair
(Supplementary Figures 2 and 3). Scatter and funnel plots
are presented in Supplementary Figures 4 to 7.
Multivariable MR was subsequently performed to assess
whether the effects of the lipid subsets on the outcome were
Figure 2. Mendelian randomization inverse variance weighted estimates
for the effect of 1 SD increase in genetically predicted elevated LDL-c,
TG, and HDL-c, 1 mm Hg increase in SBP, and DBP, and T2DM liability
on risk of IHD.
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The American Journal of Cardiology (www.ajconline.org)
Table 1
Multivariable mendelian randomisation estimates for the direct effect of one standard deviation increase in genetically predicted elevated low-density lipoprotein cholesterol, triglycerides and high-density lipoprotein cholesterol respectively, accounting for the other lipid subsets
Ischemic heart
disease Odds
(95% CI)
Low-density lipoprotein cholesterol
Triglycerides
High-density lipoprotein cholesterol
2.06 (1.71-2.48)
1.21 (0.95-1.55)
0.69 (0.56-0.86)
Low-density lipoprotein cholesterol
Triglycerides
High-density lipoprotein cholesterol
2.01 (1.75-2.31)
1.27 (1.05-1.52)
0.78 (0.67-0.92)
Ischemic stroke
Odds (95% CI)
East Asian
0.94 (0.80-1.13)
1.40 (1.12-1.77)
1.09 (0.93-1.29)
European
1.32 (1.07-1.63)
1.15 (0.88-1.51)
0.86 (0.68-1.09)
independent of each other (Supplementary Tables 2 and 4,
Table 1). Only SNPs that were available in all lipid subsets
and outcome summary statistic datasets were considered. Of
these, variants associated with at least one lipid trait at
p <5 £ 10 8 were extracted, clumped after ordering from
lowest to highest p value of association with any trait
(r2 <0.001, 10 megabase distance cutoff, East Asian, or European ancestry participants of the 1,000 genomes project), and
harmonized, before multivariable IVW MR was performed.
Statistical analyses were performed using R version
1.4.1106 with the TwoSampleMR package (The R Foundation for Statistical Computing, Vienna, Austria).
Results
In the main IVW analyses, a significant association was
observed between nearly all traditional cardiovascular risk
factors and IHD in East Asians (LDL-c: odds ratio [OR]
2.13, 95% confidence interval [CI] 1.65 to 2.75, p <0.0001;
TG: OR 1.29, 95% CI 1.13 to 1.48, p = 0.00026; HDL-c:
OR 0.75, 95% CI 0.62 to 0.90, p = 0.0016; SBP: OR 1.04,
95% CI 1.02 to 1.06, p = 0.00032; DBP: OR 1.07, 95% CI
1.03 to 1.10, p = 0.00030) (Figure 2). The association
between T2DM and IHD did not reach Bonferroni-corrected statistical significance in East Asians on IVW analysis (OR 1.08, 95% CI 1.02 to 1.16, p = 0.016). In the
European analyses, all genetically predicted risk factors,
including T2DM, were significantly associated with IHD
risk. For both the East Asian and European analyses, multivariable MR accounting for all 3 lipid subsets in the same
model demonstrated a similar association between genetically predicted higher LDL-c and lower HDL-c with
increased risk of IHD, but there was no strong association
between genetically predicted TG and IHD risk in the East
Asian analysis (Table 1).
In East Asians, a significant association was observed
between the genetically predicted BP parameters and IS on
univariable IVW analysis (SBP: OR 1.05, 95% CI 1.04 to
1.06, p <0.0001; DBP: OR 1.09, 95% CI 1.08 to 1.11,
p <0.0001), but there was no association between any of
the genetically predicted lipid parameters or T2DM on IS
risk (Figure 3). This is in contrast to the European analysis,
in which significant associations were identified between
all risk factor variables, except LDL-c and IS.
