Every Covid-19 patient who has died of the disease shows signs of blood clotting, a leading scientist has claimed.
Professor Graham Cooke, an infectious disease specialist at Imperial College London, has analysed post-mortems of patients who have succumbed to the life-threatening illness.
Results showed ‘very clearly’ that all Covid-19 patients had some form of thrombosis, the medical term for a blood clot.
It may not have been the direct cause of each death — but the findings, which have yet to be released, support the theory Covid-19 causes vascular complications.
Although the coronavirus is considered a respiratory illness that attacks the lungs, in severe cases it can damage other organs.
Blood clots have emerged as one of many surprising complications and has led to the trial of a drug designed to stop blockages in vessels.
Every Covid-19 patient who has died of the disease shows evidence of blood clotting (stock illustration), a London scientist involved in a post mortem study has claimed
Professor Cooke discussed Imperial’s research at a webinar for the Royal Society of Medicine.
‘We did a very large post mortem series which showed very clearly that every patient we looked at had evidence of thrombosis somewhere,’ he said.
‘Obviously there is an element of chance for each patient for how that plays out.
‘We’ve seen patients who have coronary thrombosis [a blood clot in a heart vessel] and vascular thrombosis [a blood clot in a vein generally].
‘So it does appear to be a very important part of the disease and we see that in terms of activation of the coagulation system.’
Blood clotting involves a series of steps, the first of which is known as ‘activation’ —
This occurs when platelets — blood-clotting cells — change shape from a flat disk to a ball and congregate together to form a plug.
Professor Cooke, involved with the National Institute for Health Research, a research arm of the NHS, added: ‘It’s important to note Covid is a multi-system disease.
‘I think one of the features that seems to separate it from other severe viral disease is this more hypercoagulable state that seems to be associated with later disease.’
A hypercoagulable state occurs when the blood is clotting more than necessary, and can be part of a blood disorder or triggered by medications, cancer, heart attacks or HIV, for example.
It’s dangerous because it can lead to the formation of a blood clot in the veins which can travel through the bloodstream and cause deep vein thrombosis — a blood clot in the veins of the pelvis, leg, arm, liver, intestines or kidneys.
It can also cause a pulmonary embolism — a blood clot in the lungs — and raise the risk of stroke, heart attack, severe leg pain, difficulty walking, or even the loss of a limb.
Doctors say they have noticed a considerable amount of Covid-19 patients with blood clotting problems, sparking concern the disease is a vascular infection as well as a respiratory one.
Professor Roopen Arya, from King’s College London, estimated in May that as many as 30 per cent of coronavirus hospital patients had blood clots.
‘I think it has become apparent that thrombosis is a major problem,’ he told the BBC.
While experts are unsure why the virus causes the blockages, the prevailing theory is that it is the result of a an immune overreaction called a ‘cytokine storm’.
When the immune response goes into overdrive, it can damage healthy tissue. if blood vessels are affected they can leak, causing blood pressure to drop and driving up the chance of clots forming.
Scientists at the University of Utah suggested inflammation is triggering a change in the behaviour of blood cells.
They made the ‘important’ discovery that platelets were ‘hyper active’ in Covid-19 patients compared with healthy people.
In petri dish experiments, the platelets of infected patients stuck together faster.
The virus was not found in the platelets themselves, which suggested that the virus indirectly causes changes to the blood, perhaps through altering hormones.
But Dr Robert Campbell, senior author of the study published in early July, said: ‘Our finding adds an important piece to the jigsaw puzzle that we call Covid-19.’
It could explain why up to 62 per cent of hospitalised Covid-19 patients in the UK suffer a stroke during their stay, according to figures from 125 patients investigated by British researchers.
Professor Cooke said there are studies ongoing to look at whether anti blood-clotting therapies could improve outcomes for Covid-19 patients.
It follows the British Heart Foundation launching a trial of TRV027, which could work by maintaining a healthy balance of hormones that regulate the thickness and pressure of someone’s blood.
This is usually done by proteins called ACE-2 receptors.
Coincidentally, ACE-2 receptors are the doorway for the coronavirus to enter human cells. The virus latches onto the proteins that coat cell surfaces before infecting them.
The fact that both the drug and the virus interact with the same receptor has given scientists hope that the treatment could work.
TRV027 has already worked for heart failure by keeping a healthy balance between two key hormones which regulate the thickness of someone’s blood.
The drug functions by maintaining a healthy balance between the two hormones angiotensin II and angiotensin 1-7.
If angiotensin II becomes too dominant, the blood gets stickier and more likely to clot.
Seriously-ill coronavirus patients tend to have a balance that seems to tip towards higher amounts of angiotensin II, studies have shown.