European Journal of Cardiovascular Medicine

Epicardial fat is a visceral adipose tissue depot located between the myocardium and visceral pericardium and is supplied by branches of the coronary arteries. Iacobellis G et al.¹ Epicardial adipose tissue (EAT), in contrast to subcutaneous fat, is metabolically active and serves as an endocrine organ that secretes vasoactive chemicals, adipokines, and pro-inflammatory cytokines. Two Bioactive molecules may readily flow into the artery wall thanks to this special position, which creates a direct paracrine connection between the coronary arteries and epicardial adipose depots. Talman AH et al.² An increasing amount of research indicates that plaque vulnerability, coronary atherosclerosis, and the beginning of acute coronary events are all influenced by increased epicardial fat thickness. Konwerski M et al.³

Acute coronary syndrome (ACS), a spectrum including ST-elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina, remains a major cause of morbidity and mortality worldwide. Singh A et al.⁴ Plaque erosion, fissuring, or rupture that results in thrombosis and myocardial ischaemia is the pathophysiological underpinning of ACS. 4 Plaque instability is mostly caused by inflammation, and it is now well known that epicardial fat acts as a local inflammatory reservoir. Ortega-Gil J et al.⁵ Higher levels of interleukin-6, tumour necrosis factor-alpha, plasminogen activator inhibitor-1, and other mediators that hasten atherosclerosis are frequently seen in patients with elevated EAT. Talman AH et al.²

Usually assessed over the right ventricular free wall in parasternal long-axis views, echocardiography provides a straightforward and repeatable evaluation of epicardial fat thickness. EFT measurement has been verified against cardiac MRI in a number of studies, showing a good correlation. Echocardiographic EFT may improve cardiovascular risk assessment and offers a practical, affordable method in clinical settings. Eroğlu S. et al. (2015)⁶

Elevated EFT has been shown in several studies to be significantly correlated with recognised cardiovascular risk factors, such as obesity, central adiposity, hypertension, dyslipidaemia, metabolic syndrome, and type 2 diabetes mellitus. Increased EFT may indicate a common pathophysiological mechanism connecting metabolic problems and coronary artery disease, as these risk factors converge in many ACS patients. Akhter AN et al. (2025)⁷ 

Epicardial fat has both local pro-atherogenic effects and systemic metabolic consequences. It increases oxidative stress by secreting free fatty acids straight into the heart. Additionally, it increases endothelial dysfunction by decreasing the bioavailability of nitric oxide. Furthermore, the closeness of epicardial fat to coronary artery adventitia promotes the spread of inflammatory signals that cause plaques to become unstable. Bodenstab ML et al. (2024)⁸

Recent studies indicate that epicardial fat volume is higher in patients with ACS compared with those with stable coronary artery disease. Harada K et al. (2025)⁹ Increased EFT is associated with culprit-vessel occlusion, multi-vessel involvement, and impaired left ventricular systolic function. In STEMI patients, higher EFT is linked to larger infarct size and reduced post-thrombolysis myocardial perfusion. Singh A et al.⁴

EFT's diagnostic, prognostic, and therapeutic implications provide justification for evaluating it in ACS patients. EFT measurement detects high-risk individuals, sheds light on the underlying atherosclerotic load, and may direct early intervention tactics. Harada K et al. (2025)⁹ Moreover, statins, anti-inflammatory medications, antidiabetic medications, and lifestyle modifications have all shown promise in lowering the amount of epicardial fat. In light of this, assessing epicardial fat thickness in patients with ACS has important therapeutic implications. The purpose of this study is to use echocardiography to analyse EFT in ACS patients and investigate its association with echocardiographic parameters and cardiovascular risk factors. Singh A et al.⁴

OBJECTIVES

1. To measure epicardial fat thickness in patients presenting with acute coronary syndrome.
2. To evaluate the association between EFT and cardiovascular risk factors including hypertension, diabetes, dyslipidemia, smoking, and obesity.
3. To correlate EFT with type of ACS (STEMI, NSTEMI, unstable angina) and left ventricular systolic function.

This cross-sectional observational study was conducted in the Department of Cardiology at a tertiary-care hospital over an 18-month period. Consecutive patients admitted with acute coronary syndrome were included after obtaining informed consent. ACS diagnosis was based on clinical presentation, ECG changes, and cardiac biomarkers according to ACC/AHA guidelines.

