Long Covid linked to increased risk of abnormal blood clotting

People suffering from long COVID may face an increased risk of abnormal blood clotting, according to a study at UCLH and UCL published in the journal Blood Advances.

Researchers also found that this blood abnormality was four times more likely in those experiencing difficulties with basic exercise more than 12 weeks after their COVID-19 infection.

The study offers important new insight into the potential mechanisms behind the longer-term effects of COVID-19 infection.

Since long COVID is an emerging condition, its biological basis is not fully understood. This research provides insight into the underlying medical mechanisms, such as damage to cells that line blood vessels, of the disease.

“By definition, this syndrome occurs when one experiences COVID-related symptoms long after the onset of infection that we can't attribute to any other cause or diagnosis,” explained study author Dr Nithya Prasannan, of the Department of Haematology at UCLH. “This study offers us laboratory and clinical evidence to begin to understand why some people experience long COVID symptoms.”

To conduct this study, a team led by UCLH’s Dr. Melissa Heightman assessed people in an outpatient post-COVID clinic between July 2020 and May 2021. Participants were said to have long COVID if they experienced symptoms three months after the onset of their original COVID-19 infection and if those symptoms persisted for at least two additional months – in the absence of other contributing diagnoses.

Researchers measured abnormal blood clotting markers by assessing the relative levels of two proteins in the body. They analyzed the ratio of Von Willebrand factor (VWF), a protein important in blood clotting, to ADAMTS13, a protein that cuts or splices VWF to prevent it from clogging blood vessels.

If there was significantly more VWF than ADAMTS13 in the bloodstream, scientists characterized patients as being in a pro-thrombotic state, meaning that they could face a greater risk of developing blood clots.

Participants also completed exercise tests, performing timed activities such as repeatedly going from sitting to standing position from a chair while wearing oxygen monitors.

Researchers measured oxygen levels and tested participants’ blood before and after exercise to measure their lactate levels, which helped describe participant response to exertion. During exercise, the body converts glucose (sugar) into energy using oxygen. However, when oxygen levels are depleted, the body starts producing lactate instead, which can be turned into energy without oxygen.

In the study, patients who exhibited a significant decrease in oxygen levels (measured by a sensor on the patient’s finger) while exercising and/or a rise in lactate afterward were said to demonstrate an impaired exercise capacity. Notably, patients with raised levels of blood clotting markers were also four times more likely to have an impaired exercise capacity.

In the future, Dr. Prasannan and her colleagues aim to assess patient bloodwork using different research platforms over the course of their long COVID illness to assess how their risk of thrombosis might change with the progression of their symptoms. She suggested that this additional monitoring could not only help confirm possible mechanisms underlying long COVID, but also offer insight into the effects of potential treatment options for the condition.

“I hope that people will view this research as a step forward in understanding what causes long COVID, which will hopefully help us guide future treatment options,” explained Dr. Prasannan. “I encourage people experiencing long COVID to participate in clinical trials when available because the more data we have, the better we can understand this condition.”