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  • Ovid Technologies (Wolters Kluwer Health)  (9)
  • 2020-2024  (9)
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  • Ovid Technologies (Wolters Kluwer Health)  (9)
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  • 2020-2024  (9)
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  • 1
    Online Resource
    Online Resource
    Risk of Midlife Stroke After Adverse Pregnancy Outcomes: The FinnGen Study
    Ovid Technologies (Wolters Kluwer Health) ; 2023
    In:  Stroke Vol. 54, No. 7 ( 2023-07), p. 1798-1805
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 54, No. 7 ( 2023-07), p. 1798-1805
    Abstract: Adverse pregnancy outcomes (APO) contribute to higher risk of maternal cerebrovascular disease, but longitudinal data that include APO and stroke timing are lacking. We hypothesized that APO are associated with younger age at first stroke, with a stronger relationship in those with 〉 1 pregnancy with APO. METHODS: We analyzed longitudinal Finnish nationwide health registry data from the FinnGen Study. We included women who gave birth after 1969 when the hospital discharge registry was established. We defined APO as a pregnancy affected by gestational hypertension, preeclampsia, eclampsia, preterm birth, small for gestational age infant, or placental abruption. We defined stroke as first hospital admission for ischemic stroke or nontraumatic intracerebral or subarachnoid hemorrhage, excluding stroke during pregnancy or within 1 year postpartum. We used Kaplan-Meier survival curves and multivariable-adjusted Cox and generalized linear models to assess the relationship between APO and future stroke. RESULTS: We included 144 306 women with a total of 316 789 births in the analysis sample, of whom 17.9% had at least 1 pregnancy with an APO and 2.9% experienced an APO in ≥2 pregnancies. Women with APO had more comorbidities including obesity, hypertension, heart disease, and migraine. Median age at first stroke was 58.3 years in those with no APO, 54.8 years in those with 1 APO, and 51.6 years in those with recurrent APO. In models adjusted for sociodemographic characteristics and stroke risk factors, risk of stroke was greater in women with 1 APO (adjusted hazard ratio, 1.3 [95% CI, 1.2–1.4]) and recurrent APO (adjusted hazard ratio, 1.4 [95% CI, 1.2–1.7] ) compared with those with no APO. Women with recurrent APO had more than twice the stroke risk before age 45 (adjusted odds ratio, 2.1 [95% CI, 1.5–3.1]) compared with those without APO. CONCLUSIONS: Women who experience APO have earlier onset of cerebrovascular disease, with the earliest onset in those with more than 1 affected pregnancy.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.123.043052
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 80381-9
    detail.hit.zdb_id: 1467823-8
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  • 2
    Online Resource
    Online Resource
    Genetic Risk Score for Intracranial Aneurysms: Prediction of Subarachnoid Hemorrhage and Role in Clinical Heterogeneity
    Ovid Technologies (Wolters Kluwer Health) ; 2023
    In:  Stroke Vol. 54, No. 3 ( 2023-03), p. 810-818
    Details
    In: Stroke, Ovid Technologies (Wolters Kluwer Health), Vol. 54, No. 3 ( 2023-03), p. 810-818
    Abstract: Recently, common genetic risk factors for intracranial aneurysm (IA) and aneurysmal subarachnoid hemorrhage (ASAH) were found to explain a large amount of disease heritability and therefore have potential to be used for genetic risk prediction. We constructed a genetic risk score to (1) predict ASAH incidence and IA presence (combined set of unruptured IA and ASAH) and (2) assess its association with patient characteristics. Methods: A genetic risk score incorporating genetic association data for IA and 17 traits related to IA (so-called metaGRS) was created using 1161 IA cases and 407 392 controls from the UK Biobank population study. The metaGRS was validated in combination with risk factors blood pressure, sex, and smoking in 828 IA cases and 68 568 controls from the Nordic HUNT population study. Furthermore, we assessed association between the metaGRS and patient characteristics in a cohort of 5560 IA patients. Results: Per SD increase of metaGRS, the hazard ratio for ASAH incidence was 1.34 (95% CI, 1.20–1.51) and the odds ratio for IA presence 1.09 (95% CI, 1.01–1.18). Upon including the metaGRS on top of clinical risk factors, the concordance index to predict ASAH hazard increased from 0.63 (95% CI, 0.59–0.67) to 0.65 (95% CI, 0.62–0.69), while prediction of IA presence did not improve. The metaGRS was statistically significantly associated with age at ASAH (β=−4.82×10 −3 per year [95% CI, −6.49×10 −3 to −3.14×10 −3 ]; P =1.82×10 −8 ), and location of IA at the internal carotid artery (odds ratio=0.92 [95% CI, 0.86–0.98]; P =0.0041). Conclusions: The metaGRS was predictive of ASAH incidence, although with limited added value over clinical risk factors. The metaGRS was not predictive of IA presence. Therefore, we do not recommend using this metaGRS in daily clinical care. Genetic risk does partly explain the clinical heterogeneity of IA warranting prioritization of clinical heterogeneity in future genetic prediction studies of IA and ASAH.
