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Combination therapy reduces cardiovascular risk factors in people with type 2 diabetes

Combination therapy reduces cardiovascular risk factors in people with type 2 diabetes

Publication date: Friday, 06 October 2017
Contributor(s): Jeremy Bray

In people with type 2 diabetes, Xultophy® (insulin degludec/liraglutide) significantly reduced a number of risk factors associated with an increased risk of cardiovascular disease (CVD), compared to basal insulin.

A new post-hoc analysis of the DUAL II and DUAL V trials presented at the 53rd Annual Meeting of the European Association for the Study of Diabetes (EASD 2017), shows that people treated with the insulin-liraglutide combination given by injection had significantly lower systolic blood pressure, total cholesterol and LDL-C and significant weight loss compared to people treated with basal insulin (insulin glargine U100 or insulin degludec). A small but statistically significant increase in heart rate was also observed.

Professor Tina Vilsbøll, Steno Diabetes Center Copenhagen, Denmark said, "People with type 2 diabetes have a higher risk of a heart attack or stroke compared to the general population, so reducing this risk as much as possible should be a central goal of treatment. I am very pleased to see the beneficial effects on cardiovascular risk markers.”

Cardiovascular markers DUAL II treatment difference vs insulin DUAL V treatment difference vs insulin
Systolic blood pressure (mmHg) -3.7 (-6.1, -1.3)* -3.6 (-5.5,-1.6)*
Total cholesterol 1 (0.9, 1.0)* 1 (0.9, 1.0)*
LDL-cholesterol 0.9 (0.9,1.0)* 0.9 (0.9,1.0)*
Table: Improvements in CVD markers with insulin-liraglutide vs insulin alone. *p<0.05

CVD is the principal cause of death and disability among people with type 2 diabetes globally, with approximately two-thirds of deaths in people with diabetes attributable to CVD. Treatments for type 2 diabetes should not only lower blood sugar levels but also aim to decrease CV risk.

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Category: Have You Heard
Edition: Volume 2 Number 10 PCCJ Online 2017
Contributor(s): Jeremy Bray

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