Unplug the machine

Why a low ten-year cardiovascular risk should be the beginning of a prevention conversation, not the end of one

As a preventive cardiologist I spend a lot of time talking to patients about risk. The analogy I use is this: imagine a machine in the corner of your bedroom. It hums quietly and emits a small amount of radiation every day. It is unlikely to give you cancer today, or this year. But the exposure accumulates, and every year it runs your lifetime risk rises.

Would you wait until that risk reached 10% before doing something about it? Nobody would. The question answers itself.

Prevention is more complicated than pulling a plug. But the analogy asks a question we rarely put to ourselves: how much preventable exposure do we allow to accumulate while waiting for someone’s short-term risk to become high enough to act on?

The threshold

In the UK, NICE recommends offering a statin when estimated ten-year cardiovascular risk reaches 10% (1). The European guidance uses SCORE2 with age-shifting thresholds (2). Estimate risk, set a bar, and treat when the estimate clears it.

The threshold has a respectable origin. Absolute benefit scales with absolute risk. When you add the cost of the drug, the daily tablet and the possibility of side effects, and somewhere the benefit stops justifying the intervention. Ten per cent is where a committee, reasonably, drew the line.

Nor does NICE treat the line as absolute: it allows treatment below 10% for informed preference or where the calculation may underestimate risk (1). Ten per cent is a threshold for routinely offering treatment, not a boundary between healthy arteries and diseased ones.

My concern is what happens when a useful threshold becomes the whole conversation. It quietly assumes three things. It assumes risk is a level, a reading on a dial we watch until it crosses a mark. It assumes the harm of waiting is small, because we can always start later. And it assumes the cost of acting early is high enough to justify the wait.

All three were defensible twenty years ago. None survives contact with what we now know.

Risk is not a level. It is an integral.

The machine in the corner harms you in proportion to the total dose you have absorbed, not today’s reading. Atherosclerosis behaves the same way. The best evidence comes from genetics. Ference and colleagues found that lifelong genetically lower LDL was associated with roughly three times the reduction in coronary disease per unit of LDL seen in statin trials that began later in life (3,4).

That does not prove a statin started thirty years earlier triples its benefit as genes and prescriptions are not interchangeable. But it is a powerful reason to take the duration of exposure as seriously as the level. A cholesterol result is a snapshot. The reading in a 55-year-old is the sum of everything that happened between 20 and 55, and none of it can be un-happened.

REACT, published in the New England Journal of Medicine in August, makes that history visible (5). Among 16,808 adults with no known heart disease, silent atherosclerosis was present in one in thirteen in their twenties, a third of men in their thirties and nine in ten in their sixties, with plaque volume rising roughly exponentially with age. That is the shape of cumulative dose, not of a process that waits politely for a threshold.

The cost of waiting is not zero

The second assumption is that delay is cheap, i.e.  if risk is low now, start later and lose nothing. The genetics say otherwise. Every year of exposure adds plaque, and plaque is far harder to remove than to prevent. Intensive lipid lowering can stabilise and possibly regress atheroma, but it does not restore a 55-year-old’s arteries to what they would have been. We are treating the consequences of decades we chose not to act in.

The threshold model also has a blind spot REACT exposes precisely as it is anchored to age, because age dominates every calculator. A 38-year-old with a high lipoprotein(a), a family history and established coronary plaque can have a ten-year risk of 3%. The calculator says wait. The arteries say the machine has been running for twenty years.

The cost of acting is now very small

The third assumption is that early treatment carries enough cost to justify caution. It did when statins were expensive and unfamiliar. Not now. A generic statin costs pennies a day. Blinded trials show most symptoms attributed to statins occur just as often on placebo (6), NICE describes severe muscle effects as extremely uncommon (1), and safety data span three decades.

Taking a medicine for years is still a commitment, and prevention is never shorthand for a prescription – exercise, nutrition, not smoking and blood pressure control remain the foundation.But set the arithmetic out plainly. On one side, a cheap, safe, well-understood intervention whose benefit grows the earlier it starts. On the other, a threshold that guarantees it starts late, to avoid a cost that has largely disappeared.

The unplugging is nearly free. The waiting is not.

Common is not normal

The usual reply is that atherosclerosis is simply part of ageing, like grey hair and wrinkles. Nine in ten sixty-year-olds have it. Surely that makes it normal?

Grey hair doesn’t kill you.

Something that happens to almost everyone can still be a disease if it is caused by an exposure and prevented by removing it. People born with lifelong low cholesterol do not get atherosclerosis a bit later, they largely do not get it. It is common because the exposure is common, not because the arteries are following a script.

A low score should open a conversation

None of this argues for statins in the water. It argues for a different question: not “is this person’s risk high enough yet”, but “is the machine running, and how long has it been on”?

Someone in their forties with plaque on a scan may still have a low ten-year risk, and that number is useful. But so is the finding that disease is present, and both belong in the discussion, alongside lipids, blood pressure, family history, lipoprotein(a), ApoB and the person’s own priorities. Some will choose medication and others will not. Our job is to lay out the evidence, including the cost of postponing treatment as well as its burden, clearly enough for that choice to be informed.

Where the plug is

In my last article I argued that we should measure the disease rather than estimate the risk. Once you have measured it, a low ten-year score is not a reason to wait. Atherosclerosis is cumulative, largely irreversible and, in most adults, already present. The tools to arrest it are cheap and safe. The only thing between a young patient with early disease and effective prevention is a rule that says their risk is not yet high enough. When I explain the machine in the corner, nobody asks me to wait until the risk is higher. They ask where the plug is.

The machine is running. Unplug it.

References

1. National Institute for Health and Care Excellence. Cardiovascular disease: risk assessment and reduction, including lipid modification. NICE guideline NG238. December 2023.
2. SCORE2 working group and ESC Cardiovascular risk collaboration. SCORE2 risk prediction algorithms: new models to estimate 10-year risk of cardiovascular disease in Europe. Eur Heart J 2021;42:2439-54.
3. Ference BA, Ginsberg HN, Graham I, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease: evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J 2017;38:2459-72.
4. Ference BA, Yoo W, Alesh I, et al. Effect of long-term exposure to lower low-density lipoprotein cholesterol beginning early in life on the risk of coronary heart disease: a Mendelian randomization analysis. J Am Coll Cardiol 2012;60:2631-9.
5. Bundgaard H, García-Lunar I, Kofoed KF, et al. Prevalence of silent atherosclerosis across adult life. N Engl J Med 2026. doi: 10.1056/NEJMoa2609059.
6. Wood FA, Howard JP, Finegold JA, et al. N-of-1 trial of a statin, placebo, or no treatment to assess side effects. N Engl J Med 2020;383:2182-4.

Dr Andrew Mitchell is a consultant cardiologist and clinical lead for the Jersey Heart Team at Jersey General Hospital and an honorary consultant cardiologist at Oxford University Hospitals. October 2026.