    Type of Medium: Online Resource
    ISSN: 0039-2499 , 1524-4628
    URL: Article
    DOI: 10.1161/STROKEAHA.122.040715
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 80381-9
    detail.hit.zdb_id: 1467823-8
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  • 3
    Online Resource
    Online Resource
    How Communicating Polygenic and Clinical Risk for Atherosclerotic Cardiovascular Disease Impacts Health Behavior: an Observational Follow-up Study
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Circulation: Genomic and Precision Medicine Vol. 15, No. 2 ( 2022-04)
    Details
    In: Circulation: Genomic and Precision Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 15, No. 2 ( 2022-04)
    Abstract: Prediction tools that combine polygenic risk scores with clinical factors provide a new opportunity for improved prediction and prevention of atherosclerotic cardiovascular disease, but the clinical utility of polygenic risk score has remained unclear. Methods: We collected a prospective cohort of 7342 individuals (64% women, mean age 56 years) and estimated their 10-year risk for atherosclerotic cardiovascular disease both by a traditional risk score and a composite score combining the effect of a polygenic risk score and clinical risk factors. We then tested how returning the personal risk information with an interactive web-tool impacted on the participants’ health behavior. Results: When reassessed after 1.5 years by a clinical visit and questionnaires, 20.8% of individuals at high ( 〉 10%) 10-year atherosclerotic cardiovascular disease risk had seen a doctor, 12.4% reported weight loss, 14.2% of smokers had quit smoking, and 15.4% had signed up for health coaching online. Altogether, 42.6% of persons at high risk had made one or more health behavioral changes versus 33.5% of persons at low/average risk such that higher baseline risk predicted a favorable change (OR [CI], 1.53 [1.37–1.72] for persons at high risk versus the rest, P 〈 0.001), with both high clinical ( P 〈 0.001) and genomic risk (OR [CI], 1.10 [1.03–1.17] , P =0.003) contributing independently. Conclusions: Web-based communication of personal atherosclerotic cardiovascular disease risk-data including polygenic risk to middle-aged persons motivates positive changes in health behavior and the propensity to seek care. It supports integration of genomic information into clinical risk calculators as a feasible approach to enhance disease prevention.
