Simplified glycaemic management for patients with type 2 diabetes admitted for acute decompensated heart failure using linagliptin

2021 ◽  
Author(s):  
Luis M. Pérez-Belmonte ◽  
Julio Osuna-Sánchez ◽  
Juan Ignacio Rico-Robles ◽  
Michele Ricci ◽  
José P. Lara ◽  
...  
Keyword(s):  
Heart Failure ◽  
Type 2 Diabetes ◽  
Acute Decompensated Heart Failure ◽  
Decompensated Heart Failure

scholarly journals Efficacy And Safety of Empagliflozin Continuation in Patients With Type 2 Diabetes Hospitalised For Acute Decompensated Heart Failure

2021 ◽  
Author(s):  
Luis M Pérez-Belmonte ◽  
Michele Ricci ◽  
Jaime Sanz-Cánovas ◽  
Mercedes Millán-Gómez ◽  
Julio Osuna-Sánchez ◽  
...  
Keyword(s):  
Heart Failure ◽  
Type 2 Diabetes ◽  
Urine Output ◽  
Acute Decompensated Heart Failure ◽  
Decompensated Heart Failure ◽  
Insulin Regimen ◽  
Propensity Matching ◽  
Bolus Insulin ◽  
Basal Bolus

Abstract Background: Sodium−glucose cotransporter 2 inhibitors have been shown to reduce hospitalisations for acute decompensated heart failure in patients with and without type 2 diabetes. However, there is little evidence on their use in hospitalised patients. This work aims to analyse the glycaemic and clinical efficacy and safety of empagliflozin continuation in patients with type 2 diabetes hospitalised for acute decompensated heart failure.Methods: This real-world study included non-critically ill patients with diabetes hospitalised for acute decompensated heart failure and treated with empagliflozin for at least three months prior to the hospitalisation between 2017 and 2020. According to our in-hospital antihyperglycaemic protocol, patients could be treated with two possible regimens: a basal-bolus insulin regimen and an empagliflozin-basal insulin regimen. Our primary endpoints were difference in glycaemic control, as measured via mean daily blood glucose level, and differences in the visual analogue scale dyspnoea score, NT-proBNP levels, diuretic response, and cumulative urine output. Safety endpoints were also analysed. A propensity matching analysis was used to match a patient on one regimen with a patient on the other regimen. The probability of starting the regimes was estimated with a logistic regression model including variables that could have affected treatment assignment or outcomes as independent variablesResults: After a propensity matching analysis, 91 patients were included in each group. There were no differences in mean blood glucose levels (152.1 ± 17.8 vs 155.2 ± 19.7 mg/dl, p=0.289). At discharge, NT-proBNP levels were lower and cumulative urine output greater in the empagliflozin group versus the basal-bolus insulin group (1,652 ± 501 vs 2,101 ± 522 pg/mL, p=0.032 and 16,100 ± 1,510 vs 13,900 ± 1,220 ml, p=0.037, respectively). Patients who continued empagliflozin had a lower total number of hypoglycaemic episodes (36 vs 64, p<0.001). No differences were observed in adverse events, length of hospital stay, or in-hospital deaths.Conclusions: For patients with acute heart failure, an in-hospital antihyperglycaemic regimen that includes continuation of empagliflozin achieved effective glycaemic control, lower NT-proBNP, and greater urine output. It was also safer, as it reduced hypoglycaemic episodes without increasing other safety endpoints.

Effect of Empagliflozin as an Add-On Therapy on Decongestion and Renal Function in Patients With Diabetes Hospitalized for Acute Decompensated Heart Failure

2021 ◽  
Author(s):  
Shunsuke Tamaki ◽  
Takahisa Yamada ◽  
Tetsuya Watanabe ◽  
Takashi Morita ◽  
Yoshio Furukawa ◽  
...  
Keyword(s):  
Heart Failure ◽  
Type 2 Diabetes ◽  
Renal Function ◽  
Acute Decompensated Heart Failure ◽  
Decompensated Heart Failure ◽  
Conventional Group ◽  
Time Points ◽  
Percent Change ◽  
Subsequent Time

