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1.
ESC Heart Fail ; 11(3): 1352-1376, 2024 Jun.
Article in English | MEDLINE | ID: mdl-38419326

ABSTRACT

Heart failure is the final stage of several cardiovascular diseases, and the key to effectively treating heart failure is to reverse or delay ventricular remodelling. Levosimendan is a novel inotropic and vasodilator agent used in heart failure, whereas the impact of levosimendan on ventricular remodelling is still unclear. This study aims to investigate the impact of levosimendan on ventricular remodelling in patients with left ventricular systolic dysfunction. Electronic databases were searched to identify eligible studies. A total of 66 randomized controlled trials involving 7968 patients were included. Meta-analysis results showed that levosimendan increased left ventricular ejection fraction [mean difference (MD) = 3.62, 95% confidence interval (CI) (2.88, 4.35), P < 0.00001] and stroke volume [MD = 6.59, 95% CI (3.22, 9.96), P = 0.0001] and significantly reduced left ventricular end-systolic volume [standard mean difference (SMD) = -0.52, 95% CI (-0.67, -0.37), P < 0.00001], left ventricular end-diastolic volume index [SMD = -1.24, 95% CI (-1.61, -0.86), P < 0.00001], and left ventricular end-systolic volume index [SMD = -1.06, 95% CI (-1.43, -0.70), P < 0.00001]. In terms of biomarkers, levosimendan significantly reduced the level of brain natriuretic peptide [SMD = -1.08, 95% CI (-1.60, -0.56), P < 0.0001], N-terminal pro-brain natriuretic peptide [SMD = -0.99, 95% CI (-1.41, -0.56), P < 0.00001], and interleukin-6 [SMD = -0.61, 95% CI (-0.86, -0.35), P < 0.00001]. Meanwhile, levosimendan may increase the incidence of hypotension [risk ratio (RR) = 1.24, 95% CI (1.12, 1.39), P < 0.0001], hypokalaemia [RR = 1.57, 95% CI (1.08, 2.28), P = 0.02], headache [RR = 1.89, 95% CI (1.50, 2.39), P < 0.00001], atrial fibrillation [RR = 1.31, 95% CI (1.12, 1.52), P = 0.0005], and premature ventricular complexes [RR = 1.86, 95% CI (1.27, 2.72), P = 0.001]. In addition, levosimendan reduced all-cause mortality [RR = 0.83, 95% CI (0.74, 0.94), P = 0.002]. In conclusion, our study found that levosimendan might reverse ventricular remodelling when applied in patients with left ventricular systolic dysfunction, especially in patients undergoing cardiac surgery, decompensated heart failure, and septic shock.


Subject(s)
Simendan , Ventricular Dysfunction, Left , Ventricular Remodeling , Simendan/therapeutic use , Simendan/pharmacology , Simendan/administration & dosage , Humans , Ventricular Dysfunction, Left/drug therapy , Ventricular Dysfunction, Left/physiopathology , Ventricular Remodeling/drug effects , Ventricular Function, Left/physiology , Ventricular Function, Left/drug effects , Stroke Volume/physiology , Stroke Volume/drug effects , Cardiotonic Agents/therapeutic use , Systole
2.
Mol Cell Endocrinol ; 576: 111996, 2023 10 01.
Article in English | MEDLINE | ID: mdl-37406985

ABSTRACT

BACKGROUND: Myocardial interstitial fibrosis is an important manifestation of diabetic heart disease, and insulin resistance is one of the mechanisms of myocardial interstitial fibrosis. Some studies have found that miR-543 is associated with insulin resistance, but whether it plays a role in diabetic myocardial interstitial fibrosis remains unclear. This study aimed to investigate the role of miR-543 in diabetic myocardial interstitial fibrosis. METHODS: The combination of high glucose and high insulin was used to establish an insulin-resistant myocardial fibroblast model. The expression levels of miR-543, α-SMA, collagen Ⅰ, collagen Ⅲ and PTEN were detected. Cell proliferation and migration were detected. Luciferase reporter gene assay was used to verify the targeting relationship between miR-543 and PTEN. RESULTS: The expression of miR-543 was up-regulated in myocardial fibroblasts with insulin resistance, which was consistent with the results of bioinformatics analysis. The proliferation and migration levels of myocardial fibroblasts in insulin-resistant states were increased, and the expression levels of α-SMA, collagen Ⅰ and collagen Ⅲ were also increased. Inhibition of miR-543 expression could reverse the above changes. Target gene prediction and dual luciferase reporter assay demonstrated that miR-543 could bind to the 3'UTR region of PTEN. Moreover, the effect of miR-543 on insulin-resistant myocardial fibroblasts is mediated by targeting PTEN. CONCLUSIONS: Inhibition of miR-543 can reduce myocardial fibroblast-myofibroblast transformation and collagen expression in insulin-resistant states by targeting PTEN.