    Type of Medium: Online Resource
    ISSN: 2574-8300
    URL: Article
    DOI: 10.1161/CIRCGEN.121.003459
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 2927603-2
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  • 4
    Online Resource
    Online Resource
    Abstract 14346: The Cardiovascular Disease Associations and Genetic Determinants of Pericardial Adipose Tissue
    Ovid Technologies (Wolters Kluwer Health) ; 2023
    In:  Circulation Vol. 148, No. Suppl_1 ( 2023-11-07)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 148, No. Suppl_1 ( 2023-11-07)
    Abstract: Introduction: While previous studies have reported associations of pericardial adipose tissue (PAT) with cardiovascular diseases such as atrial fibrillation (AF) and coronary artery disease (CAD), they have been limited in sample size or drawn from selected populations. Additionally, the genetic determinants of PAT remain largely unknown. Hypothesis: PAT is associated with cardiovascular diseases and genetic loci influence variation in PAT. Methods: A deep learning model was trained to quantify PAT area from four-chamber CMR images in the UK Biobank using semantic segmentation. Cross-sectional and prospective cardiovascular disease associations were evaluated, controlling for sex and age. A genome-wide association study was performed, and a polygenic score (PGS) for PAT was examined in 453,733 independent FinnGen study participants. Results: A total of 44,725 UK Biobank participants (51.7% female, mean [SD] age 64.1 [7.7] years) were included. PAT was positively associated with male sex (β = +0.76 SD in PAT), age (r = 0.15), body mass index (BMI; r = 0.47) and waist-to-hip ratio (r = 0.55) (P 〈 1x10 -230 for all). PAT was more elevated in prevalent heart failure (β = +0.46 SD units) and type 2 diabetes (T2D; β = +0.56) than in CAD (β = +0.22) or AF (β = +0.18). Baseline PAT was associated with incident heart failure (HR = 1.29 per +1 SD in PAT [95% CI 1.17-1.43]) and T2D (HR = 1.63 [1.51-1.76] ) during mean (SD) 3.2 (1.5) years of follow-up; the associations remained significant when controlling for BMI. We replicated 2/2 known genetic loci and identified 5 novel loci, implicating transcriptional regulators of adipocyte morphology and brown adipogenesis ( EBF1 , EBF2 and CEBPA ) and regulators of visceral adiposity ( WARS2 and TRIB2 ). The PAT PGS was associated with T2D, HF, CAD and AF in FinnGen (ORs 1.03-1.06 per +1 SD in PGS, P 〈 2x10 -10 for all). Conclusions: PAT shares genetic determinants with abdominal obesity and is an independent predictor of incident T2D and heart failure.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.148.suppl_1.14346
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 1466401-X
    detail.hit.zdb_id: 80099-5
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  • 5
    Online Resource
    Online Resource
    Abstract 14515: Distinct Genetic Mechanisms for Bradyarrhythmias From Multi-Center Multi-Ancestry Meta-Analyses
    Ovid Technologies (Wolters Kluwer Health) ; 2023
    In:  Circulation Vol. 148, No. Suppl_1 ( 2023-11-07)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 148, No. Suppl_1 ( 2023-11-07)
    Abstract: Background: With an increasing prevalence in older adults, bradyarrhythmias pose a major public health problem. Hypothesis: Genetics can inform on disease pathophysiology and implicate targets for therapeutic development for bradyarrhythmias. Methods: We first performed ancestry-specific genome-wide association studies (GWAS) and combined the results in meta-analyses of up to 1.3 million individuals including 9,511 sinus node dysfunction (SND) cases, 34,086 distal conduction disease (DCD) cases, and 28,899 pacemaker implantation (PM) cases. We evaluated the biological relevance of bradyarrhythmia loci by analyses of transcriptomes, pleiotropy, and partitioned heritability based on cardiac single cell RNA sequencing data. Finally, we performed rare variant burden testing in 460,000 whole exome sequenced individuals (cases: 1,766 SND, 12,422 DCD & 5,646 PM) from UK Biobank and Mass General Brigham Biobank. Results: Common variant analyses identified 13, 28, and 21 loci for SND, DCD, and PM, respectively. SND