Federica Galimberti (Italy)

University of Milan - Epidemiology and Preventive Pharmacology Service (SEFAP) Department of Pharmacological and Biomolecular Sciences
Federica Galimberti has a solid multidisciplinary background acquired during her Master’s degree in Pharmaceutical Chemistry and Technology (University of Milan, 2016). During her 3-year PhD program in Experimental and Clinical Pharmacological Sciences at the Department of Pharmacological and Biomolecular Sciences (University of Milan, 2016-2019), she expanded her knowledge on pharmacoepidemiology and pharmaco-utilization, in the frame of prevention of cardiovascular diseases and associated risk factors. In details, she gained expertise in the design, conduction and monitoring of drug use and safety profile studies, and prescribing appropriateness studies, mainly through healthcare utilization databases analyses. The expertise in analysing data acquired during her PhD experience led her to spend a period at Cardiovascular Epidemiology Unit of University of Cambridge, where she enhanced her knowledge on genomic and pharmacogenomic topic related to the cardiovascular system, and experienced the conduction of studies based on the principles of Mendelian randomization to identify risk factors that have both a causal and a cumulative effect of the risk of cardiovascular disease, and to model “naturally randomized trials” that attempt to frame and answer clinical questions to fill evidence gaps when an actual clinical trial would be impractical or impossible to conduct.

Author Of 1 Presentation

O016 - Mendelian randomization mediation analysis of the direct and indirect effects of adiposity on coronary artery disease (ID 1136)

Session Type
Genetics
Session Time
15:00 - 16:30
Date
Mon, 31.05.2021
Room
Live Streamed
Lecture Time
16:05 - 16:13

Abstract

Background and Aims

Increased adiposity is associated with an increased risk of coronary artery disease (CAD). Whether adiposity has a direct causal effect on the risk of CAD, or whether the effect of adiposity on CAD is mediated indirectly through the effect of adiposity on other risk factors is unknown.

Methods

We constructed a body mass index (BMI) instrumental variable genetic score composed of 96 variants associated with BMI. We used this instrument to conduct a multivariable Mendelian randomization (MR) mediation analysis to estimate the direct and indirect effects of BMI on CAD. The study included individual level data on 445,774 participants including 23,032 cases of CAD and 28,563 cases of type II diabetes (T2D); and summary data on up to 877,643 participants including 63,746 cases of CAD and 26,676 cases of T2D.

Results

A one unit increase in BMI was associated with a 7% increased odds of CAD (OR:1.07; 95%CI:1.05-1.09, p=1.6E-10), a 25% increased odds of T2D (OR:1.25, 95%CI:1.23-1.28, p=2.2E-131); and 0.34 mmHg increase in systolic blood pressure (SBP) (95%CI:0.25-0.42, p=8.5E-15). A one unit increase in BMI was also associated with a 0.02 mmol/L increase in triglycerides (95%CI:0.02-0.03, p=4.9E-21), but not with increased apolipoprotein B levels. In MR mediation analyses, 80.0% of the effect of BMI on the risk of CAD was mediated through BMI induced increases in SBP (29.6%) and T2D risk (50.4%).

Conclusions

The vast majority of the effect of increased BMI on the risk of CAD appears to be mediated indirectly through the effect of BMI on SBP and T2D.

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Presenter of 1 Presentation

O016 - Mendelian randomization mediation analysis of the direct and indirect effects of adiposity on coronary artery disease (ID 1136)

Session Type
Genetics
Session Time
15:00 - 16:30
Date
Mon, 31.05.2021
Room
Live Streamed
Lecture Time
16:05 - 16:13

Abstract

Background and Aims

Increased adiposity is associated with an increased risk of coronary artery disease (CAD). Whether adiposity has a direct causal effect on the risk of CAD, or whether the effect of adiposity on CAD is mediated indirectly through the effect of adiposity on other risk factors is unknown.

Methods

We constructed a body mass index (BMI) instrumental variable genetic score composed of 96 variants associated with BMI. We used this instrument to conduct a multivariable Mendelian randomization (MR) mediation analysis to estimate the direct and indirect effects of BMI on CAD. The study included individual level data on 445,774 participants including 23,032 cases of CAD and 28,563 cases of type II diabetes (T2D); and summary data on up to 877,643 participants including 63,746 cases of CAD and 26,676 cases of T2D.

Results

A one unit increase in BMI was associated with a 7% increased odds of CAD (OR:1.07; 95%CI:1.05-1.09, p=1.6E-10), a 25% increased odds of T2D (OR:1.25, 95%CI:1.23-1.28, p=2.2E-131); and 0.34 mmHg increase in systolic blood pressure (SBP) (95%CI:0.25-0.42, p=8.5E-15). A one unit increase in BMI was also associated with a 0.02 mmol/L increase in triglycerides (95%CI:0.02-0.03, p=4.9E-21), but not with increased apolipoprotein B levels. In MR mediation analyses, 80.0% of the effect of BMI on the risk of CAD was mediated through BMI induced increases in SBP (29.6%) and T2D risk (50.4%).

Conclusions

The vast majority of the effect of increased BMI on the risk of CAD appears to be mediated indirectly through the effect of BMI on SBP and T2D.

Hide