I wanted to share a story of a patient I saw this week. Very fit man aged 52, previous marathon runner, suspected mild #COVID19 March 2020. Extensively investigated by cardiology in 2020 for symptoms of chest pain, dizziness and struggling to exercise 1/
Cardiac MR showed some fibrosis suggestive of previous myocarditis, but all other Ix were normal. By November 2021 he was back to running 15km, but very slow improvement. Dec 2021 had booster followed by COVID re-infection over a couple of weeks (again mild symptoms) 2/
After this he developed similar symptoms to 2020, dizziness on walking up stairs, chest pain (anginal sounding). We did his spirometry and gas transfer - completely normal. On the 1 minute sit-to-stand he desaturated to 92%, HR increased from 49 to 110 and he became quite SOB 3/
Put him through the CT scanner, CTPA was negative for PEs but showed some possible right heart strain. I discussed this with some colleagues and given the desaturation we decided to perform a VQ scan. This showed extensive clots 4/
He had been referred to Resp as non-urgent. It was a chance discussion that the appointment was expedited. He was walking around with PEs and RH strain! I am really concerned about the number of people with 'mild COVID' out there who may have undiagnosed thromboembolic disease 5/
causing non-specific chest pain and SOB. This chap's symptoms were not alarming, in fact he thought it was all a bit of a fuss about nothing 6/
This paper is a multi-national report of over 900,000 people indicating propensity of risk for arterial and venous thrombi is in men, with increasing age, and association with fatalities (4-fold in non-hospitalized) thelancet.com/journals/lanin… 7/
We also know that beyond the first 30d after infection, individuals with COVID-19 are at increased risk of cardiovascular disease spanning several categories, even in the non-hospitalised 8/
There is mounting evidence that COVID19 is a pro-thrombotic, vascular/endothelial disease. The question is, are the tests we are currently doing in #LongCOVID clinics good enough? If CTPA and lung function are normal, should we be looking harder? Do people have access to VQ? 9/
On a microvascular level there is evidence of abnormal clotting and platelet hyperactivation. Why is it that the 'knowns' are not translating into treatment options? We know that dual anti platelet therapy & anticoagulation are effective in preventing vascular events 10/
In the absence of any other treatment, why are we not prescribing these drugs to people with #LongCOVID? With monitoring / risk benefit discussion of course. RCTs are not the only type of evidence. Real-world studies could be set up quickly via LC clinics 11/
Surely we should be thinking about primary prevention of 'known' vascular and thrombotic complications? I worry for the people out there with #LongCOVID. The lucky ones will have access to the best care and treatment, but how many others don't? END/
(Everything shared in this thread is with express permission from the patient.)
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