Plate Nº 52 · recorded October 10, 2026

Health & Medicine ResearchReported finding

Chronic Inflammation Raises Heart Attack Risk by 43%, Study Finds

A study of nearly 480,000 UK adults links chronic inflammation to silent structural heart changes and a 43% higher risk of heart attack and stroke, years before symptoms appear.

By Priya Raman5 min read911 words

In brief

  1. People with the highest inflammation levels (top 20%) had a 43% higher risk of heart attack and stroke than the bottom 20%.
  2. The study analysed UK Biobank data from nearly 480,000 adults, the largest of its kind.
  3. Higher inflammation was linked to thicker heart walls, smaller chambers and poorer filling — changes that can precede heart failure.
  4. Inflammatory proteins in the interleukin-1 and TNF families are already targeted by drugs in clinical trials.
  5. The study was published in the European Journal of Preventive Cardiology in 2026.

People with the highest levels of chronic inflammation faced a 43% greater risk of heart attack and stroke than those with the lowest levels, according to one of the largest heart-imaging studies ever conducted. The study, published in the European Journal of Preventive Cardiology on data from nearly 480,000 UK adults, found that inflammation may silently reshape the heart's structure years before any symptoms appear.

Researchers at the MRC Laboratory of Medical Sciences (LMS) and Imperial College London believe their analysis is the largest of its kind. Their results suggest that everyday pressures — stress, smoking, obesity, mental health problems and socioeconomic disadvantage — may leave a measurable physical mark on the heart through a biological route that scientists are only beginning to target with drugs.

What did the researchers actually measure?

The team drew on UK Biobank data from almost 480,000 adults. Instead of asking people about stress directly, they measured chronic inflammation in the blood using a marker called glycoprotein acetyls, or GlycA — a plain-English way of tracking whether the immune system stays mildly switched on for long periods.

Chronic inflammation is the body's immune response failing to shut down after an immediate threat has passed. Researchers have linked this persistent, low-level immune activity to several diseases, including cancer and diabetes, and they increasingly suspect it plays a role in heart disease too.

The researchers combined GlycA measurements with heart imaging scans and genetic information, which allowed them to connect inflammation levels to physical changes in the heart and to inherited susceptibility.

How does inflammation change the heart?

The imaging revealed a pattern the researchers describe as adverse remodeling. People with higher inflammation tended to have:

  • thicker heart walls
  • smaller heart chambers
  • poorer heart filling

All three changes can develop quietly over years before progressing to heart failure. Notably, people whose inflammation stayed elevated over time had a 43% greater risk of heart attack and stroke even when they had no existing heart disease at the start.

Inflammation was also strongly associated with socioeconomic disadvantage and psychological distress. Familiar cardiovascular risk factors, including smoking and excess body fat, were linked to higher inflammation as well.

What role do social factors and genetics play?

Professor Declan O'Regan, British Heart Foundation Chair of Cardiovascular AI at Imperial College London and Head of the Computational Cardiac Imaging Group at the LMS, said: "Our study, which is the largest of its kind, suggests that millions of people could be living with hidden inflammation, which is slowly changing their heart and causing long-term damage — increasing the risk of heart attack and stroke."

"Chronic inflammation is complicated, but we know it's tied to our health and driven by a range of lifestyle and economic factors — meaning people may be at more risk just because of their surroundings, their economic status, their family's health and their lifestyle," O'Regan said.

The genetic dimension surprised the team. "The surprising thing was how much social factors and mental health are linked to inflammation and damage to the heart — as well as more well-known risk factors like smoking and inactivity," O'Regan added. "There was also a strong genetic factor, with some people being naturally more resilient or susceptible to the inflammatory damage that comes from different lifestyles."

The researchers stress that genetic susceptibility or difficult circumstances do not make heart disease inevitable. Reducing persistent inflammation remains possible, and O'Regan points to practical steps: "While tackling health inequalities remains an issue, there are things that we can do about inflammation, including reducing risk factors like smoking and obesity."

Could blood tests and existing drugs help?

The analysis flagged inflammatory proteins in the interleukin-1 and TNF families as possible contributors to the observed heart damage. Several of these proteins are already the target of drugs being tested in clinical trials, raising the possibility that anti-inflammatory therapies could eventually help prevent cardiovascular disease before symptoms begin.

The researchers also suggest that simple inflammation blood tests could be combined with genetic risk scores to identify people who would benefit most from early intervention.

Professor Bryan Williams, Chief Scientific and Medical Officer at the British Heart Foundation, said: "Inflammation is part of the body's healing process, but there is also a darker side to it. This large-scale study found people with higher levels of inflammation experienced silent changes to the structure of their hearts and had a higher risk of major cardiac events including heart attacks and strokes."

Williams added that the research identifies several inflammatory proteins that appear to play a key role in the heart changes linked to chronic inflammation, and that "it is to be hoped that anti-inflammatory medicines could become an important tool in preventing cardiovascular disease."

What are the study's limitations?

The findings come from observational data, meaning the study shows associations between inflammation and heart changes rather than proof that inflammation directly causes the damage. The possibility of prevention through anti-inflammatory drugs remains a hope, not an established treatment. The study population is drawn from the UK Biobank, and the results may not translate to every population group.

Still, the scale of the analysis — nearly half a million adults — gives researchers unusual confidence that the link between chronic inflammation and silent heart remodeling is real. The study was funded by the Medical Research Council and the British Heart Foundation, with additional support from the NIHR Imperial Biomedical Research Centre.

via dx.doi.org (Original)

Filed under

  • chronic-inflammation
  • cardiovascular-disease
  • heart-attack-risk
  • uk-biobank
  • anti-inflammatory-therapy
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Priya Raman

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Senior reporter covering industry trends and analytics at SciBeat.

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