Inclusion Criteria

• Adults aged ≥18 years
• Diagnosed ACS (STEMI, NSTEMI, unstable angina)
• Underwent transthoracic echocardiography within 48 hours of admission

Exclusion Criteria

• Prior myocardial infarction
• History of coronary revascularization
• Pericardial disease
• Poor echocardiographic windows
• Severe valvular heart disease
• Chronic kidney disease stage 4–5

Echocardiographic Assessment

Epicardial fat thickness was measured using a GE Vivid or equivalent echocardiography machine with a 3.5-MHz transducer. EFT was recorded in:

• Parasternal long-axis view
• Parasternal short-axis view
• Over the right ventricular free wall

Thickness was measured perpendicularly at end-systole over three cardiac cycles. The mean value was used for analysis. Left ventricular ejection fraction (LVEF) was calculated using the modified Simpson’s method.

Data Collection

Demographic details, cardiovascular risk factors, anthropometry (BMI, waist circumference), and fasting biochemical profile were recorded. Patients were classified into STEMI, NSTEMI, and unstable angina categories.

Statistical Analysis

Data were analyzed using SPSS version 24. Continuous variables were expressed as mean ± SD. Categorical variables were compared using chi-square test. Pearson correlation was used to assess association between EFT and continuous variables. p < 0.05 was considered statistically significant

Table 1: Baseline Characteristics of Study Participants

Table 1 summarizes the demographic and clinical profile of the 100 patients included in the study. The mean age of the cohort was 56.3 ± 10.2 years, indicating that ACS predominantly affected middle-aged to older adults. A male predominance (72%) was observed, consistent with the known epidemiology of ACS. The prevalence of major cardiovascular risk factors was high, with 58% hypertensive, 46% diabetic, and 52% dyslipidemic. Smoking history was reported in 40% of patients. The mean body mass index (BMI) was 27.8 ± 3.4 kg/m², suggesting that the majority of patients were either overweight or obese. These findings reflect a risk factor–rich population, highlighting the clustering of metabolic and lifestyle-related contributors in ACS patients.

Table 2: Distribution of ACS Subtypes

Table 2 shows the distribution of acute coronary syndrome subtypes in the study population. STEMI was the most common presentation, accounting for 48% of cases. This was followed by NSTEMI at 32%, while 20% of patients presented with unstable angina. The predominance of STEMI indicates that a substantial proportion of patients experienced complete coronary occlusion or severe ischemia requiring urgent intervention. This distribution aligns with typical presentations observed in tertiary-care cardiac centers.

Figure 1: Distribution of ACS Subtypes

Table 3: Epicardial Fat Thickness Across ACS Subtypes

Table 3 compares mean epicardial fat thickness (EFT) across different ACS subtypes. Patients with STEMI had the greatest EFT (6.8 ± 1.4 mm), followed by those with NSTEMI (6.1 ± 1.2 mm) and unstable angina (5.3 ± 1.1 mm). The difference in EFT values between groups was statistically significant (p = 0.01). This suggests a strong relationship between increasing epicardial adiposity and the severity of ACS presentation. Higher EFT in STEMI patients supports the hypothesis that epicardial fat contributes to plaque instability and acute coronary occlusion.

Figure 2: Epicardial Fat Thickness Across ACS Subtypes

Table 4: Correlation of EFT With Risk Factors

Table 4 presents the association between epicardial fat thickness and major cardiovascular risk factors. Patients with diabetes had significantly higher EFT (7.1 ± 1.3 mm, p = 0.004), indicating enhanced visceral adiposity and metabolic inflammation. Hypertensive patients also exhibited elevated EFT (6.5 ± 1.1 mm, p = 0.03). Individuals with dyslipidemia had a mean EFT of 6.7 ± 1.2 mm (p = 0.01). The highest EFT values were observed in obese patients (BMI ≥ 25 kg/m²) at 7.3 ± 1.4 mm, which was highly significant (p < 0.001). These findings reinforce the close link between epicardial fat accumulation and cardiometabolic derangements.

Table 5: Correlation of EFT with Left Ventricular Function

Table 5 demonstrates the relationship between epicardial fat thickness and left ventricular systolic function. The mean left ventricular ejection fraction (LVEF) in the study population was 48 ± 8%. A significant negative correlation was observed between EFT and LVEF (r = –0.42, p = 0.002). This indicates that higher epicardial fat thickness is associated with poorer left ventricular systolic performance. The inverse relationship supports the theory that epicardial adiposity promotes myocardial dysfunction through local inflammation, impaired coronary circulation, and adverse metabolic effects.

