Tele-rehabilitation for Type II diabetics with heart failure with preserved ejection fraction.

Objective: This study aims to determine whether tele-rehabilitation has similar effects to conventional face-to-face physical rehabilitation for diabetic patients with heart failure with preserved ejection fraction (HFpEF). Materials and methods: Demographic, laboratory, diagnostic and rehabilitation information for patients with type 2 diabetes with HFpEF were extracted from disease-specific databases. Outcome measures, including the Short Physical Performance Battery (SPPB), 6-minute walk distance, frailty status, European Quality of Life 5-Dimension 5-Level questionnaire (EQ-5D-5L) and reduction in HbA1c from admission, patients who received tele-rehabilitation therapy were compared to those received face-to-face rehabilitation. Results: In this study, 90 patients with type 2 diabetes and HFpEF using tele-rehabilitation were matched with 90 patients with type 2 diabetes and HFpEF using face-to-face physical rehabilitation. Improvements in the results of the SPPB scores, 6-min walk distance and gait speed and EQ-5D-5L were noted from the follow-up time point 3 months to 6 months in both two groups. There were no significant differences in functional tests and quality of life between the two groups. Conclusion: Our study proved that mobile-based tele-rehabilitation programs are non-inferior to face-to-face physical rehabilitation for diabetes patients after HFpEF. In addition, adherence to the telerehabilitation program showed that the novel technology was accepted well and could be an alternative to the conventional face-to-face rehabilitation program.

Metformin suppresses cardiac fibroblast proliferation under high-glucose conditions via regulating the mitochondrial complex I protein Grim-19 involved in the Sirt1/Stat3 signaling pathway.

Hyperglycemia associated with myocardial oxidative stress and fibrosis is the main cause of diabetic cardiomyopathy. Currently, no approved drug is available for preventing or treating diabetes-induced cardiac fibrosis. Metformin has been reported to improve glycemic control and ameliorate diabetic cardiomyopathy. This study aimed to investigate the effects and mechanism of metformin on diabetes-induced cardiac fibrosis and high glucose-induced proliferation of cardiac fibroblasts (CFs). In this study, db/db mice were treated with metformin [250 mg/kg⋅d, gavage]. CFs were cultured in high-glucose medium to mimic an in vitro diabetes model and then subjected to treatment with or without metformin. Cardiac fibrosis was analyzed using immunohistochemistry, Masson's trichrome staining, and Western blot analysis. Cell Counting Kit-8 (CCK-8) assays and cell colony formation assays were used to examine cell proliferation capacity. Transwell and scratch-wound assays were used to detect the migration ability of CFs. Retinoid-interferon-induced mortality-19 (Grim-19), sirtuin1 (Sirt1), and signal transducer and activator of transcription 3 (Stat3) were detected using Western blot analysis. The genes downstream of the Stat3 pathway were detected using quantitative reverse transcription PCR (qRT‒PCR). Metformin treatment markedly attenuated cardiac fibrosis in db/db mice and the proliferation and migration of CFs under high-glucose conditions. Mechanistically, we found an intersection between metformin and Grim-19 using bioinformatics. Metformin was found to suppress the expression of p-Stat3 and elevate the expression of mitochondrial complex I protein Grim-19 and Sirt1, thus inhibiting the proliferation and migration of CFs under high-glucose conditions. Our data suggested that metformin inhibited the proliferation and migration of CFs by regulating the expression of mitochondrial complex I Grim-19 protein involved in the Sirt1/Stat3 signaling pathway under high-glucose conditions, thus providing new ideas for treating diabetes-induced cardiac fibrosis.

Protective Effects of Salvianolate on Contrast-Induced Nephropathy after Primary Percutaneous Coronary Intervention: A Prospective Multicenter Randomized Controlled Trial.

OBJECTIVES: This study's aim was to evaluate the protective effects of salvianolate on contrast-induced nephropathy after primary percutaneous coronary intervention (PPCI) compared with normal saline (NS) hydration. METHODS: We enrolled patients with acute myocardial infarction who underwent PPCI in 3 centers in Shanghai. The patients were randomly assigned to the salvianolate group or the NS group. The incidence of CIN, the changes in renal function parameters, and the occurrence of adverse events after the procedure were compared between the 2 groups. We used a multivariate logistic regression analysis to determine the independent correlates of CIN after PPCI. RESULTS: A total of 484 patients were finally included in the statistical analysis. Compared with the control group, salvianolate reduced the incidence of CIN (9.1 vs. 16.3%, p = 0.018) after PPCI. The renal function parameters after PPCI in the salvianolate group were superior to those of the control group (p < 0.05). The composite adverse events rate was significantly lower in the salvianolate group within 1 month after the procedure (9.5 vs. 15.5%, p = 0.046). A higher peak of troponin I and loop diuretic therapy were the independent correlates of CIN after PPCI. CONCLUSIONS: Salvianolate reduces the incidence of CIN and protects renal function after PPCI, and the effects were superior to those of NS hydration.

Protective effects of salvianolate on microvascular flow in a porcine model of myocardial ischaemia and reperfusion.

BACKGROUND: Microvascular reflow is crucial for myocyte survival during ischaemia/reperfusion injury. AIMS: We aimed to assess if salvianolate, a highly purified aqueous extract from Radix salviae miltiorrhizae, could improve impaired microvascular reflow induced by ischaemia/reperfusion injury, using a porcine closed-chest model. METHODS: Left anterior descending coronary artery ligation was created by balloon occlusion for 2 h followed by reperfusion for 14 days. Salvianolate was administrated intravenously for 7 days at low dose (5 mg/kg/day), high dose (10 mg/kg/day) or high dose combined with one 20 mg intracoronary bolus injection just at the beginning of reperfusion. Control-group animals were only given the same volume of saline. RESULTS: After 14 days of reperfusion, animals treated with high-dose salvianolate showed improved myocardial perfusion assessed by real-time myocardial contrast echocardiography and coloured microspheres. The beneficial effect was further supported by increased capillary density and decreased infarct size. All these effects eventually resulted in well-preserved cardiac function detected by echocardiography. Moreover, we also demonstrated that salvianolate administration was associated with elevated superoxide dismutase activity, thioredoxin activity and glutathione concentration, and reduced malondialdehyde concentration, which, in turn, resulted in a significant decrease in terminal deoxynucleotide transferase-mediated dUTP nick end labelling-positive cells and an increased ratio of Bcl-2 to Bax expression. CONCLUSION: Intravenous salvianolate at a dose of 10 mg/kg/day for 7 days had significant beneficial effects on myocardial microvascular reflow, which were associated with decreased oxidative stress and apoptosis.