The effect of continuous glucose monitoring-guided glycemic control on progression of coronary atherosclerosis in type 2 diabetic patients with coronary artery disease: The OPTIMAL randomized clinical trial.

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• This trial did not show a statistically significant difference in total plaque volume or plaque lipid metrics between CGM-guided glycaemic control and HbA1c-guided glycaemic control groups in patients with CAD at 48 weeks.

• CGM guided glycaemic control could still be useful for individuals with CAD who are experiencing recurrent hypoglycaemia or large day to day glucose fluctuations.

• In this study, CGM use enabled doctors to optimise anti-diabetic medication choices for improved glycaemic variability and risk of hypoglycaemia.

Introduction

This prospective, randomised, parallel-group, single-centre OPTIMAL trial compared the effects of continuous Glucose Monitoring (CGM) versus HbA1c-guided glucose control on coronary artery disease (CAD) in Type 2 Diabetes Mellitus (T2DM) patients by using serial intravascular ultrasound (IVUS) and near-infrared spectroscopy (NIRS) imaging.

Method

94 participants, aged 18-85, with T2DM and CAD were recruited. Participants had to:

• have undergone heart artery procedure (percutaneous coronary intervention)

• had lesions causing more than 20% narrowing

• have blood sugar (HbA1c) between 7-10% while medicated

After imaging of plaques, participants were randomly assigned to CGM or HbA1c-guided glucose control groups for 48 weeks.

• CGM group - CGM and HbA1c measurement were performed at baseline and at 12, 24, 36, and 48 weeks.

• HbA1c-guided glycaemic control group - HbA1c was measured at baseline and at 12, 24, 36, and 48 weeks.

• Based on results, glucose-lowering medications were prescribed to keep average glucose levels between 70-180 mg/dL and HbA1c below 7.0%.

Results

82 participants had evaluable images at 48 weeks.

Compared to HbA1c-guided glycaemic control, CGM-guided control achieved:

• greater reduction in glucose variability ( % coefficient of variation) [-0.1 % (-1.8 to 1.6) vs. -3.3 % (-5.1 to -1.5), p =0.01]

• more time with glucose in a healthy range (between 70 and 180 mg/dL) [-1.5 % (-6.0 to 2.9) vs. 6.7 % (1.9 to 11.5), p =0.02].

Changes in total (TAV) and percent (PAV) atheroma volume did not reach statistical significance.   TAV increased by 0.11 ±1.9 mm³ in the HbA1c-guided group and decreased by -3.29 ±2.00 mm³ in the CGM-guided group [difference = -3.4 mm³ (95%CI: -8.9 to 2.0 mm³), p =0.22].

MaxLCBI_4mm, measures the lipid core build-up in coronary arteries. It increased by 90.1 ±25.6 in the HbA1c-guided group and by 50.6 ±25.6 in the CGM-guided group (difference = -45.6 (95%CI: 118.1 to 26.7) p =0.21], meaning it regressed in both groups, but by a greater margin in the HbA1c-guided group. A post-hoc analysis showed a greater regression of maxLCBI_4mm in the CGM-guided group [difference = 20.4 % (95%CI:1.3 to 39.5 %), p =0.03].

Conclusion:

CGM guided control did not slow CAD progression in patients with T2DM when compared to standard HbA1c monitoring.

• CGM can help individuals monitor their own postprandial glucose responses and therefore adjust their dietary intake to allow them to maintain healthy blood sugar levels.

• CSG can help prevent and mitigate the risks of hypoglycaemia.

• Other interventions, aside from glycaemic management, are required to help limit progression of CVD and diabetic atheromas.

• Further research is required to understand the post-hoc analysis findings of greater regression of lipid in plaques under CGM-guided glycaemic control.

• Participants in this study had low baseline HbA1c, which makes it difficult to determine the benefits of CGM in helping to reduce HbA1c.

• Longer follow-up studies may help to better determine the benefit of CGM guided glycaemic control in CAD.