Background: Empagliflozin reduces the risk of hospitalization for heart failure in patients with type 2 diabetes and cardiovascular disease. We sought to elucidate the effect of empagliflozin as an add-on therapy on decongestion and renal function in patients with type 2 diabetes admitted for acute decompensated heart failure. Methods: The study was terminated early due to COVID-19 pandemic. We enrolled 59 consecutive patients with type 2 diabetes admitted for acute decompensated heart failure. Patients were randomly assigned to receive either empagliflozin add-on (n=30) or conventional glucose-lowering therapy (n=29). We performed laboratory tests at baseline and 1, 2, 3, and 7 days after randomization. Percent change in plasma volume between admission and subsequent time points was calculated using the Strauss formula. Results: There were no significant baseline differences in left ventricular ejection fraction and serum NT-proBNP (N-terminal pro-B-type natriuretic peptide), hematocrit, or serum creatinine levels between the 2 groups. Seven days after randomization, NT-proBNP level was significantly lower in the empagliflozin group than in the conventional group ( P =0.040), and hemoconcentration (≥3% absolute increase in hematocrit) was more frequently observed in the empagliflozin group than in the conventional group ( P =0.020). The decrease in percent change in plasma volume between baseline and subsequent time points was significantly larger in the empagliflozin group than in the conventional group 7 days after randomization ( P =0.017). The incidence of worsening renal function (an increase in serum creatinine ≥0.3 mg/dL) did not significantly differ between the 2 groups. Conclusions: In this exploratory analysis, empagliflozin achieved effective decongestion without an increased risk of worsening renal function as an add-on therapy in patients with type 2 diabetes with acute decompensated heart failure. REGISTRATION: URL: https://www.umin.ac.jp/ctr/index.htm ; Unique identifier: UMIN000026315.

scholarly journals Risk factors for acute decompensated heart failure in type 2 diabetes patients

2020 ◽  
Vol 25 (4) ◽  
pp. 3717
Author(s):  
N. A. Koziolova ◽  
A. S. Veklich ◽  
P. G. Karavaev
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Type 2 Diabetes ◽  
Acute Decompensated Heart Failure ◽  
Diuretic Therapy ◽  
Decompensated Heart Failure ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Coronary Syndrome

Aim. To identify risk factors for acute decompensated heart failure (ADHF) in patients with type 2 diabetes (T2D).Material and methods. In the cardiology department, 129 patients with ADHF were registered within 8 months, 59 (45,7%) of them had T2D. The study included 117 ADHF patients who were divided into two groups depending on the presence of T2D: group 1 (n=49; 41,9%)  — patients with T2D, group 2 (n=67; 55,9%) without T2D. The ADHF was verified by rapid progress of hypoperfusion and congestion, which required emergency hospitalization and inotropic and/or intravenous diuretic therapy. In the first 48 hours of hospitalization, echocardiography was performed, levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) and creatinine were determined; the glomerular filtration rate was estimated.Results. The incidence of T2D among patients with ADHF was 45,7%. There were following risk factors for ADHF in T2D patients: diabetic ketoacidosis (p=0,002), hypertensive crisis (p=0,017), history of acute coronary syndrome (p=0,048), atrial fibrillation (p=0,030), chronic kidney disease (p=0,003), pneumonia (p=0,035), progression of anemia (p=0,049), low prevalence of beta-blockers use (p=0,001), use of inappropriate antidiabetic drugs for HF patients (sulfonylureas, insulin). ADHF, assessed by NT-proBNP level, was significantly more severe in T2D patients (p=0,001) with pronounced congestion symptoms (p=0,001), which led to an increase in the need for diuretic therapy (p=0,002). Cardiac remodeling in T2D patients with ADHF is characterized mainly by the preserved left ventricular ejection fraction (LVEF), severe LV diastolic dysfunction (LVDD) and LV hypertrophy (LVH).Conclusion. The development of ADHF in T2D patients is associated with various risk factors and is characterized by severe congestion symptoms, high need for diuretic therapy, mainly preserved LVEF in combination with severe LVDD and LVH. 

scholarly journals Effect of empagliflozin as add-on therapy on transtubular potassium concentration gradient in patients with type 2 diabetes hospitalized for acute decompensated heart failure

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Tamaki ◽  
T Yamada ◽  
T Watanabe ◽  
T Morita ◽  
Y Furukawa ◽  
...  
Keyword(s):  
Heart Failure ◽  
Type 2 Diabetes ◽  
Concentration Gradient ◽  
Potassium Concentration ◽  
Acute Decompensated Heart Failure ◽  
Decompensated Heart Failure ◽  
Left Ventricular ◽  
Urine Samples ◽  
Left Ventricular Ejection