and DCD were moderately genetically correlated (r g = 0.64). Common variant loci included genes underlying familial forms of bradyarrhythmias (HCN4 and SCN5A) and genes regulating population-level variation in electrocardiographic traits. Four well-known common variant arrhythmia loci ( SCN5A / SCN10A , CCDC141 , TBX20 , and CAMK2D ) were shared for SND and DCD, while other loci were more specific for SND ( PITX2 , HCN4 , ZFHX3 ) or DCD ( CAV1 and NKX2 - 5 ). We observed an inverse association between predicted cardiac expression of SCN10A and risk of SND and DCD, and positive associations of predicted cardiac expression of CEP68 and STRN with risk of SND and DCD, respectively. Among 9 cardiac cell types, cardiomyocyte-expressed genes were enriched for contributions to DCD heritability. Rare variant analyses implicated LMNA for all bradyarrhythmia subtypes; SMAD6 and SCN5A for DCD; and TTN , MYBPC3 , and SCN5A for PM. Conclusions: We identify novel genes and loci associated with bradyarrhythmias. The genetic architectures of SND and DCD are both overlapping and distinct. Multiple genetic mechanisms involving ion channels, sarcomeric components, cellular homeostasis, and cardiac development may influence the development of bradyarrhythmias.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.148.suppl_1.14515
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 1466401-X
    detail.hit.zdb_id: 80099-5
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  • 6
    Online Resource
    Online Resource
    Cardiovascular Risk Factors and MRI Markers of Cerebral Small Vessel Disease : A Mendelian Randomization Study
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Neurology Vol. 98, No. 4 ( 2022-01-25)
    Details
    In: Neurology, Ovid Technologies (Wolters Kluwer Health), Vol. 98, No. 4 ( 2022-01-25)
    Type of Medium: Online Resource
    ISSN: 0028-3878 , 1526-632X
    URL: Article
    DOI: 10.1212/WNL.0000000000013120
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 1491874-2
    detail.hit.zdb_id: 207147-2
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  • 7
    Online Resource
    Online Resource
    Meta-Analysis of Genome-Wide Association Studies Reveals Genetic Mechanisms of Supraventricular Arrhythmias
    Ovid Technologies (Wolters Kluwer Health) ; 2024
    In:  Circulation: Genomic and Precision Medicine Vol. 17, No. 3 ( 2024-06)
    Details
    In: Circulation: Genomic and Precision Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 17, No. 3 ( 2024-06)
    Abstract: Substantial data support a heritable basis for supraventricular tachycardias, but the genetic determinants and molecular mechanisms of these arrhythmias are poorly understood. We sought to identify genetic loci associated with atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular accessory pathways or atrioventricular reciprocating tachycardia (AVAPs/AVRT). METHODS: We performed multiancestry meta-analyses of genome-wide association studies to identify genetic loci for AVNRT (4 studies) and AVAP/AVRT (7 studies). We assessed evidence supporting the potential causal effects of candidate genes by analyzing relations between associated variants and cardiac gene expression, performing transcriptome-wide analyses, and examining prior genome-wide association studies. RESULTS: Analyses comprised 2384 AVNRT cases and 106 489 referents, and 2811 AVAP/AVRT cases and 1,483 093 referents. We identified 2 significant loci for AVNRT, which implicate NKX2-5 and TTN as disease susceptibility genes. A transcriptome-wide association analysis supported an association between reduced predicted cardiac expression of NKX2-5 and AVNRT. We identified 3 significant loci for AVAP/AVRT, which implicate SCN5A , SCN10A , and TTN/CCDC141 . Variant associations at several loci have been previously reported for cardiac phenotypes, including atrial fibrillation, stroke, Brugada syndrome, and electrocardiographic intervals. CONCLUSIONS: Our findings highlight gene regions associated with ion channel function (AVAP/AVRT), as well as cardiac development and the sarcomere (AVAP/AVRT and AVNRT) as important potential effectors of supraventricular tachycardia susceptibility.
