Chronic inflammation tied to stress, lifestyle, mental health, and socio-economic conditions may silently change the heart for years before any symptoms appear, say British scientists, after a study of nearly half a million adults in the United Kingdom.
They said people with the highest inflammation levels faced a 43% greater risk of heart attack and stroke, raising hopes that earlier testing and anti-inflammatory treatments could help prevent serious heart disease.
Their findings, that chronic stress linked to everyday life may potentially damage cardiovascular health and shorten lifespan, were published in the European Journal of Preventive Cardiology.
The researchers were led by teams at the MRC Laboratory of Medical Sciences (LMS) and Imperial College London.
These changes to the heart may begin years before a person notices any cardiovascular symptoms, allowing the damage to build silently over time, said 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.
“Our study 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.
“But while tackling health inequalities remains an issue, there are things that we can do about inflammation, including reducing risk factors like smoking and obesity.”
Chronic inflammation occurs when the immune system remains mildly activated for long periods rather than switching off after an immediate threat has passed. This persistent, low-level immune activity has been associated with several diseases, including cancer and diabetes, and researchers increasingly suspect that it may also play an important role in heart disease.
For the new study, the team examined UK Biobank data from nearly 480 000 adults. They assessed inflammation using a blood marker called glycoprotein acetyls (GlycA) and combined those measurements with heart imaging and genetic information.
A 43% higher risk of heart attack and stroke
People with the highest inflammation levels (the top 20%) had a 43% higher risk of heart attack and stroke than those with the lowest levels (the bottom 20%).
The researchers also found signs that inflammation was associated with physical remodelling of the heart. People with higher inflammation tended to have thicker heart walls, smaller heart chambers and poorer heart filling, all changes which may develop quietly for years before progressing to heart failure.
Inflammation was also strongly associated with socio-economic disadvantage and psychological distress. More familiar cardiovascular risk factors, including smoking and excess body fat, were linked to higher inflammation as well.
People whose inflammation remained elevated over time had a 43% greater risk of heart attack and stroke, even when they had no previously existing heart disease.
The findings suggest that inflammation may provide one biological route through which pressures from everyday life, including poverty and mental health problems, can affect the body and increase cardiovascular risk.
Social factors, mental health, and genetics
O’Regan added, “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. 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 emphasise, however, that genetic susceptibility or difficult life circumstances do not make heart disease inevitable. There are still opportunities to reduce persistent inflammation and lower cardiovascular risk.
The analysis also highlighted inflammatory proteins in the interleukin-1 and TNF families as possible contributors to the observed heart damage.
Several of these proteins are already being targeted by drugs being tested in clinical trials. That raises the possibility that anti-inflammatory therapies could eventually help prevent cardiovascular disease before symptoms begin.
Blood tests could help ID people at risk
The researchers also suggest that inflammation blood tests could potentially be combined with genetic risk scores to identify people who may 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.
“The research provides valuable insights into how our genes and lifestyle factors, such as smoking, poor mental health and socio-economic status, can converge to trigger inflammation. It also identifies several inflammatory proteins that appear to play a key role in the heart changes linked to chronic inflammation, and it is to be hoped that anti-inflammatory medicines could become an important tool in preventing cardiovascular disease.
“The findings reinforce the importance of tackling the causes of inflammation and poor cardiovascular health, while also supporting people to make lifestyle changes that can help protect their hearts.”
Study details
Gene–environment interactions shape cytokine-mediated inflammation and cardiovascular risk
Mattia Corianò, Shamin Tahasildar, Ling Huang et al.
Published in the European Journal of Preventive Cardiology on 18 September 2026
Abstract
Background
Chronic inflammation is a major driver of cardiovascular diseases, but mechanisms linking systemic inflammation to cardiac remodelling remain incompletely understood. We aimed to evaluate the role of cytokine-mediated signalling and the influence of environmental and genetic factors on inflammation and cardiac phenotypes in a large population-based cohort.
Methods
We analysed subsets of 488 079 UK Biobank participants with metabolomic and proteomic profiling, cardiac magnetic resonance (CMR) imaging, and longitudinal outcomes. Chronic inflammation was quantified using glycoprotein acetyls (GlycA) by nuclear magnetic resonance spectroscopy. Machine learning-based analysis extracted CMR phenotypes. Multivariable linear regression assessed GlycA-cardiac associations. Mediation analysis tested 80 inflammatory proteins as potential mediators. Cox models evaluated GlycA levels and major adverse cardiovascular events (MACEs). An exposome-wide association study identified environmental determinants of inflammation, and gene–environment interactions were assessed using multi-ancestry polygenic risk scores.
Results
Higher GlycA levels were associated with reduced left ventricular indexed end-diastolic volume (_=−2.09) and stroke volume (_=−1.12), with compensatory increased heart rate (_=1.38; all _<10−228). Interleukin (IL)-1 receptor antagonist statistically mediated 27% of the GlycA effect on end-diastolic volume (average causal mediated effect -0.53 [95% CI, -0.64 to -0.41]; _<10−16). The highest GlycA quintile had 43% higher MACE risk versus the lowest (adjusted HR, 1.43 [95% CI, 1.38–1.49]). Trunk fat mass (_=0.35), current smoking (_=0.39), psychological distress, and low socioeconomic status were the strongest GlycA determinants (all _<10−50). Cardiovascular polygenic risk scores modified associations between environmental exposures, inflammation, and MACE.
Conclusions
Chronic systemic inflammation is associated with reduced left ventricular volumes and increased cardiovascular risk in the community, with circulating cytokines and growth factors including IL-1 and TNF identified as potential mediators of these associations. Exposure-gene interactions are associated with inflammatory responses such that risk may reflect the convergence of inherited and acquired factors.
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