Cardiovascular disease (CVD) is the leading global cause of mortality and morbidity, with ischemic heart disease (IHD) representing approximately half of all CVD-related deaths. Precise, personalized risk assessment and treatment recommendations are crucial for addressing the diverse population at risk of CVD. Current standard approaches rely on algorithms that incorporate a limited set of traditional risk factors to estimate CVD and IHD risk. However, significant cardiovascular events often occur in individuals categorized as low risk, underscoring the need for ongoing research to enhance preventive strategies.

The Focus
The MyDigiTwin initiative aims to provide individuals with personalized insights into their cardiac health, enabling proactive monitoring and management of cardiovascular conditions. This integrated digital health platform empowers individuals to take control of their cardiac health by offering accessible, data-driven insights and tools.

The Research
MyDigiTwin is a pioneering research initiative focused on revolutionizing cardiac health management by integrating advanced AI technologies with extensive patient data. The development of MyDigiTwin involves harnessing large-scale longitudinal datasets from over 500,000 patients, combined with sophisticated AI algorithms. This approach enables the platform to analyze diverse health parameters and generate tailored recommendations for users based on their unique health profiles. By leveraging AI and comprehensive patient data, MyDigiTwin represents an innovative approach to preventive and personalized healthcare, facilitating early detection and intervention for cardiovascular conditions.

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Contact person:

Prof. Dr. P. van der Harst (Pim)

Principal investigators

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The SARS-CoV-2 pandemic has a high burden of morbidity and mortality due to development of the acute respiratory distress syndrome (ARDS). The reninangiotensin-system (RAS) plays an important role in the development of ARDS, with ACE2 (angiotensin-converting enzyme 2) being a key enzyme within this. The virus's spike protein binds to ACE2, facillitating cellular internalization. Downregulation of ACE2 results in the excessive accumulation of angiotensin II, which in turn increases pulmonary vascular permeability through stimulation of the angiotensin II type 1a receptor (AT1R), thereby exacerbating lung pathology associated with decreased ACE2 activity. Currently available AT1R blockers (ARBs) such as valsartan, have shown potential to block this pathological process mediated by angiotensin II. The Focus The primary aim of the PRAETORIAN-COVID trial is to investigate the effect of the ARB valsartan compared to placebo on the composite end point of admission to an intensive care unit, mechanical ventilation, or death of COVID-19 patients. The Research Participants receiving active treatment are administered valsartan at a dosage titrated to blood pressure, with a maximum of 160 mg twice daily. Participants receiving placebo are provided with a matching placebo. The treatment duration was 14 days or until reaching the primary endpoint, or until hospital discharge, if applicable within 14 days.Two complementary mechanisms underpin the potential efficacy of angiotensin II type 1 receptor blockers (ARBs) in preventing acute respiratory distress syndrome (ARDS) and reducing morbidity and mortality: ARBs block excessive angiotensin-mediated activation of the AT1R. ARBs upregulate ACE2 expression, leading to reduced angiotensin II levels and increased production of the protective vasodilator angiotensin 1–7. Given these mechanisms, ARBs show promise in preventing ARDS development, potentially reducing the need for intensive care unit (ICU) admission and mechanical ventilation, and ultimately lowering mortality rates associated with SARS-CoV-2 infection.
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