I have become increasingly uncomfortable with the term “Long COVID.”
Not because the condition is not real. Quite the opposite. I think the term has become too small, too vague, and too politically loaded for what we are actually trying to understand. Many people hear “Long COVID” and immediately place it into a box. Some think of fatigue. Some think of anxiety. Some think of a post-viral syndrome. Some simply switch off because they are tired of the entire subject.
But when I look at the science now, I do not think the most important question is whether symptoms have lasted a long time after COVID. The more important question is this: what if COVID has left a persistent injury pattern in the smallest blood vessels of the body?
That is why I prefer the phrase post-COVID vascular damage. It is not perfect, but it moves us closer to mechanism. It forces us to ask what is happening in the microcirculation, in the capillaries, in the tissue-level blood flow that standard tests often fail to capture.
The Battleground Is Smaller Than We Thought
In my discussion with Dr Beate Jaeger and Joachim Gerlach, the central idea was simple but deeply uncomfortable. The main battleground may not be the large arteries, the obvious organs, or the routine scans. It may be the microcirculation.
Capillaries are the final delivery system. They are the smallest vessels, the point at which oxygen and nutrients actually reach the cells. You can think of them as the last tiny pipes supplying each street in a city. If the main water pipe is open but the last few metres are blocked, the house still has no water.
This is why the post-COVID picture can be so confusing. A patient may have a normal oxygen saturation, a normal echocardiogram, a normal CT scan, and routine blood tests that do not explain the severity of their symptoms. But if the capillary network is impaired, the body can still be failing at the level that matters most: tissue oxygen delivery.
The paper we discussed separates this into two forms of microvascular rarefaction. One is functional rarefaction, where the capillary is still there but blood does not flow properly through it. The other is structural rarefaction, where the capillary itself may be damaged or lost. That distinction is crucial. A blocked vessel may reopen. A lost capillary is a very different problem.
Microclots Are Not the Whole Story
For several years, much of the discussion has focused on microclots. That was necessary, because microclots gave us a way to understand why patients could feel profoundly unwell despite normal routine investigations.
But I think we now have to go beyond microclots alone.
The model that is emerging is more complex. There may be platelet activation, fibrin amyloid microclots, neutrophil extracellular traps, red blood cells becoming less deformable, endothelial inflammation, pericyte constriction, and macrophage activation all feeding into the same problem. Blood does not simply clot or not clot. It becomes rheologically abnormal. It becomes harder to move through the smallest vessels. It becomes inflammatory.
This matters because a red blood cell is roughly the size of the capillary it needs to pass through. It must deform to squeeze through that space. If the red cell becomes stiff, if the vessel entrance constricts, if platelets are activated, or if fibrin structures are forming inside that system, then oxygen delivery begins to fail even before we see obvious organ damage.
That is the pattern clinicians are not trained to look for.
Why the Patient Looks Well Until They Don’t
One of the most important clinical observations is that many patients do not collapse immediately. They deteriorate over weeks and months. They may describe a mild infection, a day or two of feeling unwell, then apparently recover. Two or three weeks later, something shifts. Fatigue appears. Exercise tolerance collapses. Palpitations start. Brain fog appears. They cannot understand why they have moved from functioning to struggling.
The problem is that we are still thinking in old timelines. We look for the acute infection. We look for the obvious complication. We do not always trace the delayed immune-vascular effect back to the preceding viral exposure.
I see this repeatedly in medicine. The event and the consequence are separated by time, so the connection is missed. If a patient has a stroke or cardiac event two weeks after a mild respiratory illness, the infection is often treated as irrelevant. If a patient becomes housebound after a viral episode that seemed trivial, we may look for psychological explanations rather than ask whether the microcirculation has changed.
That is a major blind spot.
The Difference Between Damage and Dysfunction
I think we need to be very careful here. Not every post-COVID symptom means permanent capillary loss. That would be too simplistic and probably wrong.
Some patients may have primarily functional obstruction. Their capillaries remain present, but blood flow is impaired by microclots, platelet activation, inflammatory constriction, or red-cell stiffness. These patients may have a better chance of meaningful recovery if the process is identified early and treated appropriately.
