Because other coronaviruses enter the cells by binding to dipeptidyl‐peptidase‐4 (DPP‐4), it has been speculated that DPP‐4 inhibitors (DPP‐4is) may exert an activity against severe acute respiratory syndrome coronavirus 2. In the absence of clinical trial results, we analysed epidemiological data to support or discard such a hypothesis. We retrieved information on exposure to DPP‐4is among patients with type 2 diabetes (T2D) hospitalized for COVID‐19 at an outbreak hospital in Italy. As a reference, we retrieved information on exposure to DPP‐4is among matched patients with T2D in the same region. Of 403 hospitalized COVID‐19 patients, 85 had T2D. The rate of exposure to DPP‐4is was similar between T2D patients with COVID‐19 (10.6%) and 14 857 matched patients in the region (8.8%), or 793 matched patients in the local outpatient clinic (15.4%), 8284 matched patients hospitalized for other reasons (8.5%), and when comparing 71 patients hospitalized for COVID‐19 pneumonia (11.3%) with 351 matched patients with pneumonia of another aetiology (10.3%). T2D patients with COVID‐19 who were on DPP‐4is had a similar disease outcome as those who were not. In summary, we found no evidence that DPP‐4is might affect hospitalization for COVID‐19.
IntroductionSodium glucose cotransporter-2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1RA) protect type 2 diabetic (T2D) patients from cardiovascular events, but no trial has directly compared their cardiovascular effects. We aimed to address this gap using real-world data.Research design and methodsWe performed a retrospective real-world study on a population of ~5 million inhabitants from North-East Italy. We identified T2D patients who received new prescription of SGLT2i or GLP-1RA from 2014 to 2018. SGLT2i and GLP-1RA initiators were matched 1:1 by propensity scores. The primary outcome was a composite of all-cause death, myocardial infarction, and stroke (three-point major adverse cardiovascular events (3P-MACE)). Secondary endpoints were each component of the primary endpoint, hospitalization for heart failure (HF), revascularization, hospitalization for cardiovascular causes, and adverse events.ResultsFrom a population of 330 193 diabetic patients, we followed 8596 SGLT2i and GLP-1RA matched initiators for a median of 13 months. Patients in both groups were on average 63 years old, 63% men, and 18% had pre-existing cardiovascular disease. T2D patients treated with SGLT2i versus GLP-1RA, experienced a lower rate of 3P-MACE (HR 0.68; 95% CI 0.61 to 0.99; p=0.043), myocardial infarction (HR 0.72; 95% CI 0.53 to 0.98; p=0.035), hospitalization for HF (HR 0.59; 95% CI 0.35 to 0.99; p=0.048), and hospitalization for cardiovascular causes (HR 0.82; 95% CI 0.69 to 0.99; p=0.037). Adverse events were not significantly different between the two groups.ConclusionsIn the absence of dedicated trials, this observational study suggests that SGLT2i may be more effective than GLP-1RA in improving cardiovascular outcomes of T2D.Trial registration numberNCT04184947.
Background: Cardiovascular outcome trials in high-risk patients showed that some GLP-1 receptor agonists (GLP-1RA), but not dipeptidyl-peptidase-4 inhibitors (DPP-4i), can prevent cardiovascular events in type 2 diabetes (T2D). Since no trial has directly compared these two classes of drugs, we performed a comparative outcome analysis using real-world data. Methods: From a database of ~ 5 million people from NorthEast Italy, we retrospectively identified initiators of GLP-1RA or DPP-4i from 2011 to 2018. We obtained two balanced cohorts by 1:1 propensity score matching. The primary outcome was the 3-point major adverse cardiovascular events (3P-MACE; a composite of death, myocardial infarction, or stroke). 3P-MACE components and hospitalization for heart failure were secondary outcomes. Results: From 330,193 individuals with T2D, we extracted two matched cohorts of 2807 GLP-1RA and 2807 DPP-4i initiators, followed for a median of 18 months. On average, patients were 63 years old, 60% male; 15% had pre-existing cardiovascular disease. The rate of 3P-MACE was lower in patients treated with GLP-1RA compared to DPP4i (23.5 vs. 34.9 events per 1000 person-years; HR: 0.67; 95% C.I. 0.53-0.86; p = 0.002). Rates of myocardial infarction (HR 0.67; 95% C.I. 0.50-0.91; p = 0.011) and all-cause death (HR 0.58; 95% C.I. 0.35-0.96; p = 0.034) were lower among GLP-1RA initiators. The as-treated and intention-to-treat approaches yielded similar results. Conclusions: Patients initiating a GLP-1RA in clinical practice had better cardiovascular outcomes than similar patients who initiated a DPP-4i. These data strongly confirm findings from cardiovascular outcome trials in a lower risk population.
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