Serological mechanisms underlying cardiotoxicity in COVID-19
Study code
NBR113
Lead researcher
Dr. Sanjay Sinha
Study type
Samples and data
Institution or company
University of Cambridge
Researcher type
Academic
Speciality area
Cardiovascular Disease, Infection, COVID
Recruitment Site
Cambridge
Summary
With global COVID-19 cases rising and a further projected increase for the months to come, therapeutic strategies to combat the disease are urgently needed. Despite the likely approval of a small number of COVID-19 vaccines, the NHS will inevitably need to cope with large numbers of COVID-19 patients over many months, as a broad rollout of national vaccine programs will take a considerable amount of time, and uptake and effectiveness are unlikely to reach 100%.
Heart complications occur in up to 30% of COVID-19 critically ill patients and therefore hospitals will continue to treat these patients for which no satisfactory therapy exists. The cause of the heart damage remains poorly understood. One idea is that the inflammation following infection by SARS-CoV2 (the virus causing COVID-19) might be causing the heart damage.
Our project will use the serum (fluid part of the blood) collected from COVID-19 patients to see whether this damages heart cells that we generate from stem cells in a tissue culture dish. We think that cytokines (the proteins that cause the inflammatory process) in the serum of these patients might cause heart muscle damage or interfere with their beating.
These experiments will identify the specific cytokines or combination of cytokines that might be responsible for the heart injury. We can then identify drugs that can be employed to block the damaging cytokines to ultimately prevent or ameliorate heart damage. Furthermore, the results will be useful to predict which COVID-19 patients will be more likely to develop heart complication and will ultimately result in reduced disability and death from heart problems.