Chronic Inflammation Linked to Heart Changes and Risks

By Dr. Chinta SidharthanReviewed by Laura ThomsonSep 25 2026

Inflammation often goes unnoticed, but growing research indicates that it may increase the risk of cardiovascular events. In a recent study published in the European Journal of Preventive Cardiology, a team of researchers from the United Kingdom analyzed subsets of U.K. Biobank participants to determine how a blood marker of long-term inflammation relates to the structure of the heart and to future cardiovascular risk.

Chronic low-grade inflammation is a contributor to cardiovascular disease. Inflammation that persists regardless of cholesterol levels is linked to elevated risk of cardiovascular events in people with and without a prior cardiac event. In individuals with metabolic conditions such as diabetes, widespread inflammation is also associated with ischemic heart failure

Earlier biomarker studies that tracked outcomes do not clarify how inflammation arises and is regulated in adults. As a result, the heart changes tied to inflammation and the proteins involved remain uncharacterized at population scale.

The environmental and inherited influences on chronic inflammation are also poorly defined. Individual exposures show links with inflammation and mortality, but surveys that rank the main environmental exposures and their interactions with genetic risk factors are missing. Because genetic and metabolic information improves risk prediction, understanding what shapes inflammation is important for tailored prevention and prioritizing new treatments in groups with different risk profiles.

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The Study

The researchers used subsets from the U.K. Biobank, which enrolled roughly 500,000 adults aged 40 to 69 from 2006 to 2010. They analyzed the blood samples from over 488,000 participants using nuclear magnetic resonance spectroscopy to detect glycoprotein acetyls (GlycA), which served as the marker of chronic inflammation, with high-sensitivity C-reactive protein (hsCRP) included in parallel analyses.

To assess heart structure and function, the researchers applied machine learning to cardiac magnetic resonance images to derive 33 measures, including chamber volumes, wall thickness, and aortic stiffness, along with 16 traits from electrocardiogram recordings. This imaging data, which was available for 70,809 participants, was tested against GlycA using multivariable linear regression adjusted for confounders.

Eighty inflammatory proteins, selected in advance for their known roles in inflammation, were measured through a proteomic platform in participants with matching metabolic data. Mediation analysis then estimated the extent to which each protein statistically accounted for GlycA's effect on heart measures and cardiovascular outcomes.

The outcome data was obtained from hospital records, self-reported history, and death registries. The primary endpoint combined cardiac arrest, heart failure, stroke or other cerebrovascular events, myocardial infarction, and cardiovascular death, with all-cause mortality as a secondary endpoint. Participants were divided into GlycA quintiles and the cardiovascular event risk was estimated after adjusting for lipid profiles and imaging findings.

Finally, an exposome-wide association study examined eight body fat measures and 169 environmental exposures against GlycA in 478,941 individuals. Exposures showing significant associations were then tested for interaction with 10 multi-ancestry polygenic risk scores, which reflected inherited cardiovascular susceptibility, in relation to both GlycA levels and major cardiovascular events.

The Findings of the Study

The study found that chronic inflammation, based on GlycA levels, was associated with a distinct pattern of cardiac change and higher cardiovascular risk. Participants with higher levels of GlycA had smaller chamber volumes, lower stroke volume, mildly impaired filling of the heart, and a faster heart rate, which likely compensated for the smaller volume of blood pumped with each beat. The patterns were consistent across sexes, in people with and without diabetes or obesity, and after accounting for hsCRP.

Several immune proteins statistically explained part of these links. Interleukin-1 receptor antagonist accounted for 27% of the effect of GlycA on the left ventricle's filling volume, and hepatocyte growth factor accounted for the largest share for the volume remaining after each contraction. For cardiovascular events, 63 proteins acted as statistical mediators, with interleukin-6 showing the largest share at 33%. Proteins in the interleukin-1 and tumor necrosis factor families were the predominantly observed inflammatory factors, and drugs targeting some of these pathways were already in clinical trials.

Over a median follow-up of 15.3 years, people in the highest GlycA quintile had roughly 43% higher risk of a major cardiovascular event than those in the lowest quintile. Moreover, the risk remained stable at lower levels and climbed markedly above the median.

Body fat, current smoking, psychological distress, and low socioeconomic status showed the strongest links with GlycA, whereas higher socioeconomic status and physical activity were linked to lower levels, as was a healthier diet. Genetic risk scores modified many of these relationships, so the same exposure carried different inflammatory and cardiovascular consequences depending on inherited susceptibility.

However, the cohort was mostly White European and healthier than the general population, which limits the generalizability of the results. Furthermore, GlycA testing is currently not routine in clinics, since it requires nuclear magnetic resonance imaging.

Conclusion

Overall, the findings showed that chronic inflammation was tied to reduced heart chamber volumes and higher cardiovascular risk in a community population, with interleukin-1 and tumor necrosis factor pathways emerging as possible contributors.

Genetic susceptibility shaped how strongly environmental stressors increased inflammation, so the estimated risk reflected inherited and acquired factors together. Although the findings need to be validated in other populations, they suggest that pairing inflammation markers with genetic data could help identify people who would have the most cardiovascular health gains from early interventions.