A new study in Journal of Clinical Medicine shows that after COVID-19, many patients have persistent impairment of oxygen transfer in the lungs (DLCO/KCO) - lasting 12 to 22 months, even when basic spirometry looks almost normal🧵
Key point?
FEV1 remains largely stable, while FVC improves only slowly over time.
This doesn’t look like classic airway obstruction. It points instead to restrictive and diffusion-level damage.
FEV1 remains largely stable, while FVC improves only slowly over time.
This doesn’t look like classic airway obstruction. It points instead to restrictive and diffusion-level damage.
In simple terms.
Patients may breathe fine on spirometry, yet oxygen doesn’t pass efficiently from the lungs into the blood.
Patients may breathe fine on spirometry, yet oxygen doesn’t pass efficiently from the lungs into the blood.
That’s why reduced DLCO/KCO matters.
It reflects dysfunction at the alveolar–capillary interface - where air, blood vessels, and endothelium meet.
It reflects dysfunction at the alveolar–capillary interface - where air, blood vessels, and endothelium meet.
This also explains the typical long-COVID pattern.
Exertional shortness of breath, fatigue, reduced exercise tolerance
- despite near-normal basic lung tests!
Exertional shortness of breath, fatigue, reduced exercise tolerance
- despite near-normal basic lung tests!
Importantly, patients with moderate or severe acute COVID had significantly worse long-term lung function than those with mild disease.
Acute severity translates into chronic physiological damage.
Acute severity translates into chronic physiological damage.
The most sensitive markers weren’t standard spirometry.
They were lung volumes and diffusion metrics (TLC, alveolar volume, KCO) - tests that are often not routinely performed.
They were lung volumes and diffusion metrics (TLC, alveolar volume, KCO) - tests that are often not routinely performed.
Statistical analysis shows post-COVID lung damage isn’t one thing. There are different phenotypes - small airway involvement, diffusion impairment, restrictive volume loss - often overlapping.
SARS-CoV-2 is often described as a respiratory virus.
This kind of data makes it hard to avoid the conclusion that it is fundamentally a vascular disease, with the lungs as the clearest window into the damage.
This kind of data makes it hard to avoid the conclusion that it is fundamentally a vascular disease, with the lungs as the clearest window into the damage.
If this were mainly an airway problem, we’d expect FEV1 to fall.
Instead, what persists is impaired gas exchange - a hallmark of microvascular and endothelial dysfunction.
Instead, what persists is impaired gas exchange - a hallmark of microvascular and endothelial dysfunction.
The lungs are essentially a massive vascular organ.
Huge surface area + dense capillary network = the perfect place to detect microangiopathy and endothelial injury.
Huge surface area + dense capillary network = the perfect place to detect microangiopathy and endothelial injury.
And the same vascular pattern shows up elsewhere.
Brain - hypometabolism, cognitive slowing
Heart - reduced exercise capacity
Muscles - early fatigue
Different organs. Same bottleneck - impaired microcirculation.
Brain - hypometabolism, cognitive slowing
Heart - reduced exercise capacity
Muscles - early fatigue
Different organs. Same bottleneck - impaired microcirculation.
That’s why patients can have normal breathing tests and still feel profoundly unwell.
The air moves.
The oxygen delivery fails downstream.
The air moves.
The oxygen delivery fails downstream.
Long COVID makes far more sense when start recognizing it as a systemic vascular–immune disorder, with the lungs acting as a window into the damage.
Daniela Robu Popa at al., Journal of Clinical Medicine 2026. Impact of COVID-19 on Respiratory Function: A Post-Recovery Comparative Assessment. mdpi.com/2077-0383/15/2…
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