Introduction In a recent meta-analysis of patients treated with lipid lowering therapies to achieve contemporary targets, 76% of whom had diabetes, high-sensitivity CRP (hsCRP) was a stronger predictor of cardiovascular risk than low-density lipoprotein (LDL) cholesterol. Although, on average, patients with type 2 diabetes (T2D) have higher levels of CRP, little is known about the relationship between the quality of glucose control and hsCRP as a measure of inflammation. We therefore performed continuous glucose monitoring (CGM) on patients presenting with acute coronary syndrome (ACS) with and without T2D to explore this relationship. Methods Patients who were admitted to Oxford University Hospital with ACS were consented to the INFLAMED study. Continuous glucose monitoring (CGM) was performed during admission and/or at home for a median duration of 21 days, using Dexcom G7 glucose sensors. Participants were blinded to the glucose readings. Clinical data including hsCRP during admission were recorded. Peripheral blood was also sampled during hospital admission and PBMCs isolated and stored in liquid nitrogen for future downstream experiments. Results 89 patients were consented to the study, 45 with T2D and 44 without, and of whom 38 had CGM. hsCRP was significantly higher in patients with T2D (4.7 (IQR: 1.80–8.30) vs 2.3 (IQR: 1.00–4.50) mg/L, p-value 0.023) (table 1) and showed an increasing trend with higher number of vessels with disease that was significant when comparing single versus triple vessel disease (2.0 (IQR: 1.00–4.78) vs 4.5 (IQR: 2.00–10.90) p-value 0.0393) (figure 1A). Different metrics of characterising hyperglycaemia, when separated to high vs low based on median values, showed differences in hsCRP but only 'Time Above Range (TAR) (%)', a metric derived from CGM, with a derived median value in this cohort of 4% (IQR: 1–37%), showed a significant difference (1.8(IQR: 0.73–5.88) vs 6.15(IQR: 2.43–12.25) mg/L, p-value 0.0267) (figure 1B). CGM demonstrated heterogeneity of patterns of glycaemia among patients with T2D (figure 2). Conclusion/Implications We demonstrated that hsCRP was associated with increasing extent of coronary artery disease and CGM provided additional characterisation of patterns of glycaemia, one of which showed significant association with hsCRP. We aim to perform these analyses in a larger sample size and characterise the pro-inflammatory state in diabetes at the level of transcription and cytokine secretion in immune cells and investigate how they associate with patterns of glycaemia and complexity of coronary artery disease.
Chai et al. (Wed,) studied this question.