    Type of Medium: Online Resource
    ISSN: 2574-8300
    URL: Article
    DOI: 10.1161/CIRCGEN.123.004320
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2024
    detail.hit.zdb_id: 2927603-2
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  • 8
    Online Resource
    Online Resource
    Abstract 13873: Deep Learning-Based GWAS of Aortic Valve Function Links 81 Loci to Aortic Stenosis Risk
    Ovid Technologies (Wolters Kluwer Health) ; 2023
    In:  Circulation Vol. 148, No. Suppl_1 ( 2023-11-07)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 148, No. Suppl_1 ( 2023-11-07)
    Abstract: Background & Aims: The genetic influences on normal aortic valve (AV) function and their impact on aortic stenosis (AS) risk are of significant interest. We sought to identify common genetic determinants of normal variation in AV function, and to understand their relationship with clinical disease. Methods: We used deep learning to measure peak velocity, mean gradient, and aortic valve area from MRI in UK Biobank participants. We conducted genome-wide association studies (GWAS) in a subset of 44,780 participants without cardiovascular disease. We performed multi-trait analysis of GWAS (MTAG) to incorporate data from AV measurements and AS diagnoses in UK Biobank and FinnGen, and applied PRScs to construct polygenic scores (PGS). Results: In the unadjusted analysis, 26 loci were associated with at least one AV measurement. Incorporating the AS GWAS using MTAG, we identified 81 distinct loci (62 with AV traits, 54 with AS, 35 overlapping), including PCSK9 (β=0.032, P=5.8E-09) and LDLR (β=0.018, P=2.3E-10). Additional loci were associated with lipid metabolism (LPA, FADS2, SORT1), atherosclerosis (CDKN2B, ARHGEF26, OTUD7B, PRDM16), inflammation (IL6, KLF2, TRAF1), and cardiac development and aortic root function (SMAD3, GATA4, ELN, TBX20, TEX41). The PGS for the unadjusted mean gradient was predictive of AS in FinnGen (HR 1.36 for the top 5% of participants vs all others, P=1.8E-14). All of Us participants in the top 5% of the MTAG-adjusted peak velocity PGS had an HR of 2.5 for incident AS (P=4.4E-08). Mendelian randomization showed association between Lp(a) and LDL—but not ApoA—on greater peak velocity (P=2.7E-13, P=1.6E-16, and P=0.60, respectively). Conclusion: We identified 81 genetic loci linked to AV function or AS. AV measurement PGS were strong predictors of AS risk. ApoB and Lp(a) showed causal association with higher peak velocity. These findings have implications for the early pathogenesis of AS and suggest modifiable pathways as targets for prevention.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.148.suppl_1.13873
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 1466401-X
    detail.hit.zdb_id: 80099-5
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  • 9
    Online Resource
    Online Resource
    Polygenic Hyperlipidemias and Coronary Artery Disease Risk
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Circulation: Genomic and Precision Medicine Vol. 13, No. 2 ( 2020-04)
    Details
    In: Circulation: Genomic and Precision Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 13, No. 2 ( 2020-04)
    Abstract: Hyperlipidemia is a highly heritable risk factor for coronary artery disease (CAD). While monogenic familial hypercholesterolemia associates with severely increased CAD risk, it remains less clear to what extent a high polygenic load of a large number of LDL (low-density lipoprotein) cholesterol (LDL-C) or triglyceride (TG)-increasing variants associates with increased CAD risk. Methods: We derived polygenic risk scores (PRSs) with ≈6M variants separately for LDL-C and TG with weights from a UK Biobank–based genome-wide association study with ≈324K samples. We evaluated the impact of polygenic hypercholesterolemia and hypertriglyceridemia to lipid levels in 27 039 individuals from the National FINRISK Study (FINRISK) cohort and to CAD risk in 135 638 individuals (13 753 CAD cases) from the FinnGen project (FinnGen). Results: In FINRISK, median LDL-C was 3.39 (95% CI, 3.38–3.40) mmol/L, and it ranged from 2.87 (95% CI, 2.82–2.94) to 3.78 (95% CI, 3.71–3.83) mmol/L between the lowest and highest 5% of the LDL-C PRS distribution. Median TG was 1.19 (95% CI, 1.18–1.20) mmol/L, ranging from 0.97 (95% CI, 0.94–1.00) to 1.55 (95% CI, 1.48–1.61) mmol/L with the TG PRS. In FinnGen, comparing the highest 5% of the PRS to the lowest 95%, CAD odds ratio was 1.36 (95% CI, 1.24–1.49) for the LDL-C PRS and 1.31 (95% CI, 1.19–1.43) for the TG PRS. These estimates were only slightly attenuated when adjusting for a CAD PRS (odds ratio, 1.26 [95% CI, 1.16–1.38] for LDL-C and 1.24 [95% CI, 1.13–1.36] for TG PRS). Conclusions: The CAD risk associated with a high polygenic load for lipid-increasing variants was proportional to their impact on lipid levels and partially overlapping with a CAD PRS. In contrast with a PRS for CAD, the lipid PRSs point to known and directly modifiable risk factors providing additional guidance for clinical translation.
    Type of Medium: Online Resource
    ISSN: 2574-8300
    URL: Article
    DOI: 10.1161/CIRCGEN.119.002725
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 2927603-2
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