Abstract Background The transtubular potassium concentration gradient (TTKG) has been reported to be a marker of renal aldosterone bioactivity, and has been shown to be a surrogate of arterial underfilling in patients with acute decompensated heart failure (ADHF). Moreover, high TTKG at discharge has been shown to be associated with poor prognosis in ADHF patients. Empagliflozin, one of the sodium glucose cotransporter 2 inhibitors, has been shown to reduce the risk of cardiovascular mortality in patients with type 2 diabetes mellitus (T2D) and cardiovascular disease. However, little is known about the effect of empagliflozin as add-on therapy on TTKG in T2D patients with ADHF. Purpose We sought to elucidate the effect of empagliflozin as add-on therapy on TTKG in T2D patients with ADHF. Methods We enrolled 58 consecutive T2D patients admitted for ADHF. On admission, enrolled patients were randomly assigned in a 1:1 ratio to either empagliflozin add-on therapy (EMPA(+)) or conventional glucose-lowering therapy (EMPA(−)). All patients in EMPA(+) group received empagliflozin (10 mg/day) throughout the study period. Left ventricular ejection fraction (LVEF) was measured at baseline using echocardiography. Body weight and vital signs, such as blood pressure and heart rate, were measured, and blood and urine samples were collected at baseline and 1, 2, 3 and 7 days after randomization. The TTKG was measured using the first morning urine samples collected on each day. TTKG was calculated according to the following equation: TTKG = (Ku/Ks)×(plasma osmolality/urine osmolality), where Ku is urine potassium concentration and Ks is serum potassium concentration, as previously reported. Results Thirty patients were assigned to the EMPA(+) group, and 28 patients were assigned to the EMPA(−) group. There were no significant baseline differences in LVEF, plasma B-type natriuretic peptide (BNP) level, body mass index, or serum creatinine level between the EMPA(+) and EMPA(−) groups. TTKG did not significantly differ between the two groups at baseline. However, seven days after randomization, plasma BNP level was significantly lower in the EMPA(+) group than in the EMPA(−) group (median 227 [IQR 114–381] pg/mL vs 362 [227–554] pg/mL, p=0.0294). Furthermore, TTKG of the EMPA(+) group was significantly lower at 2, 3 and 7 days after randomization (Figure). Conclusions This study demonstrated that empagliflozin as add-on therapy can lower TTKG in T2D patients with ADHF. Figure 1 Funding Acknowledgement Type of funding source: None

scholarly journals Impact of canagliflozin in natriuretic peptides in patients with type 2 diabetes after hospitalization for acute heart failure

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
E Martin Dorado ◽  
R Gonzalez Manzanares ◽  
J.C Castillo Dominguez ◽  
J Lopez Aguilera ◽  
J Perea ◽  
...  
Keyword(s):  
Heart Failure ◽  
Type 2 Diabetes ◽  
Ejection Fraction ◽  
Acute Decompensated Heart Failure ◽  
Signs And Symptoms ◽  
Sglt2 Inhibitors ◽  
Control Group ◽  
Dipeptidyl Peptidase 4 ◽  
Reduced Ejection Fraction

Abstract Background Sodium-glucose cotransporter 2 (SGLT2) inhibitors have demonstrated to reduce the risk of hospitalization for heart failure (HF) in patients with type 2 diabetes mellitus (T2D). We aimed to assess the changes in N-terminal pro-B-type natriuretic peptide (NT-ProBNP) concentrations in a cohort of patients hospitalized for HF according to whether or not they received canagliflozin at discharge. Methods This cohort study included all patients with T2D admitted for HF from January 2017 to December 2019 in a single center. We excluded patients whose treatment with SGLT2 inhibitors were contraindicated (eGFR ≤45 ml/min/1.73 m2) and those who had other SGLT2 inhibitors than canagliflozin in their treatment at discharged. All patients had received a primary diagnosis of acute decompensated heart failure, including signs and symptoms of fluid overload and a concentration of NT-ProBNP of 1400 pg/mL at least. NT-ProBNP concentrations were collected at 3 months, 6 months, and 1 year after hospitalization with laboratory records if available. The aim of this study is to compare mean NT-ProBNP levels at hospital discharge and 3, 6 and 12 moths of follow-up in patients treated with and without canagliflozin. Results We included a total of 102 patients, 45 patients (44.1%) were prescribed canagliflozin and the remaining 57 (55.9%) were not prescribed any SGLT2 inhibitors (control group). There were no significant differences in clinical and comorbidities in both groups, except for age; slightly younger in the canagliflozin group (69,2±10,3 vs 73,2±11,1; p=0,04). Treatment at discharge was also similar, patients in the control group received more dipeptidyl peptidase-4 (DPP-4) inhibitors (21.1% vs 6.7%; p=0.04). Low rate of patients received sacubitril-valsartan (15,6%) in the canagliflozin group and 14% in the control group. More than a half of patients in both groups have HF with reduced ejection fraction. Mean levels of peptides were similar in both groups at hospital admission and discharge. During the first period of 3 months, we observed a decreased of NT-ProBNP concentration in both groups, but significantly inferior in canagliflozin group (p&lt;0,001). At 6 and 12 months, NT-ProBNP levels were practically maintained in patients treated with canagliflozin, whereas levels in patients in the control group were increased. Difference in both groups at a 12 month-period was significantly superior (p=0,004), with a median reduction of concentration levels at discharge of 64.3% in the canagliflozin group and 15,8% in control group. There were no differences in patients with HF from those with reduced ejection fraction and preserved. Conclusions Canagliflozin therapy at discharge was associated with a significant reduction in NT-ProBNP concentration in patients with diabetes after hospitalization for HF. FUNDunding Acknowledgement Type of funding sources: None. NT-ProBNP according to canagliflozin

