Silvia Di Maio (Austria)
Medical University of Innsbruck
Department of Genetics and Pharmacology, Institute of Genetic Epidemiology
Silvia Di Maio, M.Sc., is a PhD Student at the Institute of Genetic Epidemiology, Medical University of Innsbruck, Austria. She received her Bachelor Degree in Biological Sciences at the University of Milano-Bicocca, Italy, and her Master Degree in Biology Applied to Nutritional Sciences at the University of Milan, Italy. Her research focuses on the cardiovascular risk factor Lipoprotein(a) [Lp(a)]. Silvia Di Maio investigates genetic variants influencing the plasma concentration of Lp(a) and its causal role in human diseases, using molecular, statistical and computational approaches in large population studies.

Presenter of 1 Presentation

 Conference Calendar

LIPOPROTEIN(A) AND SARS-COV-2 INFECTIONS: RISK FOR ISCHEMIC HEART DISEASE AND THROMBOEMBOLIC EVENTS.

Session Name
0360 - Atherothrombosis and myeloid cells (ID 11)
Session Type
Workshop - Risk factors
Date
Mon, 23.05.2022
Session Time
15:45 - 17:15
Room
Attilio Maseri - Blue room
Presenter
Lecture Time
16:45 - 16:55

Abstract

Background and Aims

SARS-CoV-2 positive patients show high frequency of thromboembolic complications. Comorbidities like ischemic heart disease (IHD) associate with worse outcome. Since lipoprotein(a) [Lp(a)] is a strong risk factor for IHD and has possibly thrombogenic properties, we investigated in UK Biobank whether SARS-CoV-2 infections alter the Lp(a)‑driven risk for IHD and thromboembolic events.

Methods

Follow-up study from March 16, 2020 to November 30, 2020 in 6,937 positive patients and 435,104 population controls (negative or non‑tested) from UK Biobank. We compared the median of baseline Lp(a) (measured long before the pandemic) in the two groups by Wilcoxon test and the frequency of IHD and thromboembolic events by chi‑square test. The Lp(a)‑driven risks for IHD and thromboembolic events were estimated by logistic regression models using Lp(a) both as a continuous variable and in categories.

Results

The Lp(a) concentration were similarly distributed in positive patients and population controls. Thromboembolic events were five‑times more frequent in SARS-CoV-2 positive patients (1.54% vs. 0.31%, p=4.68e-74), but did not associate with Lp(a) (OR=1.00; p=0.90). However, the IHD risk was significantly associated with the Lp(a) concentration in both groups. Interestingly, the risk increase was steeper in SARS‑CoV‑2 positive patients (interaction p-value=0.030) (Figure). The OR for IHD of the top 5% to the bottom 20% of the Lp(a) distribution was 48% higher within positive patients (OR[95%CI]=2.22[1.40‑3.54], p=0.00067) versus population controls (OR[95%CI]=1.50[1.34‑1.69), p=2.20e-12).figure.png

Conclusions

SARS-CoV-2 infections enhance the association between Lp(a) and IHD. Baseline Lp(a) does not affect the risk for thromboembolic events in SARS-CoV-2 patients.

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