Epicardial fat thickness has emerged as a powerful marker of cardiovascular risk, particularly in patients presenting with acute coronary syndrome. The present study demonstrates that patients with ACS have significantly higher epicardial fat thickness compared with established normal reference ranges, supporting the mechanistic role of epicardial adiposity in coronary atherosclerosis and plaque destabilization. Singh A et al.⁴

The discovery that STEMI patients had the highest EFT is consistent with other research indicating a link between higher epicardial obesity and more severe coronary events. Coronary plaque instability is directly caused by the paracrine production of pro-inflammatory mediators, such as resistin, TNF-α, interleukin-6, and monocyte chemoattractant protein-1. These mediators permeate into the coronary adventitia because there are no fascial barriers, which accelerates atherosclerosis and promotes endothelial dysfunction. El-Naggar HM et al. (2025)¹⁰

Strong correlations between EFT and conventional cardiovascular risk factors, such as diabetes, hypertension, dyslipidaemia, and obesity, were also discovered in our study. This finding is consistent with a number of other research showing a strong correlation between increasing epicardial fat and components of the metabolic syndrome.Eroğlu S. et al. (2015)⁶ Insulin resistance increases the flow of free fatty acids from epicardial fat depots straight into the heart and encourages adipocyte hypertrophy. Lipotoxicity, elevated oxidative stress, and compromised myocardial energetics result from this. Zhao X et al. (2023)¹¹ The risk of plaque development and rupture is increased by certain metabolic abnormalities. Additionally, patients with greater EFT showed more widespread regional wall motion abnormalities and a lower left ventricular ejection percentage. These results imply that the buildup of epicardial fat may not only precede coronary artery disease but also contribute to myocardial dysfunction by impairing coronary perfusion and increasing local inflammation. Epicardial fat volume has been linked to bigger infarct sizes in STEMI patients and worse myocardial salvage after reperfusion treatment, according to earlier cardiac MRI investigations. de Luca C et al. (2008)¹²

The idea that epicardial fat acts as a measure of visceral adiposity is supported by the study's substantial association between BMI and EFT. However, epicardial fat has a higher metabolic activity than subcutaneous fat. In fact, a number of studies have demonstrated that EFT has a stronger correlation with cardiometabolic risk variables than either measurements of the waist or BMI alone, demonstrating its distinct role in cardiovascular pathophysiology.

The usefulness of echocardiography for quick assessment of EFT in acute situations is another significant conclusion of our work. Meenakshi K et al.(2016)¹³ Echocardiography is less costly, more accessible, and radiation-free than CT and MRI. High sensitivity and specificity have been demonstrated by several investigations that have confirmed echocardiographic EFT measures versus MRI-based evaluations.

Our findings align with prior research indicating that EFT values above 5 mm represent a high-risk phenotype. Eroğlu S. et al. (2015)⁶ STEMI, multi-vessel coronary artery disease, and poor clinical outcomes are more common in these patients. As a result, including EFT measurement into the standard echocardiographic assessment of ACS patients may improve risk assessment and direct early treatment.Singh A et al.⁴

In conclusion, there is a clear correlation between increased epicardial fat thickness and cardiovascular risk factors, acute coronary syndrome, and compromised heart function. A straightforward, repeatable, and therapeutically useful method that might enhance early risk assessment in ACS patients is echocardiographic evaluation of EFT.

Patients with acute coronary syndrome have markedly increased epicardial fat thickness, which is strongly correlated with important cardiovascular risk factors such as obesity, diabetes, hypertension, and dyslipidaemia. Increased EFT is inversely correlated with left ventricular ejection fraction, indicating its connection to myocardial dysfunction, and it corresponds with the severity of ACS, being greatest among STEMI patients. A quick, non-invasive diagnostic method that offers important insight into the inflammatory and metabolic milieu causing coronary atherosclerosis and plaque instability is echocardiographic evaluation of EFT. Routine cardiac examination that incorporates EFT measurement may improve risk classification and enable early start of curative and preventative treatments. To confirm epicardial fat as an independent predictor of unfavourable cardiovascular outcomes and investigate the effects of therapeutic manipulation of epicardial adiposity on ACS prognosis, further extensive prospective trials are advised.

