Vaccination, Stiff Arteries, Wuhan and the COVID Legacy
When the European Heart Journal recently published the CARTESIAN study, headlines quickly followed: “COVID infection ages your arteries—especially in women. Vaccination protects”
For many, this was another reassuring message in a long line of narratives about the life-saving power of the COVID ‘vaccines’.
But if we pause and look more closely, the claim of “protection against vascular stiffening” is far less clear than the soundbite suggests.
The Nature of the Evidence
The CARTESIAN study is a sprawling, multinational cohort: nearly 2,400 participants across 16 countries, recruited during the tumultuous waves of the pandemic.
Researchers measured arterial stiffness using pulse wave velocity (PWV), a well-validated surrogate marker for vascular aging. Unsurprisingly, people who had contracted COVID—whether mild or severe—tended to have stiffer arteries than those who had never been infected.
That part of the finding is both credible and biologically plausible.
Where things become more contentious is in the interpretation that vaccination provided a protective buffer, particularly in women. Here, the story is murkier.
Confounding Factors Everywhere
Unlike a randomised trial, CARTESIAN was observational. Vaccinated and unvaccinated groups differed in important ways: the vaccinated were more likely to be older, ‘health-conscious’, under medical supervision, and receiving drugs such as statins or ACE inhibitors that themselves reduce arterial stiffness.
No amount of statistical adjustment can fully scrub away such confounding. At best, the association hints; it does not prove.
The Calendar-Time Problem
Timing is everything in epidemiology. Unvaccinated infections occurred disproportionately early, in the days of Alpha and Delta, when the virus was more severe.
Vaccinated infections clustered later, in the Omicron era, when disease was typically milder and perhaps less damaging to blood vessels. If Omicron itself caused less endothelial injury, then the vaccinated group would naturally appear “protected”—not because of the vaccine, but because of the variant.
The Trap of Selection Bias
By design, CARTESIAN included only people who had been infected and then stratified them by severity. That act—conditioning on infection—introduces what statisticians call collider bias.
Once you select only those who “made it through the infection door,” apparent associations can flip direction, magnifying or even manufacturing protective effects that aren’t truly causal. This is a well-described pitfall of COVID research, and it looms large here.
Heterogeneity in Measurement
Cohorts spanned dozens of centers using different devices—SphygmoCor, Complior, Vicorder—to measure PWV. Each machine produces systematically different absolute values. If the mix of devices correlated with vaccination uptake (say, certain hospitals being more vaccination-compliant), then the observed differences could be partly technical noise.
Medication, Lifestyle, and Multiplicity
Consider also that vaccinated participants were likelier to be prescribed medications known to soften arteries, or to pursue healthier lifestyles generally. And remember: the study tested multiple outcomes across multiple subgroups.
The “signal” that vaccination helped women, but not men, could simply be statistical happenstance—an artefact of multiple testing dressed up as discovery.
The Grand Leap of Interpretation
Finally, translating small changes in PWV into “years of arterial aging” is seductive but imprecise. PWV reference curves depend on device type, population, and arterial length assumptions.
A difference of 0.5 m/s may look dramatic when equated to five years of aging, but in reality sits near the threshold of device variability and confounding influence.
So What Should We Conclude?
Does this mean vaccination had no protective effect on vascular stiffening? Not necessarily. But it does mean the evidence is far from definitive. The safest reading is that vaccination and arterial stiffness are correlated in this cohort, but we cannot confidently say one caused the other.
Variant timing, measurement differences, medical care patterns, and statistical artifacts all offer equally plausible explanations.
The Broader Lesson
The COVID era has shown us, again and again, how quickly preliminary findings morph into definitive headlines. The danger is not in the research itself—CARTESIAN is a valuable, well-conducted study—but in the over-interpretation of complex data into simplified slogans.
When science is used to reinforce policy narratives, rather than to interrogate them, public trust erodes.
My Conclusion
The finding that COVID can stiffen arteries is serious, and it deserves public attention. But the notion that vaccination specifically “protects” against this effect remains unproven.
It may one day be validated by better data, or it may be revealed as an artefact of timing and confounding. Until then, we should resist the temptation to turn associations into absolutes. Science, and the public, deserve better.
And here is the crucial point: naturally circulating coronaviruses have never been shown to stiffen human arteries. Decades of exposure to endemic strains, and even outbreaks of SARS-1 and MERS, left no such vascular legacy.
The only coronavirus now documented to accelerate vascular aging is SARS-CoV-2, and that is because it is not a naturally evolved virus at all.
It is a laboratory-modified pathogen, almost certainly originating from the Wuhan Institute of Virology, built on a natural coronavirus backbone but altered in ways that unleashed unique vascular and immunological havoc.
Many experts and observers now regard SARS-CoV-2 as a de facto bioweapon: a biological organism that has been deliberately engineered and given so-called “gain-of-function” properties to increase its infectivity and pathogenicity.
To gloss over this reality, and to imply that such arterial injury is a generic property of coronaviruses, is not just misleading—it is scientific negligence.
The CARTESIAN study should have made this distinction abundantly clear: we are not dealing with “just another coronavirus,” but with an engineered virus whose man-made features are directly responsible for these unprecedented vascular consequences.
See more here substack.com
Header image: Getty Images
Some bold emphasis added
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