scholarly journals Mendelian randomization analysis to characterize causal association between coronary artery disease and COVID-19

2020 ◽  
Author(s):  
Lang Wu ◽  
Jingjing Zhu ◽  
Chong Wu
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Observational Studies ◽  
Mendelian Randomization ◽  
Causal Association ◽  
Mendelian Randomization Analysis ◽  
Log Odds ◽  
Individual Decisions ◽  
Artery Disease ◽  
Randomization Analysis

AbstractObservational studies have suggested that having coronary artery disease increases the risk of Coronavirus disease 2019 (COVID-19) susceptibility and severity, but it remains unclear if this association is causal. Inferring causation is critical to facilitate the development of appropriate policies and/or individual decisions to reduce the incidence and burden of COVID-19. We applied Two-sample Mendelian randomization analysis and found that genetically predicted CAD was significantly associated with higher risk of COVID-19: the odds ratio was 1.29 (95% confidence interval 1.11 to 1.49; P = 0.001) per unit higher log odds of having CAD.

scholarly journals Mendelian Randomization Analysis of Hemoglobin A1cas a Risk Factor for Coronary Artery Disease

Diabetes Care ◽  
2019 ◽  
Vol 42 (7) ◽  
pp. 1202-1208 ◽  
Author(s):  
Aaron Leong ◽  
Ji Chen ◽  
Eleanor Wheeler ◽  
Marie-France Hivert ◽  
Ching-Ti Liu ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Risk Factor ◽  
Coronary Artery ◽  
Mendelian Randomization ◽  
Mendelian Randomization Analysis ◽  
Artery Disease ◽  
Randomization Analysis

scholarly journals Mendelian randomization analysis supports the causal role of dysglycaemia and diabetes in the risk of coronary artery disease

2015 ◽  
Vol 36 (23) ◽  
pp. 1454-1462 ◽  
Author(s):  
Stephanie Ross ◽  
Hertzel C. Gerstein ◽  
John Eikelboom ◽  
Sonia S. Anand ◽  
Salim Yusuf ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Mendelian Randomization ◽  
Causal Role ◽  
Mendelian Randomization Analysis ◽  
Artery Disease ◽  
Randomization Analysis

scholarly journals The Impact of Serum 25-hydroxyvitamin D, Calcium, and Parathyroid Hormone Levels on the Risk of Coronary Artery Disease in Patients With Diabetes: A Mendelian Randomization Study

2020 ◽  
Author(s):  
Songzan Chen ◽  
Fangkun Yang ◽  
Tian Xu ◽  
Yao Wang ◽  
Kaijie Zhang ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Parathyroid Hormone ◽  
Coronary Artery ◽  
Mendelian Randomization ◽  
Causal Association ◽  
Serum 25Ohd ◽  
Hydroxyvitamin D ◽  
Patients With Diabetes ◽  
25 Hydroxyvitamin D ◽  
Artery Disease

Abstract BackgroundTo investigate the causal association between serum 25-hydroxyvitamin D (25OHD), calcium (Ca), and parathyroid hormone (PTH) levels and the risk of coronary artery disease (CAD) in patients with diabetes using a Mendelian randomization approach.MethodsGenetic signatures associated with serum 25OHD, Ca, and PTH levels were extracted from recently published genome-wide association study (GWAS), including 79,366, 39,400, 29,155 individuals, respectively. Genetic association estimates for CAD in patients with diabetes were obtained from a GWAS of 15,666 individuals with diabetes (3,968 CAD cases, 11,696 controls). The inverse-variance-weighted method was employed for the primary analysis, and other robust methods were applied for sensitivity analyses.ResultsSix, seven and five single nucleotide polymorphisms were identified as instrumental variables for serum 25OHD, Ca and PTH levels, respectively. There was no significant association between genetically predicted serum 25OHD levels and the risk of CAD in patients with diabetes (odds ratio (OR) = 1.04, 95% confidence interval (CI): 0.58 - 1.87, P = 0.888). Similarly, genetically predicted serum Ca (OR = 1.83, 95% CI: 0.62 – 5.35, P = 0.273) and PTH levels (OR = 1.27, 95% CI: 0.67 – 2.44, P = 0.464) were not significantly associated with the risk of CAD in patients with diabetes. These findings were robust in sensitivity analyses.Conclusions/interpretationThis study found no evidence to support the causal association between serum 25OHD, Ca and PTH levels and the risk of CAD in patients with diabetes.

