Did COVID Age Our Arteries? A Closer Look at the Evidence
A new study suggests COVID may stiffen arteries, especially in women. Here’s what the evidence shows — and why the headlines don’t tell the whole story
You may have seen the headlines:
"COVID-19 seems to age blood vessels – but only among women."
"COVID Infection Can Age Blood Vessels and Weaken Heart Health, Especially in Women."
"Vascular Aging May Explain Long COVID's Predominance in Women."
These stories stem from a new international study published in the European Heart Journal. The study suggests that people—specifically, the women in the study—who had COVID-19 might have stiffer arteries months after infection, which the authors interpreted as a sign of "accelerated vascular aging."
It's the kind of result that spreads fast. The idea that your arteries could silently age five or ten years from a COVID-19 virus you caught and got over is genuinely concerning.
But here's the key point: this study raises important questions, but it doesn't prove that COVID ages your arteries. There are good reasons to interpret these findings cautiously, as there are some significant methodological concerns that the headlines don't mention.
As someone who studies cardiovascular outcomes and COVID-19, among other things, let me walk you through what this research shows, what it doesn't, and why it matters.
What the Study Actually Found
The study, called the CARTESIAN study, followed over 2,000 people across 16 countries, measuring how stiff their arteries were 6 to 12 months after COVID infection.
They used a method called pulse wave velocity (PWV). Think of it like testing how bouncy a rubber ball is; a stiffer ball bounces faster. Similarly, pressure waves from your heartbeat move faster through stiffer arteries. When your heart beats, it sends a wave through your blood vessels. If your arteries are soft and flexible, the wave moves more slowly. If they're stiff, like aging pipes, it moves faster.
What the study found was modest: among women who had COVID, PWV was on average slightly higher than in those who hadn't had it. In men, there was no measurable effect.
The authors calculated these differences as equivalent to 5 to 10 years of vascular aging. But this calculation comes from comparing the PWV changes to normal aging curves in the general population, not from following people for years to see what happens. And there was a lot of individual variation: some people who had COVID showed improvements in vascular function, and some didn't. And the same was true in the control group. So even though the headline was stark, the underlying data were more nuanced.
What We Haven't Seen in the Real World
Before diving into the study's limitations, it's worth stepping back to ask: what would we expect to see if COVID were really aging arteries on a large scale?
There's growing concern that COVID might increase long-term cardiovascular risks, and this study adds to that discussion. I have been skeptical because if COVID were broadly aging our arteries, you'd expect to see its effects show up in the population: more heart attacks, more strokes, more cardiovascular deaths. Given that over 100 million Americans have had COVID, even a modest increase in cardiovascular risk should show up clearly in population data as a spike.
But we haven't.
In the U.S., age-adjusted mortality from ischemic heart disease continues to decline. Heart failure and hypertensive heart disease are rising, but those trends predate the pandemic and reflect longstanding shifts in chronic disease.
So, despite widespread infection, we haven't seen a post-COVID surge in vascular events. That doesn't mean COVID is harmless; we know severe COVID can cause heart inflammation and blood clots during acute infection. But it does suggest we shouldn't jump to conclusions about long-term vascular damage based on small shifts in this pulse wave velocity.
A Critical Design Flaw
This was a serious and ambitious study and I salute the authors for the effort. But there's a core issue in how it was designed that could have created the very result it's trying to explain.
The issue is with the control group, the group against which the COVID participants were compared.
In research, the control group is meant to represent what would happen in people just like the study group, except without the exposure you're trying to study. That way, if you see a difference, you can reasonably attribute it to the exposure, in this case the viral infection.
But here's the problem: The people in the COVID group were recruited through ads or pulled from other research cohorts, a convenience sample of people who showed up or were already in studies. This is not a representative group. But the issue is with the control group. They were not recruited in the same way. They were made up of many hospital staff (41% were healthcare professionals, compared to much lower percentages in the COVID groups).
Healthcare workers tend to be healthier, more health-literate, and more regularly monitored than the general population. So when the study finds that people who had COVID had stiffer arteries, it's hard to know: is that because of the infection? Or did it only seem that way because they were compared to an unusually healthy group? This means the study may be comparing a typical population (COVID group) to an unusually healthy one (controls), which could make normal arteries look 'aged' by comparison.
The researchers addressed this concern by comparing their COVID participants to a separate group of people from Austria who had been studied before the pandemic. They found similar results, which strengthen their case. But this doesn't fully resolve the fundamental comparison problem, as the Austrian group was drawn from a relatively healthy population without significant histories of cardiovascular disease, hypertension, dyslipidemia, or diabetes.
The Women-Only Effect: Signal or Noise?
The fact that effects showed up only in women, with no difference in men, is puzzling. The authors suggest biological explanations, for example, that women's typically stronger immune responses might make them more susceptible to prolonged inflammation after infection. But this is largely speculative.
It's also possible that unmeasured differences between groups, or statistical noise, could explain the sex difference. When you're looking at multiple subgroups and modest effect sizes, finding effects in some groups but not others can happen by chance.
What We Do Know vs. What We Don't
Here's what we do know: severe COVID can cause significant cardiovascular problems during acute infection. Heart inflammation, blood clots, and other serious complications are well-documented, especially in hospitalized patients.
The question this study is trying to answer is different: whether milder cases cause lasting, subtle changes to blood vessel function that might increase long-term risk.
And here's where the evidence gets interesting: in the CARTESIAN study, when researchers followed people over time, many participants' PWV actually improved between their first and second visits. The COVID groups showed stable or better PWV over 12 months, while the control group showed worsening.
If this were truly permanent vascular aging, you wouldn't expect to see improvement. This pattern suggests whatever changes occurred might be temporary—perhaps related to lingering inflammation that resolves over time.
What PWV Really Means
PWV is a useful research tool that correlates with age, blood pressure, and cardiovascular risk. But it's not a direct measure of arterial damage, and it can fluctuate based on temporary factors, including inflammation, hydration, stress, even time of day.
The study's suggestion that small PWV changes equal years of aging assumes these changes carry the same long-term risk as the gradual vascular stiffening that happens with normal aging. But there's no evidence yet that temporary PWV bumps after infections work the same way.
If You're Still Worried
If you've had COVID and you're concerned about your cardiovascular health, the same screenings your doctor would normally recommend still apply. The fundamentals that actually protect your arteries, or age them prematurely, haven't changed:
• Know your blood pressure and keep it controlled • Know your cholesterol levels • Don't smoke • Stay physically active • Eat a heart-healthy diet • Manage diabetes if you have it
These factors have far more impact on your long-term vascular health than a temporary infection from years ago.
If you have specific concerns, especially if you had severe COVID or have ongoing symptoms, it's worth discussing with your doctor. But for most people who had mild COVID, this study doesn't suggest any need for special cardiovascular monitoring.
The Bottom Line
This study represents important research that helps us understand how infections might affect long-term health. It raises useful questions and pushes science forward.
But it doesn't prove that COVID causes lasting vascular aging. It doesn't show that your arteries silently stiffened by years. And it doesn't mean we're headed for a wave of cardiovascular disease.
Let's keep studying these effects. Let's keep asking hard questions about long-term COVID impacts. But let's also keep our sense of proportion.
We do not yet have strong evidence that COVID-19 has aged your arteries. The bigger risks to your cardiovascular health remain the same ones we've always known about.