Abstract 16474: BP Reduction With the Sodium Glucose Co-Transporter 2 Inhibitor Empagliflozin in Type 2 Diabetes is Similar in Treatment Naïve as in Those on One or ≥ 2 Antihypertensive Agents - Further Insights From a Dedicated 24h ABPM Study

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Guiseppe Mancia ◽  
Christopher P Cannon ◽  
Illka Tikkanen ◽  
Cordula Zeller ◽  
Ludwin Ley ◽  
...  

In patients with type 2 diabetes (T2D) hypertension is accompanied by an increase in CV risk which can be substantially attenuated if BP is lowered by drug treatment. Empagliflozin (EMPA) is a new glucose-lowering agent of the sodium glucose co-transporter 2 inhibitor (SGLT2i) class, which has been shown to reduce body weight and also lower BP. It is not known, however, whether the EMPA-related BP lowering effect is preserved in patients under background antihypertensive treatment. We investigated the effect of 12 weeks with EMPA on 24 hour (h) mean BP in 823 T2D patients (age 60.2 ± 9.0 years, HbA1c 7.9 ± 0.7%, office systolic (S)/diastolic (D) BP 142.1 ± 12.3/83.9 ± 7.0 mmHg, mean ± SD) in a study with a randomized design. EMPA was given at 10mg (n=276) or 25mg (n=276) daily; 271 patients were randomized to placebo. Patients were under no, 1 or ≥ 2 antihypertensive drugs (n= 62, 353 and 408, respectively) such as an ACE inhibitor (ACEI), an angiotensin receptor antagonist (ARB) or a diuretic (D). HbA1c and weight were significantly reduced with EMPA 10 mg (mean [SE] -0.62% [0.05], -1.5 kg [0.2]) and EMPA 25 mg (-0.65 [0.05], -2.0 [0.2]) relative to placebo (all p < 0.001). As shown in the Table, compared to placebo, EMPA at the lower or higher dose reduced 24h mean SBP and DBP in all groups. With the lower dose the BP reduction was somewhat less pronounced in patients with ≥ 2 antihypertensive drugs whereas with the higher dose the BP effect was similar irrespective of the presence and intensity of background antihypertensive treatment. The antihypertensive effect of EMPA was preserved also irrespective of the type of treatment (D and ACEIs or ARBs), especially at the higher dose. Thus, EMPA reduces BP in patients with T2D regardless of whether they are untreated or more or less intensively treated for hypertension.

Author(s):  
Koichi Kitamura ◽  
Koichi Hayashi ◽  
Shinsuke Ito ◽  
Yuiko Hoshina ◽  
Masahiro Sakai ◽  
...  

AbstractRecent randomized trials demonstrating the beneficial effects of sodium-glucose cotransporter 2 inhibitors (SGLT2is) in type 2 diabetes suggest that early reductions in eGFR upon initiation of SGLT2i therapy are associated with improved renal outcomes. Multiple concomitant medications, including antidiabetic and antihypertensive agents, are commonly used, however, which may modify the renal hemodynamic action of SGLT2is. Here we found that background treatment with metformin diminished the SGLT2i-induced reductions in eGFR after 3 months of SGLT2i therapy in patients with type 2 diabetes and hypertension (−2.29 ± 0.90 vs −5.85 ± 1.27 mL/min/1.73 m2 for metformin users (n = 126) and nonusers (n = 97), respectively). Other antidiabetic agents (DPP4 inhibitors, sulfonylureas and insulin) had no effect on the eGFR response to SGLT2is. Antihypertensive drugs, including calcium channel blockers (CCBs) and β blockers, did not affect the SGLT2i-induced changes in eGFR, whereas renin-angiotensin system inhibitors (RASis) tended to enhance this response (p = 0.059). Next, we evaluated the interaction between metformin and RASis in the eGFR responses to SGLT2is. Under no background treatment with RASis, metformin abrogated the eGFR response to SGLT2is, but this response was preserved when RASis had been given along with metformin (decreases of 0.75 ± 1.28 vs. 4.60 ± 1.15 mL/min/1.73 m2 in eGFR, p = 0.028). No interaction between metformin and insulin or between metformin and DPP4 inhibitors was observed. In conclusion, metformin blunts the SGLT2i-induced decrease in eGFR, but coadministration of RASis ameliorates this response. Furthermore, the inability of CCBs to modify the SGLT2i-induced reduction in eGFR suggests that the SGLT2i-induced renal microvascular action is mediated predominantly by postglomerular vasodilation rather than preglomerular vasoconstriction.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1483-P
Author(s):  
TOSHIAKI OHKUMA ◽  
MIN JUN ◽  
MARK WOODWARD ◽  
JOHN CHALMERS ◽  
VLADO PERKOVIC ◽  
...  

2020 ◽  
Author(s):  
Luis Miguel Pérez-Belmonte ◽  
José David Torres-Peña ◽  
María D. López-Carmona ◽  
M. Mar Ayala-Gutiérrez ◽  
Francisco Fuentes-Jiménez ◽  
...  

Author(s):  
Rick I. Meijer ◽  
Trynke Hoekstra ◽  
Niels C. Gritters van den Oever ◽  
Suat Simsek ◽  
Joop P. van den Bergh ◽  
...  

Abstract Purpose Inhibition of dipeptidyl peptidase (DPP-)4 could reduce coronavirus disease 2019 (COVID-19) severity by reducing inflammation and enhancing tissue repair beyond glucose lowering. We aimed to assess this in a prospective cohort study. Methods We studied in 565 patients with type 2 diabetes in the CovidPredict Clinical Course Cohort whether use of a DPP-4 inhibitor prior to hospital admission due to COVID-19 was associated with improved clinical outcomes. Using crude analyses and propensity score matching (on age, sex and BMI), 28 patients using a DPP-4 inhibitor were identified and compared to non-users. Results No differences were found in the primary outcome mortality (matched-analysis = odds-ratio: 0,94 [95% confidence interval: 0,69 – 1,28], p-value: 0,689) or any of the secondary outcomes (ICU admission, invasive ventilation, thrombotic events or infectious complications). Additional analyses comparing users of DPP-4 inhibitors with subgroups of non-users (subgroup 1: users of metformin and sulphonylurea; subgroup 2: users of any insulin combination), allowing to correct for diabetes severity, did not yield different results. Conclusions We conclude that outpatient use of a DPP-4 inhibitor does not affect the clinical outcomes of patients with type 2 diabetes who are hospitalized because of COVID-19 infection.


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