Cardiovascular diabetologyAug 24, 2017

How ongoing statin use relates to blood sugar changes and heart risks after starting insulin in type 2 diabetes

GLP-1 Therapies Weekly Brief ↗PubMed ↗DOI ↗

Updated Apr 2, 2026

Abstract

Among 12,725 patients with Type 2 Diabetes starting insulin therapy, concurrent statin use was linked to a higher risk of major cardiovascular events.

Initial reduction in HbA1c was greater in non-statin users compared to statin users at 6 months (-0.34% vs -0.26%, p = 0.004).
No significant difference in HbA1c reduction was observed between the two groups at 3 years (-0.31% vs -0.35%, p = 0.344).
The risk of major adverse cardiovascular events (3-point MACE) was higher in statin users, with an adjusted hazard ratio of 1.36 (95% CI 1.15-1.62, p < 0.0001).
Throughout the study, HbA1c levels were consistently higher in statin users compared to non-users (p < 0.05).
Atorvastatin, simvastatin, and rosuvastatin were associated with reduced risk for MACE compared to non-users, while pravastatin's association was not statistically significant.

Simplified

AIM: Statins may increase the risk of new-onset diabetes and adversely affect glycaemic control, but their effects on the glycemic response and mortality outcomes following commencement of insulin therapy in patients with Type 2 Diabetes (T2D) are unclear.

METHODS: A retrospective cohort study was conducted in 12,725 insulin initiators with T2D using The Health Improvement Network (THIN) UK database. Changes in HbA1c at 6, 12, 24 and 36 months, and the 5-year risk of mortality and (3-point) major adverse cardiovascular events (MACE), were compared between prior users (n = 10,682) and non-users (n = 2043) of statin therapy who were newly commenced on insulin treatment. Cox proportional hazard models were used to estimate the hazard ratios of the different outcomes.

RESULTS: Mean age of the cohort was 58.7 ± 14.0 years (51% male) and mean baseline HbA1c was 8.7 ± 1.8%. A greater initial reduction in HbA1c was observed following insulin initiation in the non-users of statins compared with the users, which was significant in the short term (-0.34% vs -0.26% at 6 months; mean diff = -0.09%, p = 0.004) but not in the long term: -0.31% versus -0.35% at 3 years (mean diff = 0.05%, p = 0.344). CV events (3-point MACE) were 878 versus 217 in statin users versus non-users (20.7 vs 30.9 per 1000 person-years; adjusted Hazard Ratio (aHR) 1.36 (95% CI 1.15-1.62; p < 0.0001). In a subgroup analysis of individual statins, HbA1c was higher throughout the study duration with all statins relative to non-users of statin therapy (p < 0.05). The aHRs for 3-point MACE for atorvastatin, simvastatin, rosuvastatin and pravastatin were 0.82 (95% CI 0.68-0.98), 0.67 (0.55-0.82), 0.56 (0.39-0.81) and 0.78 (0.60-1.01), respectively.

CONCLUSIONS: Following initiation of insulin therapy in patients with T2D in routine care, concurrent use of a statin was associated with less good glycaemic control in the short-term but a much lower risk of major adverse CV events.

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How ongoing statin use relates to blood sugar changes and heart risks after starting insulin in type 2 diabetes

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