scholarly journals Physical activity, sedentary behavior and risk of coronary artery disease, myocardial infarction and ischemic stroke: a two-sample Mendelian randomization study

2021 ◽  
Author(s):  
Martin Bahls ◽  
Michael F. Leitzmann ◽  
André Karch ◽  
Alexander Teumer ◽  
Marcus Dörr ◽  
...  
Keyword(s):  
Physical Activity ◽  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Ischemic Stroke ◽  
Coronary Artery ◽  
Sedentary Behavior ◽  
Mendelian Randomization ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Artery Disease

Abstract Aims Observational evidence suggests that physical activity (PA) is inversely and sedentarism positively related with cardiovascular disease risk. We performed a two-sample Mendelian randomization (MR) analysis to examine whether genetically predicted PA and sedentary behavior are related to coronary artery disease, myocardial infarction, and ischemic stroke. Methods and results We used single nucleotide polymorphisms (SNPs) associated with self-reported moderate to vigorous PA (n = 17), accelerometer based PA (n = 7) and accelerometer fraction of accelerations > 425 milli-gravities (n = 7) as well as sedentary behavior (n = 6) in the UK Biobank as instrumental variables in a two sample MR approach to assess whether these exposures are related to coronary artery disease and myocardial infarction in the CARDIoGRAMplusC4D genome-wide association study (GWAS) or ischemic stroke in the MEGASTROKE GWAS. The study population included 42,096 cases of coronary artery disease (99,121 controls), 27,509 cases of myocardial infarction (99,121 controls), and 34,217 cases of ischemic stroke (404,630 controls). We found no associations between genetically predicted self-reported moderate to vigorous PA, accelerometer-based PA or accelerometer fraction of accelerations > 425 milli-gravities as well as sedentary behavior with coronary artery disease, myocardial infarction, and ischemic stroke. Conclusions These results do not support a causal relationship between PA and sedentary behavior with risk of coronary artery disease, myocardial infarction, and ischemic stroke. Hence, previous observational studies may have been biased. Graphic abstract

Associations of observational and genetically determined caffeine intake with coronary artery disease and diabetes

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
A Said ◽  
Y.J Van De Vegte ◽  
N Verweij ◽  
P Van Der Harst
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Mendelian Randomization ◽  
Cox Regression ◽  
Caffeine Intake ◽  
Uk Biobank ◽  
Genome Wide ◽  
Artery Disease ◽  
Genetically Determined

Abstract Background Caffeine is the most widely consumed psychostimulant and is associated with lower risk of coronary artery disease (CAD) and type 2 diabetes (T2D). However, whether these associations are causal remains unknown. Objectives This study aimed to identify genetic variants associated with caffeine intake, and to investigate possible causal links between genetically determined caffeine intake and CAD or T2D. Additionally, we aimed to replicate previous observational findings between caffeine intake and CAD or T2D. Methods Genome wide associated studies (GWAS) were performed on caffeine intake from coffee, tea or both in 407,072 UK Biobank participants. Identified variants were used in a two-sample Mendelian randomization (MR) approach to investigate evidence for causal links between caffeine intake and CAD in CARDIoGRAMplusC4D (60,801 cases; 123,504 controls) or T2D in DIAGRAM (26,676 cases; 132,532 controls). Observational associations were tested within UK Biobank using Cox regression analyses. Results Moderate observational caffeine intakes from coffee or tea were associated with lower risks of CAD or T2D compared to no or high intake, with the lowest risks at intakes of 120–180 mg/day from coffee for CAD (HR=0.77 [95% CI: 0.73–0.82; P<1e-16]), and 300–360 mg/day for T2D (HR=0.76 [95% CI: 0.67–0.86]; P=1.57e-5). GWAS identified 51 novel genetic loci associated with caffeine intake, enriched for central nervous system genes. In contrast to observational analyses, MR analyses in CARDIoGRAMplusC4D and DIAGRAM yielded no evidence for causal links between caffeine intake and the development of CAD or T2D. Conclusions MR analyses indicate caffeine intake might not protect against CAD or T2D, despite protective associations in observational analyses. Manhattan_plot_CaffeineIntake Funding Acknowledgement Type of funding source: None

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