Chronic stress and inflammation cause silent structural heart damage

Everyday life stresses and economic pressures are taking a permanent toll on human cardiovascular health, according to a large-scale study published in the European Journal of Preventive Cardiology. Researchers analyzing data from nearly 480,000 UK adults in the UK Biobank found that chronic, low-grade inflammation acts as a biological bridge linking psychological distress, poverty, and lifestyle factors to silent physical changes in the heart.

UK Biobank Study Reveals 43% Higher Risk of Heart Attacks and Strokes

Led by researchers at the MRC Laboratory of Medical Sciences (LMS) and Imperial College London, the study evaluated blood markers, heart imaging, and genetic data to measure the long-term impact of systemic immune activation. The findings indicate that individuals in the top 20% for inflammation levels—measured using the blood marker glycoprotein acetyls (GlycA)—experience a 43% higher risk of heart attacks and strokes compared to those in the bottom 20%.

Crucially, this elevated risk persists even among people with no pre-existing heart disease. The researchers noted that these physical transformations can develop quietly over many years, remaining entirely hidden until they progress toward heart failure.

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, stated that their study, the largest of its kind, suggests millions may be living with hidden inflammation causing heart damage and increasing the risk of heart attacks and strokes. Chronic inflammation, he said, is tied to health and driven by lifestyle and economic factors, placing people at greater risk based on their surroundings, economic status, family health, and lifestyle.

Silent Structural Changes in Heart Walls and Chambers

The physical damage caused by persistent immune activation alters the architecture of the heart itself. Participants with high inflammation markers demonstrated distinct structural modifications, including thickened heart walls, smaller heart chambers, and poorer heart filling capacity.

Professor Bryan Williams, chief scientific and medical officer at the British Heart Foundation, emphasized the insidious nature of these developments.

Professor Bryan Williams noted that the study found individuals with higher inflammation levels experienced silent heart structure changes and a higher risk of cardiac events.

The data demonstrated that higher inflammation levels strongly correlate with socioeconomic disadvantage, psychological distress, and established physical risk factors like smoking and excess body fat. However, researchers also identified a strong genetic component, noting that some individuals possess natural resilience or susceptibility to inflammatory damage.

Targeting Inflammatory Proteins and Immune Cells

Parallel research published in Arteriosclerosis, Thrombosis, and Vascular Biology by investigators at Linköping University highlights specific cellular malfunctions that maintain this low-grade immune activation. Focusing on patients with chronic coronary syndrome who showed no symptoms and normal routine C-reactive protein (CRP) levels, the team examined the behavior of neutrophils—the body’s most abundant white blood cells.

The Linköping experiments revealed that neutrophils in these patients fail to undergo programmed cell death and remain highly active because regulatory T cells fail to suppress them. According to doctoral student Maike Schneider, routine diagnostic testing currently misses these underlying cellular mechanisms.

Backing potential future interventions, the UK study pointed to specific inflammatory proteins from the interleukin-1 and TNF families as primary drivers of structural heart damage. Because several of these proteins are already being targeted by drugs in clinical trials, researchers hope anti-inflammatory treatments may soon offer a way to prevent cardiovascular disease before initial symptoms present.