Epicardial Adipose Tissue: Functions and Health Risks

Epicardial adipose tissue (EAT) is a fat deposit located directly on the heart’s surface, between the heart muscle (myocardium) and the pericardium, the sac enclosing it. This position places EAT in direct contact with the myocardium and the coronary arteries. EAT is a metabolically active organ whose role in health is complex. It serves beneficial functions under normal conditions but becomes a source of risk when excessive or dysfunctional.

Physiological Roles of Epicardial Adipose Tissue

Under normal conditions, epicardial adipose tissue performs several supportive functions for the heart. It acts as a local energy reservoir, supplying the heart muscle with fatty acids to fuel its activity. The rate of fatty acid release from EAT is higher than from other fat depots, highlighting its specialized role in cardiac energy metabolism.

Beyond its metabolic contributions, EAT provides mechanical cushioning for the heart and the major coronary arteries, protecting them from physical forces. The tissue also has thermogenic, or heat-producing, capabilities that may help protect the heart from hypothermia. In a healthy state, EAT secretes protective molecules, such as adiponectin, that help shield heart cells and blood vessels from inflammatory and fibrotic processes.

Epicardial Adipose Tissue and Cardiovascular Disease

When epicardial adipose tissue becomes excessive, its protective qualities diminish and it contributes to cardiovascular disease. An increased volume of EAT is strongly linked to coronary artery disease (CAD). The tissue can become inflamed and release pro-inflammatory molecules directly into the adjacent coronary arteries and myocardium, promoting atherosclerotic plaques. This local signaling is possible because no fascial barrier separates EAT from the heart.

The negative influence of dysfunctional EAT is also associated with an increased risk of atrial fibrillation, a common heart rhythm disorder. The inflammatory mediators can alter the electrical properties of the nearby atrial tissue, leading to arrhythmias. Furthermore, excessive EAT is linked to diastolic dysfunction, a condition where the heart’s ventricles do not relax properly between beats.

This accumulation of fat can also exert mechanical stress, contributing to changes in the heart’s structure. Unhealthy EAT releases fewer protective molecules and more harmful free fatty acids, which can have a direct toxic effect on heart muscle cells, a process known as lipotoxicity. This combination of inflammatory, mechanical, and lipotoxic effects implicates excess EAT as a contributor to heart failure.

Factors Influencing Epicardial Adipose Tissue Accumulation

Several factors determine the amount of epicardial adipose tissue. Overall obesity, particularly central or visceral adiposity where fat is stored around abdominal organs, is a primary driver of EAT accumulation. High-calorie diets and physical inactivity are major contributors to both general obesity and the expansion of this cardiac fat depot.

Metabolic conditions are also closely intertwined with EAT volume. Individuals with metabolic syndrome and type 2 diabetes mellitus frequently exhibit increased amounts of epicardial fat. Other factors such as age and sex can influence EAT levels, with volume tending to increase with age. Genetic predispositions can also make some individuals more likely to accumulate fat in this location.

Assessment Methods for Epicardial Adipose Tissue

Clinicians and researchers use several non-invasive imaging techniques to measure epicardial adipose tissue. These measurements are becoming valuable for assessing cardiovascular risk beyond traditional factors. Echocardiography, which uses sound waves to create images of the heart, is a widely available method for estimating EAT thickness, though its accuracy can depend on the operator.

Computed tomography (CT) and magnetic resonance imaging (MRI) are considered more precise methods for quantifying the total volume of EAT. CT scans provide clear images but involve exposure to ionizing radiation. MRI also offers excellent detail for measuring EAT volume without radiation, but it is more expensive and less widely available.

Accurately quantifying EAT provides a valuable tool for risk stratification. Measuring this fat depot helps identify at-risk individuals and can be used to monitor the effectiveness of interventions, such as diet and exercise, aimed at reducing cardiovascular risk.