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Background <p>Peri- and epicardial adipose tissue (PEAT) is a metabolically active fat depot surrounding the heart and coronary arteries that may contribute to vascular dysfunction and inflammation in type 2 diabetes (T2D). We examined associations between PEAT volume, coronary calcification (CACS), myocardial flow reserve (MFR), and systemic inflammation (hsCRP).</p> Methods <p>Cross-sectional analysis of adults with T2D without overt CVD recruited 2020–2023. PEAT was quantified on non-contrast CT; CACS was calculated by the Agatston method; MFR was measured by rubidium-82 PET/CT; hsCRP assessed systemic inflammation. Associations were tested using multivariable regression adjusting for cardiovascular risk factors.</p> Results <p>Among 887 participants (mean age 65&#xa0;years; 70% male; mean BMI 30&#xa0;kg/m<sup>2</sup>; median PEAT 199&#xa0;mL [IQR 133–283]), higher PEAT (per 100&#xa0;mL) was associated with lower MFR (β − 0.04; 95% CI − 0.09 to 0.00; <i>p</i> = 0.041) and higher hsCRP, corresponding to a 38% increase (95% CI 28% to 48%; <i>p</i> &lt; 0.001) in age- and sex-adjusted models, but not with CACS &gt; 300 (OR 1.01; 95% CI 0.89–1.15). After further adjustment for diabetes duration, BMI, LDL cholesterol, systolic blood pressure, HbA1c, kidney function, smoking, and albuminuria, only the association with hsCRP remained significant at 14% (95%; CI 4% to 25%; <i>p</i> = 0.005).</p> Conclusion <p>In individuals with T2D without overt CVD, PEAT volume was not independently associated with CACS or MFR after multivariable adjustment. Higher PEAT volume was associated with higher hsCRP, suggesting a relationship with systemic inflammation; however, this exploratory finding should be interpreted in the context of established links between adiposity and inflammatory burden.</p> Graphical abstract <p></p>

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Associations between cardiac adipose tissue volume, measures of coronary calcification, myocardial microvascular function and systemic inflammation in individuals with type 2 diabetes free of overt cardiovascular disease

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月23日

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  • Morten Steen Jensen,
  • Ida K. B. Rasmussen,
  • Anne-Cathrine Skriver-Møller,
  • Philip Hasbak,
  • Martin B. Blond,
  • Adam Chebli,
  • Victor S. Wasehuus,
  • Mats C. H. Lassen,
  • Morten Lindhardt,
  • Allan Kofoed-Enevoldsen,
  • Urd L. Kielgast,
  • Emilie H. Zobel,
  • Lene Holmvang,
  • Tor Biering-Sørensen,
  • Peter Rossing,
  • Rasmus S. Ripa,
  • Andreas Kjaer,
  • Tine W. Hansen

摘要

Background

Peri- and epicardial adipose tissue (PEAT) is a metabolically active fat depot surrounding the heart and coronary arteries that may contribute to vascular dysfunction and inflammation in type 2 diabetes (T2D). We examined associations between PEAT volume, coronary calcification (CACS), myocardial flow reserve (MFR), and systemic inflammation (hsCRP).

Methods

Cross-sectional analysis of adults with T2D without overt CVD recruited 2020–2023. PEAT was quantified on non-contrast CT; CACS was calculated by the Agatston method; MFR was measured by rubidium-82 PET/CT; hsCRP assessed systemic inflammation. Associations were tested using multivariable regression adjusting for cardiovascular risk factors.

Results

Among 887 participants (mean age 65 years; 70% male; mean BMI 30 kg/m2; median PEAT 199 mL [IQR 133–283]), higher PEAT (per 100 mL) was associated with lower MFR (β − 0.04; 95% CI − 0.09 to 0.00; p = 0.041) and higher hsCRP, corresponding to a 38% increase (95% CI 28% to 48%; p < 0.001) in age- and sex-adjusted models, but not with CACS > 300 (OR 1.01; 95% CI 0.89–1.15). After further adjustment for diabetes duration, BMI, LDL cholesterol, systolic blood pressure, HbA1c, kidney function, smoking, and albuminuria, only the association with hsCRP remained significant at 14% (95%; CI 4% to 25%; p = 0.005).

Conclusion

In individuals with T2D without overt CVD, PEAT volume was not independently associated with CACS or MFR after multivariable adjustment. Higher PEAT volume was associated with higher hsCRP, suggesting a relationship with systemic inflammation; however, this exploratory finding should be interpreted in the context of established links between adiposity and inflammatory burden.

Graphical abstract