Short Term Use of Empagliflozin Does Not Improve Left Ventricular Function in Non-Diabetic Hypertensive Patients: Results from a Non-Randomised Controlled Trial

Background: A selective inhibitor of sodium-glucose cotransporter 2 (SGLT2), empagliflozin, has demonstrated its effects in reducing cardiovascular mortality and hospitalization rates for heart failure in type 2 diabetes patients. However, the cardiac-intrinsic mechanism for this cardiovascular benefit has not been sufficiently studied. We therefore aimed to investigate the effect of empagliflozin on left ventricular function in a group of patients with grade I hypertension. Methods: We carried out a single-arm non-randomized clinical trial at the National Obesity Centre in Yaoundé over a period of 8 months (October 2016 to May 2017), where patients were assigned to receive 25 mg of empagliflozin once daily. Cardiac ultrasound, 24-hour ambulatory blood pressure measurement, resting electrocardiography and biological assessment were carried out at baseline and at the end of a 6-week treatment period with empagliflozin. The primary outcome was the improvement of the left ventricular relaxation evaluation criteria. Ethical approval was obtained from the Centre Regional Ethics Committee in Yaoundé, Cameroon. Results: A total of 11 patients were treated (median observation time, 6 weeks). We noted a non-significant improvement in the early lateral annular velocity from 9.7 [9.2 - 11.4] cm/s to 9.1 [8.8 - 10.2] cm/s, p =0.21. We also noted a non-significant improvement of the mitral profile (E/A) from 0.71 [0.63 - 0.78] cm/s to 0.81 [0.58 - 0.88] cm/s, p = 0.08. There were no differences in E/E’ ratio, 5.0 [4.1 - 6.3] vs 5.6 [4.9 - 7.4], p = 0.07. There was a non-significant drop in both systolic (p = 0.06) and diastolic (p = 0.09) blood pressure. We also observed on ECG a drop of the PR interval from 200 [157 - 200] ms to 160 [143 - 186] ms, p = 0.04. Conclusion: Short-term treatment with empagliflozin does not show an improvement of the left ventricular function in grade I hypertensive patients with diastolic dysfunction. Trial registration: This study was retrospectively registered on Clinical Trial Registry with ClinicalTrials.gov Identifier: NCT04203914.

Effect of Binge Drinking on Glucose Metabolism in Occasional Drinkers: An Experimental Study

Binge drinking is a major public health problem that affects all age groups. Its relation to the risk of impaired glucose metabolism and diabetes is unclear due to controversial findings in animal models and lack of studies in humans. We performed an experimental study on 10 adult volunteers (7M/3F) under the age of 40 who were occasional binge drinkers. In all participants, we performed a baseline two-hour euglycemic hyperinsulinemic clamp at 80 mU•m−2•min−1 at baseline for comparison with an age and sex matched control population of non-drinkers. On a second occasion, before and after ingestion of 78 g of alcohol (beer) in 2 hrs we also measured insulin sensitivity using a 15-minute short insulin tolerance test in drinkers. Blood glucose was also measured every 15 mins over 2 hours during alcohol ingestion. Volunteers were aged 27.6 ± 5.7 years, with a BMI of 23.1 ± 2.8 kg/m2, and ALAT of 24.7 ± 3.0 UI/L. Insulin sensitivity evaluated by the clamp technique was higher in occasional drinkers (M = 12.7 ± 3.4 mg•kg−1•min−1 vs. 8.0 ± 2.3 mg•kg−1•min−1 in non-drinkers, p = 0.011). Acute alcohol ingestion was associated with a non-significant trends towards improved glucose disappearance during short insulin tolerance test (KITT 2.53% ± 0.22%/min before vs. 3.11% ± 1.15%/min after;p = 0.122). Beer consumption induced a significant increase in capillary glycaemia of 78% (p = 0.001). Bingeing was associated with reduced insulin secretion (Homa-β 113.5 ± 22.7 vs. 155.4 ± 57.6;p = 0.047). Binge drinking may induce an increase in insulin sensitivity but acutely decrease insulin secretion.