ArticleTrials2025
Effects of SGLT2 inhibitors on cardiac autonomic activity and ventricular remodeling in patients with acute myocardial infarction: study protocol for a clinical trial.
Article in Trials, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Dapagliflozin associates with heart rate variability decline in T2DM patients on GLP-1 receptor agonist therapy: a prospective observational study.Frontiers in endocrinology · 2026Observational
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundSodium-glucose co-transporter 2 inhibitors (SGLT2-I) exhibit significant cardiovascular protective effects in patients with acute myocardial infarction (AMI) complicated with type 2 diabetes mellitus (T2DM), mainly through enhancing cardiac function and reducing malignant arrhythmias. However, limited evidence exists regarding their efficacy in non-diabetic AMI patients. Moreover, the relationship between these benefits and improvements in cardiac autonomic function and left ventricular remodeling remains contentious, hindering a comprehensive understanding of their mechanisms of action. This study aims to fill this knowledge gap regarding dapagliflozin's effects on cardiac autonomic activity and ventricular remodeling in AMI patients.
methodsThis study is a prospective, randomized, open-label, assessor-blinded, single-center trial in AMI patients in China. A total of 110 participants will be randomly allocated in a 1:1 ratio to either receive standardized treatment alone or receive standardized treatment along with 10 mg of dapagliflozin taken once daily. The primary endpoint is the change from the baseline to 24 weeks in heart rate variability (HRV) and deceleration capacity (DC) measured by 24-h ambulatory Holter monitoring. Secondary endpoints include changes in the left ventricular remodeling index (a relative change of LV end-diastolic volume, LVRI) as measured from baseline, along with the incidence of major adverse cardiovascular events throughout the follow-up period. Changes in various variables from the baseline will also be analyzed, encompassing glucose and lipid levels, blood pressure, body weight, and biomarkers linked to diagnostic and functional parameters of AMI, such as creatine kinase, troponin I (TnI) level, and N terminal pro B type natriuretic peptide (NT-proBNP) level. DISCUSSION: This will be the first trial to evaluate the effects of dapagliflozin on cardiac autonomic function and ventricular remodeling in AMI patients. This study seeks to elucidate the mechanisms underlying dapagliflozin's cardioprotective effects, potentially informing future therapeutic strategies for improving outcomes in this population.
trial registrationClinical trial ID: ChiCTR2400084050. Registration date: May 9, 2024.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.