Even mild COVID infection increases risk of blood clots and death

A study in the UK found that mild (non-hospitalized) infections led to a 2.7x higher risk of blood clots and 10.2x higher risk of death compared to controls ( https://heart.bmj.com/node/174901.full ). H/T: @[email protected] 🧵 1/

Cardiovascular disease and mortality sequelae of COVID-19 in the UK Biobank

Objective To examine association of COVID-19 with incident cardiovascular events in 17 871 UK Biobank cases between March 2020 and 2021. Methods COVID-19 cases were defined using health record linkage. Each case was propensity score-matched to two uninfected controls on age, sex, deprivation, body mass index, ethnicity, diabetes, prevalent ischaemic heart disease (IHD), smoking, hypertension and high cholesterol. We included the following incident outcomes: myocardial infarction, stroke, heart failure, atrial fibrillation, venous thromboembolism (VTE), pericarditis, all-cause death, cardiovascular death, IHD death. Cox proportional hazards regression was used to estimate associations of COVID-19 with each outcome over an average of 141 days (range 32–395) of prospective follow-up. Results Non-hospitalised cases (n=14 304) had increased risk of incident VTE (HR 2.74 (95% CI 1.38 to 5.45), p=0.004) and death (HR 10.23 (95% CI 7.63 to 13.70), p<0.0001). Individuals with primary COVID-19 hospitalisation (n=2701) had increased risk of all outcomes considered. The largest effect sizes were with VTE (HR 27.6 (95% CI 14.5 to 52.3); p<0.0001), heart failure (HR 21.6 (95% CI 10.9 to 42.9); p<0.0001) and stroke (HR 17.5 (95% CI 5.26 to 57.9); p<0.0001). Those hospitalised with COVID-19 as a secondary diagnosis (n=866) had similarly increased cardiovascular risk. The associated risks were greatest in the first 30 days after infection but remained higher than controls even after this period. Conclusions Individuals hospitalised with COVID-19 have increased risk of incident cardiovascular events across a range of disease and mortality outcomes. The risk of most events is highest in the early postinfection period. Individuals not requiring hospitalisation have increased risk of VTE, but not of other cardiovascular-specific outcomes. Data may be obtained from a third party and are not publicly available. The UK Biobank will make the source data available to all bona fide researchers for all types of health-related research that is in the public interest, without preferential or exclusive access for any persons. All researchers will be subject to the same application process and approval criteria as specified by UK Biobank. For more details on the access procedure, see the UK Biobank website: <http://www.ukbiobank.ac.uk/register-apply> <http://www.ukbiobank.ac.uk/register-apply>.

Heart

The study looked at 17,871 COVID-19 cases in the UK between March 2020 and March 2021. People hospitalized *for* COVID-19 were at even higher risk:
118.0x = All-cause Death
27.6 = Venous Thromboembolism (blood clots)
21.6x = Heart Failure
17.5x = Stroke
14.9x = Atrial Fibrillation (AF)
13.6x = Pericarditis
9.9x = Myocardial Infarction (heart attack)

2/

The authors stated, "The associated risks were greatest in the first 30 days after infection but remained higher than controls even after this period."

It is important to note that the majority of the study was conducted *before* the COVID-19 vaccines were approved and being given in the UK. 3/

@[email protected] took data from the CDC and plotted the deaths per months in males aged 25-54 from cardiovascular or respiratory disease and found a 39% increase in deaths/month since the start of the pandemic even in this younger age group ( https://twitter.com/greg_travis/status/1602337780125908995 ). 4/
Gregory Travis -- @[email protected] on Twitter

“25-54 year old males are experiencing a nearly forty percent increase in monthly deaths from cardiovascular & respiratory diseases since the start of the pandemic Retweet of you would like public health professionals, including the CDC, to please explain why that is happening”

Twitter
Dr. Rae Duncan discusses how COVID infection causes endothelial damage (inner lining of blood vessels) happening directly from the virus infection itself and also from the immune response that is generated (cytokines) ( https://twitter.com/jeffgilchrist/status/1586321257091698688 ). 5/
Dr. Jeff Gilchrist on Twitter

