Healthy Life Webinar 2. Why the links between COVID-19 and cardiovascular risk? Clues for reducing disease severity

Click here to watch the video – speakers and discussants from the UK, Hong Kong, India and Middle East.

Healthy heart charity the Cardiovascular Research Trust has launched a regular monthly series of live webinars on healthy life and how to prevent heart disease and related illnesses.
Do please email us ( if you would like to suggest ideas for topics, questions and speakers for these live sessions.
Webinars are free and hosted on Zoom usually at 4pm UK time on the 3rd Monday of each month.

4 pm UK time Monday July 20th 2020
Session 2. Why the links between COVID-19 and cardiovascular risk?

Chair: Professor Donald Singer, Chair of the Cardiovascular Research Trust and President, FPM, London

Panel: Professor Bernard Cheung, University of Hong Kong; Dr Philip Welsby, Associate Editor, Postgraduate Medical Journal, Edinburgh; Mr K P Iyengar, Department of Orthopaedics, Southport District General Hospital; Dr Rajesh Kamath, Prasanna School of Public Health, Manipal Academy of Higher Education, India; Dr Prashanth Kulkarni, Consultant Cardiologist, Care Hospitals, Hyderabad, India; Dr Emmanual Fru Nsutebu, Infectious Disease Division, Sheikh Shakhbout Medical City, Abu Dhabi, United Arab Emirates.

Our speakers will discuss direct and indirect links between COVID-19 and cardiovascular disease and how these can be minimised. These include:

1. ACE-2 (angiotensin converting enzyme II) is the key docking protein by which the COVID-19 virus binds to cells [1]. This is also the key cell entry receptor used by the initial SARS-CoV [1]. ACE-2 is mainly found on vascular endothelial cells, the renal tubular epithelium and the Leydig cells of the testis. Copies of the ACE-2 protein are present in increased numbers in patients with risk factors for heart disease. ACE-2 could also be a therapeutic target in the treatment of COVID-19.
2. It is now clear that reasons why some people may have unexpectedly severe lung damage include pro-coagulant effect of  the COVID-19 virus [2-4]. This can cause multiple clots in lung vessels, thus reducing the ability of the lungs to absorb oxygen from the air and clear carbon dioxide from the body. Other infections are well-recognised to increase blood coagulability  however these effects may be particularly severe in COVID-19.
3. Several drugs currently being used empirically or in clinical trials may cause cardiac toxicity resulting in sudden cardiac death arrhythmias.
4. There are also indirect reasons for increased cardiovascular disease because of the COVID-19 pandemic. These include:
a. poorer recognition and control of cardiovascular risk factors and established serious disorders of the heart, brain and circulation due to reduced access to medical services.
b. malnutrition in patients self-isolating at home may also increase risk of falls, heart attack and stroke.

1. Zhou, P., Yang, X., Wang, X. et al. A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature 579, 270–273 (2020).
2. Jose, RJ,  Manuel, A. COVID-19 cytokine storm: the interplay between inflammation and coagulation. Lancet 2020; S2213-2600(20)30216-2.
3. Leonard-Lorant I, Delabranche X, Severac F, et al. Acute Pulmonary Embolism in COVID-19 Patients on CT Angiography and Relationship to D-Dimer Levels [published online ahead of print, 2020 Apr 23]. Radiology. 2020;201561. doi:10.1148/radiol.2020201561
4. Connors JM, Levy JH. COVID-19 and its implications for thrombosis and anticoagulation [published online ahead of print, 2020 Apr 27]. Blood. 2020;blood.2020006000. doi:10.1182/blood.2020006000




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