Peripheral vascular
disease Odds
(95% CI)
Heart failure
Odds (95% CI)
Atrial fibrillation
Odds (95% CI)
2.28 (1.75-2.96)
0.81 (0.61-1.08)
0.44 (0.33-0.58)
1.17 (0.98-1.40)
1.01 (0.79-1.28)
0.83 (0.70-0.99)
1.13 (0.77-1.66)
1.37 (0.94-2.00)
0.76 (0.54-1.06)
2.40 (1.24-4.63)
1.31 (0.64-2.69)
0.66 (0.41-1.07)
1.34 (1.18-1.52)
1.21 (0.99-1.46)
0.66 (0.56-0.78)
0.95 (0.79-1.15)
0.69 (0.54-0.87)
0.62 (0.50-0.77)
Significant associations were observed between
genetically predicted LDL-c, HDL-c, T2DM liability,
and SBP with risk of PVD (LDL-c: OR 1.57, 95% CI
1.30 to 1.89, p <0.0001; HDL-c: OR 0.76, 95% CI 0.68
to 0.86, p <0.0001; T2DM: OR 1.32, 95% CI 1.25 to
1.40, p <0.0001; SBP: OR 1.04, 95% CI 1.02 to 1.06,
p = 0.00027), but not genetically predicted TG or DBP
with PVD risk (TG: OR 1.17, 95% CI 1.01 to 1.36,
p = 0.043; DBP: OR 1.04, 95% CI 1.01 to 1.07,
p = 0.013) (Figure 4). On multivariable MR, there
remained a significant association between both LDL-c
and HDL-c with PVD. In contrast, for the European analysis only genetically predicted T2DM liability was significantly associated with increased PVD risk on
univariable analysis.
Similar to the results for IS, in East Asians a significant
association was observed between the genetically predicted
BP parameters and HF on univariable IVW analysis (SBP:
OR 1.05, 95% CI 1.04 to 1.06, p <0.0001; DBP: OR 1.09,
95% CI 1.07 to 1.11, p <0.0001), but no association
between any of the genetically predicted lipid subsets or
T2DM liability on HF risk (Figure 5). This contrasts the
European analysis, in which significant associations were
identified between all analyzed risk factors and HF.
In East Asians, genetically predicted higher BP was
associated with increased risk of AF (SBP: OR 1.06, 95%
CI 1.03 to 1.08; DBP: OR 1.10, 95% CI 1.06 to 1.15), with
no association between any of the genetically predicted
Figure 3. Mendelian randomization inverse variance weighted estimates
for the effect of 1 SD increase in genetically predicted elevated LDL-c,
TG and HDL-c, 1 mm Hg increase in SBP, and DBP, and T2DM liability
on risk of IS.
Preventive Cardiology/Cardiovascular risk factors in East Asians
333
Figure 4. Mendelian randomization inverse variance weighted estimates
for the effect of 1 SD increase in genetically predicted elevated LDL-c,
TG and HDL-c, 1 mm Hg increase in SBP, and DBP, and T2DM liability
on risk of PVD.
Figure 6. Mendelian randomization inverse variance weighted estimates
for the effect of 1 SD increase in genetically predicted elevated LDL-c,
TG and HDL-c, 1 mm Hg increase in SBP, and DBP, and T2DM liability
on risk of AF.
lipid subsets or T2DM liability on AF (Figure 6). In the
European analysis, genetically predicted higher SBP was
associated with increased risk of AF, but DBP, the lipid
subsets, and T2DM liability were not.
genetically predicted elevated BP, but not dyslipidemia or
T2DM, as risk factors for IS and HF in East Asians. Previous studies in East Asians have consistently demonstrated
that elevated BP contributes to a substantially higher population-attributable risk toward stroke compared with dyslipidemia and diabetes mellitus.20 Existing evidence has
additionally demonstrated that East Asians are more frequently diagnosed with masked hypertension, and East
Asian populations may experience a higher morning BP
surge than Europeans which is predictive of stroke risk.21
Indeed, the relatively increased susceptibility of East
Asians to elevated BP was recognized by Kario et al22 in a
targeted consensus statement on hypertension management
specifically for Asian populations.
The finding that the lipid subsets were significantly associated with IHD and PVD but not IS, HF, or AF in East
Asians was unexpected in the context of the results from
European ancestry individuals. This may be related to
insufficient statistical power, although comparable findings
have previously been reported. The Management of Elevated Cholesterol in the Primary Prevention Group of Adult
Japanese (MEGA) trial, which Randomized 7,832 Japanese
patients to pravastatin plus diet versus diet alone, showed a
significant reduction in risk of MI and overall coronary
heart disease but no significant difference in risk of IS in
the pravastatin group.23 In the more recent but smaller
Japan Statin Treatment Against Recurrent Stroke (JSTARS) trial, in which 1,578 Japanese patients with previous noncardioembolic IS and hypercholesterolemia were
randomized to pravastatin or control, the pravastatin group
experienced lower rates of atherothrombotic infarct but the
overall rate of stroke or transient ischemic attack was not
significantly different from the control group.24 Neither
study reported outcome rates of PVD, HF, or AF. The
inverse association between genetically predicted HDL-c
and nearly all the outcomes in the European IVW analyses
is also interesting in light of recent studies which have questioned the causal association between HDL-c and cardiovascular events.25,26 This may reflect the larger sample size
in the present study compared with previous analyses. Notably, however, these results were not consistently supported
by the sensitivity analyses, which is similar to the report by
Burgess and Davey Smith27 that demonstrated a significant
association in MR analysis between HDL-c and coronary
artery disease on IVW but not sensitivity analyses.
