A heart attack after COVID may not look like the classic heart attack we usually imagine.
A new core-lab study of patients with NSTEMI + COVID-19 suggests something more diffuse. Not just one blocked artery, but a blood-clotting and vessel inflammation problem🧵
First, two key terms.
STEMI is the type of heart attack where the ECG shows ST-segment elevation. It often means a major coronary artery is suddenly blocked.
NSTEMI is a heart attack without that classic ST elevation. It can be less obvious on ECG, but it is not minor.
So STEMI is often like a main pipe suddenly being blocked.
NSTEMI can be more complex. Partial blockage, smaller clots, multiple narrowed vessels, poor microvascular flow, or the heart being stressed by illness.
But COVID can add another layer.
COVID-19 is not just a respiratory infection.
In some patients, it affects the blood vessels, the inner vessel lining, platelets, inflammation, and clotting.
The vascular system can become more inflamed, more reactive, and more prone to clot formation.
This Canadian study looked at 155 patients with lab confirmed COVID-19 and NSTEMI.
Median age 67
Women 29.7%
COVID vacc recorded 82.6%
The study did not test vaccine effectiveness or analyze timing of vaccination.
The in-hospital death rate was 8.4%.
For context, the authors compare this with a historical pre-pandemic NSTEMI cohort where in-hospital mortality was 3.5%.
Not a perfect head-to-head comparison - but the signal is hard to ignore.
The angiograms told an important story.
Doctors often expect to find one clear culprit artery.
But in these COVID + NSTEMI patients, the picture was often messier. More clot, worse flow, and less of a simple one-artery explanation.
In the coronary arteries, blood clots were common.
Among patients who already had a stent, 25% had stent thrombosis.
And PCI - the procedure used to open a blocked coronary artery - was unsuccessful in about 22% of patients.
That matters.
PCI usually works by finding the blocked vessel and restoring blood flow.
But if the problem is more diffuse, with clotting, microvascular dysfunction, and widespread vessel inflammation, opening one spot may not solve the whole problem.
The ECG findings also fit this pattern.
Only 6 out of 155 patients had an ECG that clearly pointed to one specific heart territory.
Most had diffuse, non-localizing ST-segment changes.
That is not the usual one artery, one territory story.
Other findings were also concerning:
ST elevation in aVR 33%
Conduction abnormalities 19.4%
Q waves 16.9%
Global systolic dysfunction 32.3%
This suggests a broader hit to the heart and coronary circulation.
STEMI + COVID has looked even worse in earlier registry data.
The NACMI registry reported very high in-hospital mortality in STEMI patients with COVID-19.
That makes sense. STEMI is already a major emergency. Add COVID-related inflammation and clotting, and the risk can rise sharply.
But this new study’s message is different.
Even NSTEMI - often seen as the less dramatic heart attack - can become very serious when it happens alongside COVID-19.
The virus may change the biological environment in which the heart attack occurs.
COVID can add vascular inflammation, endothelial injury, platelet activation, increased clotting, microclots, worse coronary blood flow.
So the heart attack may not be just a local plumbing problem. It can become a more systemic vascular problem.
The study does not tell us exactly how to change treatment.
It did not test stronger anticoagulation, different antiplatelet therapy, PCI timing, or other interventions.
But it clearly describes a dangerous phenotype that deserves much more attention.
COVID can shift the body toward inflammation and clotting.
In this NSTEMI + COVID cohort, patients had more thrombus, diffuse ECG changes, more heart dysfunction, higher mortality, more PCI failure than expected from historical NSTEMI data.
For some people, COVID is also a vascular and cardiac risk event - and preventing infection and reinfection still matters.
Data were collected from April 2020 to December 2023, so the cohort likely spans multiple pandemic waves - early strains, Delta, and Omicron - but variant specific analysis was not performed.
Ellingson BKin at al., Angiographic and Electrocardiographic Characteristics of Patients With Non–ST-Segment Elevation Myocardial Infarction and COVID-19. sciencedirect.com/science/articl…
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A new narrative review in Communications Medicine sums up where the field stands on long COVID.
Not as one single, uniform diagnosis, but as a complex, multisystem condition after SARS2 infection🧵
Its value is in the synthesis. It brings together immunology, neurology, vascular biology, metabolism, and clinical medicine into one framework.
The review covers prevalence, pathophysiology, biomarkers, treatment strategies, and future research directions. It is a broad interpretation of the current literature.
For 2025, the societal cost of Long COVID and ME/CFS in Germany is estimated at €64.4 billion - about 1.44% of GDP.
For Czechia, this would roughly translate to around CZK 120 billion per year if we apply the same share of GDP - 1.44% of the Czech economy.
A simple population-based conversion would produce a higher number (200 billion), but that is an overestimate.
This should matter to you, @strakovka.
Because this is what poor public health policy costs. Ignoring prevention, ventilation, surveillance, post-COVID care, and the long-term damage caused by repeated infections.
A new systematic review looked at what happens to the heart after COVID - not during the acute infection, but months later.
The key point:
A normal ejection fraction does not always mean the heart is completely unaffected.🧵
In people assessed more than 12 weeks after PCR confirmed COVID - especially those with persistent cardiopulmonary symptoms - there is evidence of subtle, and sometimes persistent, cardiac involvement.
This may show up as
higher BNP/NT-proBNP
reduced LV-GLS
abnormalities on cardiac MRI
while LVEF often remains normal
Exertion and PEM.
A new paper studied people with long COVID using a 2-day (!) submaximal CPET protocol, combined with NIRS measurement on the calf muscle.
The authors looked at what happens to breathing, performance, and muscle oxygenation during repeated exertion🧵
The key finding.
In the long COVID group, muscle tissue oxygen saturation (TSI%) initially increased during exercise, but it did not stay elevated for as long as it did in controls. (Thomas 2026)
On day 2, this pattern was even worse. In long COVID, TSI% stayed above resting levels for a shorter period, while controls maintained elevated muscle oxygenation more effectively during exercise.
COVID-19 creates a state of immune dysregulation where the body may lose control over things it normally keeps suppressed - latent viruses, especially herpesviruses, and possibly even dormant cancer cells.
A new study on EBV and CD8 T cells fits into this bigger picture.🧵
The point is not simply that EBV can reactivate during COVID. We already have quite a lot of evidence for that.
In hospitalized patients with acute COVID, EBV reactivation was very common - around 68-73% - and it was seen not only in critical cases, but also in moderate disease.
The authors looked at EBV, CMV, HHV-6A and HHV-6B.
EBV dominated.
CMV and HHV-6B were detected only at low frequencies.
HHV-6A was not detected at all.
So this does not look like just random viral noise. EBV stands out.
In this cohort, children exposed to SARS-CoV-2 in utero showed higher rates of developmental delay and were also more likely to screen positive on an autism screening tool than pre pandemic controls🧵
The developmental delay signal comes from the group’s earlier work in the same cohort. In the abstract, the authors cite a rate of 11.6% in 172 exposed children versus 1.6% in 128 pre pandemic controls.
The newer clinical piece in this paper is the autism screening result. Among 218 SARS2 exposed children, 22 screened positive on M-CHAT-R/F (10.1%). In the control group, 30 of 527 screened positive (5.7%).