“COVID-19: Increased cardiovascular risk following even mild infection Dr. Rae Duncan (@Sunny_Rae1) discusses the serious cardiovascular damage that can happen even after a single mild infection, making prevention of infection even more important ( https://t.co/GbnZzFiy9B ). 🧵1/”

Twitter
Dr. Claire Taylor explains more about which tests are needed to detect these microclots as the more common D-Dimer and CTPA tests will frequently come back "normal" but can find them using a VQ scan ( https://twitter.com/jeffgilchrist/status/1586043185901760512 ). 6/
Dr. Jeff Gilchrist on Twitter

“Dr. Claire Taylor (@drclairetaylor) explains more about the right tests such as VQ scans ( https://t.co/pCGd86EOIO ). 23/”

Twitter
Dr. Rae Duncan provides a real world example from the cardiovascular clinic she started where all the Long COVID patients they treated had microclots and platelet activation ( https://twitter.com/jeffgilchrist/status/1586043132134576128 ). 7/
Dr. Jeff Gilchrist on Twitter

“COVID-19: Real world example of the impact of infection Everyone should watch and listen to Dr. Rae Duncan's presentation about what she has seen COVID-19 do to the body ( https://t.co/nJbaGrkby0 ). This is not a cold or the flu despite how it may initially feel. 🧵1/”

Twitter
@PutrinoLab has found a way to image #microclots and activated #platelets which can be seen with your own eyes through a microscope ( https://twitter.com/VirusesImmunity/status/1589762087597019137 ). 8/
Prof. Akiko Iwasaki on Twitter

“Delighted to host @resiapretorius and @PutrinoLab at Yale today. @ValterVSM and I learned how to image #microclots and activated platelets. Activated platelet stained with anti-CD62P antibody are evident just looking through the eyepiece 👀 This is from a #longCOVID patient👇🏽😭”

Twitter
@PutrinoLab explains how microclots and platelet hyperactivation can be used as a biomarker by taking blood, spin, stain, and look under a microscope and then process the image ( https://twitter.com/PutrinoLab/status/1601223290273398784 ). 9/
Putrino Lab on Twitter

“Them: Microclots and platelet hyperactivation in #LongCovid can't be quantified by conventional standards, so we shouldn't use it as a biomarker Us: Hold our beer(s). Step 1: Take blood, spin blood, stain blood, look at blood under a microscope and capture an image of it 1/”

Twitter
The theory is that microclots may be blocking delicate blood vessels throughout the body, preventing oxygen from getting to where it needs to go resulting in shortness of breath, organ damage, cognitive dysfunction, and debilitating fatigue ( https://www.webmd.com/lung/news/20221207/microclots-may-explain-long-covid-symptoms/ ). 10/
Tiny, Menacing Microclots May Explain Long COVID’s Symptoms

Early in the pandemic, doctors noticed the sickest patients had high numbers of blood clots, which caused problems and killed patients long after they left the hospital. Some long COVID researchers suspect something similar may cause puzzling symptoms of long COVID.

WebMD
These images show microclots (green) circulating in the blood of people. You can see there is very little in image A from the controls without Long COVID and significantly more in images B, C, and D from those patients with Long COVID ( https://pubmed.ncbi.nlm.nih.gov/35195253/ ). 11/
A central role for amyloid fibrin microclots in long COVID/PASC: origins and therapeutic implications - PubMed

Post-acute sequelae of COVID (PASC), usually referred to as 'Long COVID' (a phenotype of COVID-19), is a relatively frequent consequence of SARS-CoV-2 infection, in which symptoms such as breathlessness, fatigue, 'brain fog', tissue damage, inflammation, and coagulopathies (dysfunctions of the blood …

PubMed
Besides cardiovascular damage, mild COVID infections can also damage your lungs too ( https://mstdn.science/@jeffgilchrist/109530595557671130 ). 12/
Dr. Jeff Gilchrist :verified: (@[email protected])