Discussion
Blood pressure, lipid levels and T2DM are traditionally
considered to be modifiable risks influenced by both genetic
and lifestyle factors. The present study leveraged largescale GWAS data and the MR approach to evaluate the
association between traditional cardiovascular risk factors
and diseases in East Asian ancestry individuals. We found
similar risk factor profiles for IHD and AF between East
Asian and European ancestry populations. However, for
East Asians, in contrast to Europeans, only genetically predicted elevated BP was significantly associated with IS and
HF.
The increased risk of cardiovascular diseases because of
dyslipidemia, hypertension, and T2DM has been established in European populations through large observational
and randomized trials1−3 and extrapolated to non-Europeans in clinical practice. The present study supports this
approach for IHD and AF, demonstrating largely concordant findings between East Asian and European ancestry
populations for the association between traditional cardiovascular risk factors and these outcomes. However, the
present study provided evidence for a causal role of
Figure 5. Mendelian randomization inverse variance weighted estimates
for the effect of 1 SD increase in genetically predicted elevated LDL-c,
TG, and HDL-c, 1 mm Hg increase in SBP and DBP, and T2DM liability
on risk of HF.
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The American Journal of Cardiology (www.ajconline.org)
Genetic ancestry has previously been shown to modulate
the effect of T2DM on risk of diabetic complications. The
present study showed an association between genetically
predicted T2DM and elevated risk of PVD in East Asians
and a trend toward association with IHD that did not reach
significance after Bonferroni-correction for multiple testing. Previous studies on the relation between T2DM and
cardiovascular diseases in East Asians have not been consistent in their findings. A multiethnic study of 62,432 participants in North America found lower risk of incident MI,
congestive HF, stroke and non-traumatic lower extremity
amputation, and higher risk of end-stage renal disease in
Asian compared with European ancestry individuals.28 In
contrast, the Action in Diabetes and Vascular Disease study
found that Asian participants with T2DM had higher incidence of stroke and nephropathy, and lower incidence of
PVD and coronary disease compared with their Eastern
European and Australian counterparts.29 Notably, neither
study was specific to East Asians, and it is well-described
that within Asia there is heterogeneity regarding cardiovascular disease epidemiology.4
There are several important limitations. Statistical power
was limited particularly for the PVD outcome dataset in
Europeans, for which there were only 1,456 cases, and consequently the CIs were unsurprisingly wide (Supplementary
Table 8). Furthermore, because several of the outcome variables were extracted from biobank data, it is possible that
there were inaccuracies in the attribution of participants as
a case versus control. Moreover, the outcome definitions
between East Asian and European analyses were not identical, as the analyses were limited by the availability of large
suitable GWAS datasets. IHD, for example, was defined for
East Asians as MI (BBJ) whereas the European dataset
included MI, acute coronary syndrome, chronic stable
angina, and coronary stenosis >50% (CARDIoGRAMplusC4D). Importantly, this assumes shared pathogenesis
for the spectrum of IHD from mild coronary artery disease
to MI. Despite this, the effect of each exposure variable on
risk of IHD was comparable between East Asians and Europeans. Furthermore, HF and IS are heterogeneous diseases.
IS, for example, has several subtypes with different etiologies that may vary between ancestry groups and this may
contribute to the differing risk factor profiles between
ancestry groups. Additionally, while there is some overlap
between several of the exposure and outcome datasets, the
use of strong instruments, achieved by only using SNPs
associated with the exposure at p <5 £ 10 8 with associated high F-statistics (Supplementary Table 7), is expected
to mitigate the potential risk of bias. Although there was
evidence of significant heterogeneity in many of the analyses, determined by evaluation of the Q statistic, the concordance between the main IVW and sensitivity analyses
suggests that bias is less likely to have substantially
impacted the results.
Overall, this study used large-scale GWAS data of East
Asian individuals to evaluate the relation between traditional cardiovascular risk factors and diseases in a population that is understudied relative to the proportion of the
global population. This analysis demonstrated a similar risk
factor profile for IHD and AF between East Asians and
Europeans but suggested that elevated BP may be the more
pertinent risk factor for IS and HF in East Asians. This
study presents an important complementary research
approach that may better inform further investigation into
population-level cardiovascular disease prevention and
treatment strategies in East Asian populations.
Declaration of Competing Interest
The authors have no competing interests to declare.
Supplementary materials
Supplementary material associated with this article can
be found in the online version at https://doi.org/10.1016/j.
amjcard.2023.08.007.
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