LIMITATIONS

1. Single-center study, limiting generalizability.
2. Cross-sectional design prevents assessment of long-term outcomes.
3. Sample size was moderate.
4. EFT measurement by echocardiography is operator dependent.
5. Absence of a control (non-ACS) group.

1. Iacobellis G, Bianco AC. Epicardial adipose tissue: emerging physiological, pathophysiological and clinical features. Trends Endocrinol Metab. 2011 Nov;22(11):450-7. doi: 10.1016/j.tem.2011.07.003. Epub 2011 Aug 16. PMID: 21852149; PMCID: PMC4978122.
2. Talman AH, Psaltis PJ, Cameron JD, Meredith IT, Seneviratne SK, Wong DT. Epicardial adipose tissue: far more than a fat depot. Cardiovasc Diagn Ther. 2014 Dec;4(6):416-29. doi: 10.3978/j.issn.2223-3652.2014.11.05. PMID: 25610800; PMCID: PMC4278038.
3. Konwerski M, Gąsecka A, Opolski G, Grabowski M, Mazurek T. Role of Epicardial Adipose Tissue in Cardiovascular Diseases: A Review. Biology (Basel). 2022 Feb 23;11(3):355. doi: 10.3390/biology11030355. PMID: 35336728; PMCID: PMC8945130.
4. Singh A, Museedi AS, Grossman SA. Acute Coronary Syndrome. 2023 Jul 10. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan–. PMID: 29083796.
5. Ortega-Gil J, Pérez-Cardona JM. Unstable angina and non ST elevation acute coronary syndromes. P R Health Sci J. 2008 Dec;27(4):395-401. PMID: 19069375.
6. Eroğlu S. How do we measure epicardial adipose tissue thickness by transthoracic echocardiography? Anatol J Cardiol. 2015 May;15(5):416-9. doi: 10.5152/akd.2015.5991. PMID: 25993714; PMCID: PMC5779180.
7. Akhter AN, Aisha F, Moazzam AB, Khan SHB, Malik J, Parveen A. Epicardial Fat Thickness as a Marker of Coronary Artery Disease in Diabetics: A Single Center Study. Clin Cardiol. 2025 Jul;48(7):e70171. doi: 10.1002/clc.70171. PMID: 40616590; PMCID: PMC12228419.
8. Bodenstab ML, Varghese RT, Iacobellis G. Cardio-Lipotoxicity of Epicardial Adipose Tissue. Biomolecules. 2024 Nov 18;14(11):1465. doi: 10.3390/biom14111465. PMID: 39595641; PMCID: PMC11591820.
9. Harada K, Kato M, Terashima S, Takeda S, Matsunaga S, Kataoka T, Harada K, Nagao T, Shinoda N, Marui N, Murohara T. Association between Epicardial Adipose Tissue Volume and Changes in Left Ventricular Ejection Fraction in Patients with Acute Coronary Syndrome. J Atheroscler Thromb. 2025 Aug 5. doi: 10.5551/jat.65820. Epub ahead of print. PMID: 40769890.
10. El-Naggar HM, Abdel-Maseh JG, Hasan-Ali H, Khidr SS. Epicardial fat thickness predicts severe coronary artery disease and high mortality risk among ST-elevation myocardial infarction patients. Echo Res Pract. 2025 Jul 21;12(1):17. doi: 10.1186/s44156-025-00087-y. PMID: 40685373; PMCID: PMC12278483.
11. Zhao X, An X, Yang C, Sun W, Ji H, Lian F. The crucial role and mechanism of insulin resistance in metabolic disease. Front Endocrinol (Lausanne). 2023 Mar 28;14:1149239. doi: 10.3389/fendo.2023.1149239. PMID: 37056675; PMCID: PMC10086443.
12. de Luca C, Olefsky JM. Inflammation and insulin resistance. FEBS Lett. 2008 Jan 9;582(1):97-105. doi: 10.1016/j.febslet.2007.11.057. Epub 2007 Nov 29. PMID: 18053812; PMCID: PMC2246086.
13. Meenakshi K, Rajendran M, Srikumar S, Chidambaram S. Epicardial fat thickness: A surrogate marker of coronary artery disease - Assessment by echocardiography. Indian Heart J. 2016 May-Jun;68(3):336-41. doi: 10.1016/j.ihj.2015.08.005. Epub 2016 Jan 18. PMID: 27316487; PMCID: PMC4911429.