Abstract
BackgroundCardiovascular protection following empagliflozin therapy is not entirely attributable to the glucose lowering effect. Increased hematocrit might influence the shear stress that is the main force acting on the endothelium, regulating its anti-atherogenic function.ObjectiveWe designed the study with the aim of investigating the effect of empagliflozin on blood viscosity and shear stress in the carotid arteries. A secondary endpoint was the effect of empagliflozin on carotid artery wall thickness.MethodsThe study was a non-randomized, open, prospective cohort study including 35 type 2 diabetic outpatients who were offered empagliflozin or incretin-based therapy (7 liraglutide, 8 sitagliptin) in combination with insulin and metformin. Blood viscosity, shear stress and carotid wall thickness were measured at baseline and at 1 and 3 months of treatment. Blood viscosity was measured with a viscometer, and shear stress was calculated using a validated formula. Intima-media thickness (IMT) of the carotid artery was detected by ultrasound and was measured with dedicated software.ResultsBlood viscosity (4.87 ± 0.57 vs 5.32 ± 0.66 cP, p < 0.02) and shear stress significantly increased in the Empagliflozin group while no change was detected in the Control group (4.66 ± 0.56 vs 4.98 ± 0.73 cP, p = NS). IMT significantly decreased in the Empagliflozin group after 1 and 3 months (baseline: 831 ± 156, 1-month 793 ± 150, 3-month 766 ± 127 μm; p < 0.0001), while in the liraglutide group, IMT significantly decreased only after 3 months (baseline 879 ± 120; 1-month 861 ± 163; 3-month 802 ± 114 μm; p < 0.001). In the sitagliptin group, IMT remained almost unchanged (baseline 901 ± 135; 1-month 902 ± 129; 3-month 880 ± 140 μm; p = NS).ConclusionsThis study is the first to describe a direct effect of empagliflozin on blood viscosity and wall shear stress. Furthermore, IMT was markedly reduced early on in the Empagliflozin group.
Highlights
Cardiovascular protection following empagliflozin therapy is not entirely attributable to the glucose lowering effect
This study is the first to describe a direct effect of empagliflozin on blood viscosity and wall shear stress
The dose was up titrated to 25 mg once daily (OD) in 13 subjects (65%) at 1-month visit based on fasting plasma glucose (FPG) and self-monitoring blood glucose (SMBG)
Summary
Cardiovascular protection following empagliflozin therapy is not entirely attributable to the glucose lowering effect. Empagliflozin reduced cardiovascular death and all-cause mortality, as well as hospitalization for heart failure, whereas canagliflozin was neutral on death and heart failure [1, 2]. Canagliflozin but not empagliflozin has a moderate SGLT1 inhibitor activity, reducing the absorption of glucose in the gastrointestinal tract, where the SGLT1 is mostly located. SGLT2 inhibitors have recently been demonstrated to markedly reduce cardiovascular mortality with highly significant reduction in admissions for heart failure and end-stage renal disease, despite modest effects on long-term glycemic control [1, 2, 6]. The discrepancy between the glucose lowering effect (similar to that of other treatments) and the effect on cardiovascular events (much greater with SGLT2 inhibitors) has recently attracted great interest. Empagliflozin has been reported to reduce aortic stiffness and afterload, thereby ameliorating ventricular function and myocardial oxygenation [5, 7,8,9]
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