Attached: 2 images How even #mild #COVID-19 #infection can damage your #lungs https://twitter.com/jeffgilchrist/status/1604112214788640768 Studies are finding damage in #children and the #virus in lungs a year after infection, causing #T-cell infiltration, scarring, and a mechanism for lung injury. 🧵 1/

mstdn.science
A study just published found that mild COVID-19 induces early quantifiable persistent troponin I elevations in men age 55+ ( https://www.frontiersin.org/articles/10.3389/fcvm.2022.1053790/full ). Troponin I proteins are released in the blood when the heart muscle has been damaged. H/T: @[email protected] 13/
Mild COVID-19 induces early, quantifiable, persistent troponin I elevations in elder men

ImportanceElderly patients, especially men, are at risk of increased morbidity from coronavirus disease 2019 (COVID-19). Long-term data on troponin I levels in longitudinal observational studies of outpatients with mild to moderate COVID-19 are scarce.ObjectiveThis controlled cohort study aimed to evaluate the course of troponin I concentrations over a long period in convalescent COVID-19 outpatients with mild to moderate symptoms.Setting and participantsIn this cohort study, individuals with PCR-confirmed, mild to moderate SARS-CoV-2 infection as well as control individuals with confirmed negative PCR and negative SARS-CoV-2 serology were included. Study visits were performed from April 2020 through July 2021 (initialized during the first wave of the corona pandemic in Switzerland). A study visit in patients comprised blood draws every week in the first month and additionally after 8 weeks. This course was repeated in patients observed long-term.ResultsThis study enrolled 278 individuals from the Canton of St. Gallen, Switzerland, aged 12–92 years (59.5% women), who had mild to moderate COVID-19 symptoms (outpatients only) and a diagnosis confirmed by positive RT-PCR. Fifty-four of the participants with confirmed SARS-CoV-2 infection were followed for 14 months with repeat cycles of the testing protocol. In addition, 115 symptomatic patients that were PCR and serology negative were enrolled in the same time period as a control group. In COVID-19 patients, low-level tropon...

Frontiers

The study looked at 278 individuals in Switzerland from April 2020 to July 2021 (so the majority of the study took place before COVID vaccines were approved).

They found that troponin I levels were significantly increased in male COVID-19 patients age 55+ compared to controls from baseline until week 9 after infection and still remained elevated for at least 14 months (when the study finished). There was no significant difference found in women. 14/

"This statistically significant change in troponin I concentration was not dependent on co-morbidities in this group. ALT, Creatinine, BNP, and D-Dimer values after convalescence did not differ in comparison to the control cohort."

The study concludes, "This suggests the possibility of an ongoing, long-term, low-grade myocardial injury." 15/

The researchers believe this myocardial injury is likely the result of a combination of cytokine release, inflammation, microvascular damage, and a resulting supply/demand imbalance. Early data from their cohort revealed a gender difference in early immunological response after COVID-19 infection which may help explain why they are seeing a difference in troponin I levels between men and women post-infection. 16/
@jeffgilchrist To clarify, it looks like all of the first visits occurred in mid 2020 so this is an unvaccinated cohort. Can’t apply this data to vaccinated populations
@EliP @jeffgilchrist The issue is that MANY have been infected 2019-2021 so it absolutely still applies to those folk. I was sick with Covid in January 2020 to the point where I almost died gasping for breath with a chest that felt like it was going to explode in the chair I’m sitting in now. Had tingling in extremities/face. Terrifying shit. Now the concern is silent damage - regardless of vaccine. Current variants are very vaccine/immune evasive…
@TransitBiker @jeffgilchrist That wasn’t my point. My point was that mild cases in people with prior vaccination are different and need to be studied using separate cohorts of people.
@jeffgilchrist is there any relationship to men over 55 also suffering Atrial Fibrillation noted in other studies?
@jeffgilchrist
AARP might want to get its lobbying force on that right away, or start selling off their office furniture. One of the two.
@ddp
@noyes @jeffgilchrist @ddp
At this rate, these younger generations will never retire. They will be dead/disabled long before they reach 67 or whatever the age is.