Others may develop structural damage. That is the more concerning possibility. If capillaries are actually lost, the tissue they supplied may also be compromised. This is most frightening in tissues with poor regenerative capacity, such as myocardium and brain. Once fibrosis begins, or once highly specialised cells are lost, we are no longer talking about simple fatigue. We are talking about lost reserve.
This is the hypertension analogy I keep coming back to. Before hypertension was properly understood, people watched it silently damage the heart, kidneys, eyes and brain. By the time treatment started, some of the injury was already irreversible. I worry that post-COVID microvascular disease may be following a similar pattern. We are watching symptoms without measuring the right pathology.
Why One Protocol Will Not Solve This
One of the reasons the system struggles with this illness is that medicine wants clean protocols. One diagnosis. One mechanism. One drug. One outcome measure.
But this condition does not behave like that.
Some patients are predominantly vascular. Some are neurological. Some are gut-driven. Some have dysautonomia. Some have viral persistence. Some have autoimmune features. Many overlap. That means a single trial of a single drug against a vague label like “Long COVID” is almost guaranteed to disappoint.
This does not mean treatment is impossible. It means phenotyping is essential. We need to know whether the dominant problem is clotting, endothelial inflammation, macrophage activation, viral persistence, mast-cell activation, mitochondrial dysfunction, autoimmunity, or loss of microvascular reserve. Without that, we are not treating patients. We are guessing.
Dr Jaeger’s presentation emphasised how severe cases may require layered approaches: correcting deficiencies, addressing platelet activation and coagulation abnormalities, considering antihistamine strategies in selected patients, and in extreme cases using H.E.L.P. apheresis or related extracorporeal approaches. The important point is not that every patient needs this. Most do not. The important point is that the sickest patients show us the biology more clearly.
The Clinical Community Has to Wake Up
The most dangerous response now is the desire to move on.
I understand the fatigue. The public is tired. Doctors are tired. Institutions are tired. But biology does not care whether we are tired. If a mechanism continues, the consequences continue.
What concerns me most is the quiet accumulation of damage. A patient does not need to become critically ill to lose function. An older person who was independent may become housebound and everyone says, “They are just getting old.” A younger person who was athletic may become unable to exercise and is told to pace themselves. A patient with wound complications, poor healing, inflammatory flares, or unexplained vascular symptoms may never have the dots connected.
The missing link may be the microcirculation.
What I Think This Means
I do not think post-COVID illness is one disease. I think it is a family of overlapping pathologies triggered by SARS-CoV-2 and shaped by the patient’s underlying biology.
But I increasingly think the microvascular component may be one of the most important parts of the puzzle. It explains why symptoms can be systemic. It explains why routine tests can be normal. It explains why exertion exposes the problem. It explains why the brain, heart, muscles, lungs and gut can all appear involved without a single obvious organ diagnosis.
Most importantly, it explains why early recognition matters.
If we identify functional obstruction early, there may be a window to restore flow and prevent progression. If we ignore it until structural rarefaction has occurred, we may be trying to reverse damage that should never have been allowed to accumulate.
That is the uncomfortable message. The smallest blood vessels may be carrying the biggest clue.
Timecodes
00:00 — Opening: Why post-COVID vascular damage matters
07:00 — The new paper: microvascular damage and capillary erasure
10:01 — Organ damage vs persistent post-COVID illness
13:26 — Why H.E.L.P. apheresis entered the discussion
15:30 — Early cases: clots, children, and clinical turning points
20:10 — Mapping the full disease: spike persistence and clotting
25:00 — Platelet activation, amyloid fibrin, and endothelial damage
29:50 — Why single-drug trials miss a multi-pathway disease
40:00 — Severe cases in young athletic patients
44:40 — Heparin and H.E.L.P. apheresis: proposed mechanisms
49:20 — Antivirals, immune reactivation, and glycocalyx support
54:50 — Capillary loss and tissue hypoxia: the key concept
59:00 — Case evidence: perimyocarditis, fibrinogen, and oxygenation
1:04:50 — Why early detection matters before irreversible loss
1:10:40 — Clinical silence, wound complications, and moving on too soon
1:15:00 — What needs to happen now: family doctors, reinfections, and mitigation