P5413Effect of empagliflozin as add-on therapy on serum uric acid level in patients with type 2 diabetes hospitalized for acute decompensated heart failure: a prospective randomized controlled study

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Tamaki ◽  
T Yamada ◽  
T Morita ◽  
Y Furukawa ◽  
Y Iwasaki ◽  
...  
Keyword(s):  
Heart Failure ◽  
Uric Acid ◽  
Serum Uric Acid ◽  
Acid Level ◽  
Acute Decompensated Heart Failure ◽  
Serum Uric Acid Level ◽  
Decompensated Heart Failure ◽  
Sglt2 Inhibitors ◽  
Lower Serum

Abstract Background Elevated serum uric acid (UA) level has been shown to be associated with reduced survival among patients (pts) with heart failure. Sodium glucose cotransporter 2 (SGLT2) inhibitors have been reported to lower serum uric acid level in pts with type 2 diabetes mellitus (T2D). Empagliflozin, one of the SGLT2 inhibitors, has been shown to reduce the risk of cardiovascular mortality in T2D pts with cardiovascular disease, and involvement of UA lowering effect by empagliflozin in the reduction of cardiovascular mortality has been suggested. However, little is known about the effect of empagliflozin as add-on therapy on serum UA level in T2D pts with acute decompensated heart failure (ADHF). Purpose We sought to elucidate the effect of empagliflozin as add-on therapy on serum UA level in T2D pts with ADHF. Methods We enrolled 38 consecutive T2D pts admitted for ADHF. On admission, enrolled pts were randomly assigned in a 1:1 ratio to either empagliflozin add-on therapy (EMPA(+)) or conventional glucose-lowering therapy (EMPA(−)). All pts in EMPA(+) group received empagliflozin (10 mg/day) throughout the study period. Left ventricular ejection fraction (LVEF) was measured at baseline using echocardiography. Body weight and vital signs, such as blood pressure and heart rate, were measured, and blood and urine samples were collected at baseline and 1, 2, 3 and 7 days after randomization. Renal handling of UA was evaluated by fractional excretion of UA (FEUA). Results Twenty pts were assigned to the EMPA(+) group, and 18 pts were assigned to the EMPA(−) group. There were no significant baseline differences in LVEF, plasma brain natriuretic peptide level, body mass index, or serum creatinine level between the EMPA(+) and EMPA(−) groups. In addition, prevalence rate of hyperuricemia, serum UA level, and FEUA did not significantly differ between the two groups at baseline. However, there was significant difference in the change in serum UA level from baseline at 2, 3 and 7 days after randomization between the two groups (Figure A). As a result, serum UA level was significantly lower in the EMPA(+) group than in the EMPA(−) group at 7 days after randomization (6.2±1.8 mg/dL vs 7.8±1.8 mg/dL, p=0.0127). Moreover, FEUN of the EMPA(+) group was significantly higher at 1, 2 and 7 days after randomization (Figure B), which suggested that serum UA level was lowered in the EMPA(+) group by increased urinary excretion of UA. Figure 1 Conclusions This study demonstrated that empagliflozin as add-on therapy can lower serum UA level in T2D pts with ADHF through the effect on the urinary excretion rate of UA.

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