Meta-analyses of the effects of DPP-4 inhibitors, SGLT2 inhibitors and GLP1 receptor analogues on cardiovascular death, myocardial infarction, stroke and hospitalization for heart failure

Safety and effectiveness of ipragliflozin in elderly versus non-elderly Japanese type 2 diabetes mellitus patients: 12 month interim results of the STELLA-LONG TERM study

“…As the changes in hematocrit from baseline to 12 months between elderly and non-elderly patients were generally similar, with only a single statistical difference, it is unlikely that the increase observed is involved in the development of volume-depletion-related events. Elevated hematocrit levels generally indicate an increase in hemoconcentration owing to the diuretic action of SGLT2 inhibitors but, as reported previously [22][23][24][25][26][27][28][29] , this effect is not considered sufficient to increase the risk of stroke. However, as the data reported here are derived from an interim analysis of this study, we will continue to monitor this point.…”

Glucose-lowering medication selection in patients with diabetes and acute cerebrovascular accident

“…Следовательно, учитывая различное влияние ингибиторов иДПП-4 на исходы и снижение смертности у больных СД, перенесших инсульт, с появлением новых препаратов этого класса, наличием многих плейотропных свойств у данной группы, фактически полным отсутствием побочных явлений представляется целесообразным включить препараты этого класса в протокол ведения больных с данной патологией. Однако, по мнению исследователей, другой класс препаратов из инкретин-направленной фармакотерапии -аналоги глюкагоноподобного пептида -1 (аГПП-1) представляют наибольшую ценность для предотвращения развития инфаркта и инсульта, даже по сравнению с глифлозинами [36].…”

Critical role of the epicardium in mediating cardiac inflammation and fibrosis in patients with type 2 diabetes

“…Although incretin‐based agents reduce epicardial fat volume, glucagon‐like peptide‐1 receptor agonism promotes adverse change in the biology of adipose tissue, and dipeptidyl peptidase‐4 inhibitors can potentiate the actions of proinflammatory chemokines . Perhaps for these reasons, in the clinical setting, incretin‐based drugs have not improved ventricular diastolic filling dynamics or reduced the risk of heart failure …”

“…38 Perhaps for these reasons, in the clinical setting, incretinbased drugs have not improved ventricular diastolic filling dynamics 39 or reduced the risk of heart failure. 40…”