Scripties UMCG - Rijksuniversiteit Groningen
English | Nederlands

Inflammation in coronary artery disease and the interplay with epicardial fat

(2019) Blokland, I.V. van (Irene)

Introduction: Even though our knowledge on the pathophysiology of coronary artery disease (CAD) has
increased, the precise role of inflammation remains unclear. We approach to study the role of inflammation in
CAD from two sides by first of all the role of inflammatory cells and cytokine levels in ST-Elevated Myocardial
Infarction (STEMI). Secondly, we study the role of adipose tissue located around the heart, known as epicardial
fat, in CAD and the interplay with inflammatory cells.
Methods: Part I: A total of 24 patients presenting with a STEMI at the University Medical Centre Groningen
were included between January and December 2018. Inflammatory cells and plasma were collected at three
distinct time points: Baseline, 24 hours and 6-8 weeks after percutaneous coronary intervention. Levels of
interleukine-6 (IL-6), soluble interleukine-6 receptor (sIL-6R) and soluble glycoprotein 130 (sgp130) were
measured in the collected plasma samples. Part II: For epicardial fat analysis, a total of 60 participants were
selected from the UK Biobank cohort who were matched on age, sex and body mass index (20 healthy controls,
20 CAD and 20 STEMI). Epicardial fat was quantified on cardiac magnetic resonance image stacks (short-axis)
in end-diastolic phase using the software CVi42. Statistical significance was considered at a level of p<0.05.
Results: Part I: Baseline levels of leukocytes and neutrophils were significantly elevated in STEMI patients
compared to reference values, respectively (8.6(IQR 7.3-14.1) 109cells/L vs. 7(IQR 4-10) 109cells/L; p=0.009)
and (6.33(IQR 5.1-10.1) 109cells/L vs. 4.4(IQR 1.8-7.0) 109cells/L; p=0.007). Levels of IL-6 were significantly
elevated at 24h compared to baseline (3.76 pg/mL (IQR 1.86-11.83 pg/mL) vs. 1.33 pg/mL (IQR 0.97-2.42
pg/mL); p<0.001). Levels of sIL-6R at 24h and 6-8w correlated significantly with baseline inflammatory cells.
Part II: Epicardial fat volumes were significantly higher in CAD compared to controls (164.6(IQR 146.1-
194.4)mL vs. 120.7(IQR 103.4-137.9)mL; p<0.001) and compared to STEMI (164.6(IQR 146.1-194.4)mL vs.
143.8(IQR 113.4-159.7)mL; p=0.036).
Discussion and conclusion: After STEMI, baseline levels of leukocytes and neutrophils are increased and levels
of IL-6 are elevated after 24h. Epicardial fat is increased in individuals with CAD and is in general associated
with monocytes and neutrophils. These findings suggest that inflammation is involved in several process in CAD
and could serve as a potential new therapeutic target in the treatment of CAD as well as heart failure.

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