Subject(s)
Insulin Resistance , Insulins , MicroRNAs , Cell Proliferation/genetics , Collagen/metabolism , Collagen Type I/genetics , Collagen Type I/metabolism , Fibroblasts/metabolism , Fibrosis , Insulin Resistance/genetics , Insulins/metabolism , Luciferases/metabolism , MicroRNAs/genetics , MicroRNAs/metabolism , Myofibroblasts/metabolism , PTEN Phosphohydrolase/genetics , PTEN Phosphohydrolase/metabolism , Animals , Mice
3.
World J Pediatr ; 13(1): 49-56, 2017 Feb.
Article in English | MEDLINE | ID: mdl-27650526

ABSTRACT

BACKGROUND: Critical value reporting has been widely adopted by hospitals throughout the world, but there were few reports about neonatal critical values. This study aimed to analyze characteristics of the neonatal critical values considered at our center and to provide information on improving neonatal intensive care. METHODS: A retrospective study of critical values at a newborn tertiary center in China was conducted to assess neonatal critical values according to test, distribution, reporting time, patient outcome and the impact to the therapy. RESULTS: In total, 926 critical values were recorded. Overall, 66.52% (616/926) of the items were reported within 24 hours of admission, 50.28% (465/926) during duty times and 54.75% (507/926) in the neonatal intensive care unit (NICU). The routine coagulation test was the most frequent source of critical values. Electrocardiography, blood gas analysis and therapeutic drug monitoring of drug levels were associated with the highest rates of treatment intervention (100%); routine coagulation tests were the lowest (23.14%). Sample quality was the main cause of false-positive critical values. CONCLUSIONS: The incidence of neonatal critical values peaked during the first 24 hours post-admission and during duty periods. Each newborn center needs to enact rapid treatment guidelines to address common critical values in order to facilitate clinical interventions. Periodically reviewing critical values could help to optimize clinical practices.


Subject(s)
Critical Care/standards , Critical Illness/therapy , Infant, Premature , Intensive Care Units, Neonatal/organization & administration , Outcome Assessment, Health Care , Blood Gas Analysis , China , Cohort Studies , Critical Care/trends , Critical Care Outcomes , Critical Illness/mortality , Diagnostic Tests, Routine , Disease Management , Electrocardiography/methods , Female , Humans , Infant, Newborn , Male , Monitoring, Physiologic/methods , Retrospective Studies , Tertiary Care Centers
4.
J Pediatr Endocrinol Metab ; 28(7-8): 773-6, 2015 Jul.
Article in English | MEDLINE | ID: mdl-25781522

ABSTRACT

Neonatal thyroid storm is rare; the diagnostic criteria and management of neonatal thyroid storm have not been well established. In this paper, we report a preterm infant diagnosed with neonatal hyperthyroidism secondary to maternal Graves' disease who was discharged after therapy. Unfortunately, he was rehospitalised for neonatal thyroid storm. We will discuss the diagnosis and general therapy of neonatal thyroid storm.


Subject(s)
Anemia/etiology , Graves Disease/complications , Pregnancy Complications/etiology , Thyroid Crisis/etiology , Adult , Anemia/diagnosis , Anemia/therapy , Female , Humans , Infant, Newborn , Male , Pregnancy , Pregnancy Complications/diagnosis , Pregnancy Complications/therapy , Prognosis , Thyroid Crisis/diagnosis , Thyroid Crisis/therapy
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