Pericardial- Rather than Intramyocardial Fat Is Independently Associated with Left Ventricular Systolic Heart
Peter Wolf1, Yvonne Winhofer1, Sabina Smajis1
1Medical University of Vienna, Department of Internal Medicine III, Division of Endocrinology and Metabolism, Vienna, Austria.
Insights
Pericardial fat, not intramyocardial fat, is linked to reduced cardiac function in healthy individuals. This finding highlights pericardial fat as a key factor in myocardial health.
Area of Science:
- Cardiology
- Medical Imaging
- Metabolic Health
Background:
- Obesity is a significant risk factor for heart failure, potentially due to lipotoxicity from intramyocardial (MYCL) and pericardial (PERI) fat accumulation.
- MYCL may be a marker of metabolic disturbance rather than a direct cause of cardiac dysfunction.
- PERI fat may influence cardiac function through mechanical and paracrine effects.
Purpose of the Study:
- To investigate the association between MYCL and PERI fat accumulation and myocardial function in metabolically healthy individuals.
- To determine whether PERI or MYCL is a stronger predictor of altered cardiac function.
Main Methods:
- 1H-magnetic resonance spectroscopy and imaging were used to assess MYCL and PERI in 31 metabolically healthy subjects.
- Systolic and diastolic left ventricular function were evaluated.
- Correlation and linear regression analyses were performed to assess the relationships between fat depots and cardiac function.
Main Results:
- PERI fat showed significant negative correlations with Stroke Volume (SV) and Cardiac Index (CI).
- MYCL fat did not show significant correlations with SV or CI.
- Multiple regression analysis indicated that PERI negatively predicted CI, while MYCL had no significant impact.
Conclusions:
- Cardiac fat depots, specifically PERI fat, significantly impact left ventricular function in metabolically healthy individuals.
- PERI fat is a more critical predictor of altered myocardial function compared to MYCL.
Background:
Obesity is a major risk factor to develop heart failure, in part due to possible lipotoxic effects of increased intramyocardial (MYCL) and/or local or paracrine effects of pericardial (PERI) lipid accumulation. Recent evidence suggests that MYCL is highly dynamic and might rather be a surrogate marker for disturbed energy metabolism than the underlying cause of cardiac dysfunction. On the other hand, PERI might contribute directly by mechanic and paracrine effects. Therefore, we hypothesized that PERI rather than MYCL is associated with myocardial function.
Methods:
To avoid potential confounding of metabolic disease 31 metabolically healthy subjects (age: 29±10yrs; BMI: 23±3kg/m2) were investigated using 1H-magnetic resonance spectroscopy and imaging. MYCL and PERI, as well as systolic and diastolic left ventricular heart function were assessed. Additionally, anthropometric data and parameters of glucose and lipid metabolism were analyzed. Correlation analysis was performed using Pearson's correlation coefficient. Linear regression model was used to show individual effects of PERI and MYCL on myocardial functional parameters.
Results:
Correlation analysis with parameters of systolic heart function revealed significant associations for PERI (Stroke Volume (SV): R = -0.513 p = 0.001; CardiacIndex (CI): R = -0.442 p = 0.014), but not for MYCL (SV: R = -0.233; p = 0.207; CI: R = -0.130; p = 0.484). No significant correlations were found for E/A ratio as a parameter of diastolic heart function. In multiple regression analysis CI was negatively predicted by PERI, whereas no impact of MYCL was observed in direct comparison.
Conclusions:
Cardiac fat depots impact left ventricular heart function in a metabolically healthy population. Direct comparison of different lipid stores revealed that PERI is a more important predictor than MYCL for altered myocardial function.
Related Concept Videos
Location and Orientation of the Heart
Cardiomyopathy III: Hypertrophic Cardiomyopathy
Cholesterol: Significance and Regulation
Considering cholesterol and...
Heart Failure II: Pathophysiology
Coronary Artery Disease II: Pathophysiology

