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3.
BMC Cardiovasc Disord ; 21(1): 258, 2021 05 26.
Article de Anglais | MEDLINE | ID: mdl-34039268

RÉSUMÉ

BACKGROUND: Limited data were available on the current trends in optimal medical therapy (OMT) after PCI and its influence on clinical outcomes in China. We aimed to evaluate the utilization and impact of OMT on the main adverse cardiovascular and cerebrovascular events (MACCEs) in post-PCI patients and analyzed the factors predictive of OMT after discharge. METHODS: We collected data from 3812 individuals from 2016.10 to 2017.09 at TEDA International Cardiovascular Hospital. They were classified into an OMT group and a non-OMT group according to their OMT status, which was defined as the combination of dual antiplatelet therapy, statins, ß-blockers, angiotensin-converting enzyme inhibitors or angiotensin receptor blockers after PCI. Multivariable Cox regression models were developed to assess the association between OMT and MACCEs, defined as all-cause mortality, nonfatal myocardial infarction, stroke, and target vessel revascularization. A logistic regression model was established to analyze the factors predictive of OMT. RESULTS: Our results revealed that the proportion of patients receiving OMT and its component drugs decreased over time. A total of 36.0% of patients were still adherent to OMT at the end of follow-up. Binary logistic regression analysis revealed that baseline OMT (P < 0.001, OR = 52.868) was the strongest predictor of OMT after PCI. The Cox hazard model suggested that smoking after PCI was associated with the 1-year risk of MACCE (P = 0.001, HR = 2.060, 95% CI 1.346-3.151), while OMT (P = 0.001, HR = 0.486, 95% CI 0.312-0.756) was an independent protective factor against postoperative MACCEs. CONCLUSIONS: There was still a gap between OMT utilization after PCI and the recommendations in the evidence-based guidelines. Sociodemographic and clinical factors influence the application of OMT. The management of OMT and smoking cessation after PCI should be emphasized.


Sujet(s)
Agents cardiovasculaires/usage thérapeutique , Maladie coronarienne/thérapie , Intervention coronarienne percutanée/tendances , Types de pratiques des médecins/tendances , Sujet âgé , Agents cardiovasculaires/effets indésirables , Chine/épidémiologie , Comorbidité , Maladie coronarienne/diagnostic , Maladie coronarienne/mortalité , Utilisation médicament/tendances , Femelle , Humains , Mâle , Adhésion au traitement médicamenteux , Adulte d'âge moyen , Intervention coronarienne percutanée/effets indésirables , Intervention coronarienne percutanée/mortalité , Études prospectives , Appréciation des risques , Facteurs de risque , Fumer/effets indésirables , Fumer/mortalité , Arrêter de fumer , Facteurs temps , Résultat thérapeutique
4.
Oncotarget ; 7(32): 52179-52194, 2016 Aug 09.
Article de Anglais | MEDLINE | ID: mdl-27438148

RÉSUMÉ

Type 2 diabetes mellitus is often complicated by osteoporosis, a process which may involve osteoblast autophagy. As melatonin suppresses autophagy under certain conditions, we its investigated the effects on bone autophagy during diabetes. We first assessed different body parameters in a diabetic rat model treated with various concentrations of melatonin. Dynamic biomechanicalmeasurements, bone organization hard slice dyeing and micro-CT were used to observe the rat bone microstructure, and immunohistochemistry was used to determine levels of autophagy biomarkers. We also performed in vitro experiments on human fetal osteoblastic (hFOB1.19) cells cultured with high glucose, different concentrations of melatonin, and ERK pathway inhibitors. And we used Western blotting and immunofluorescence to measure the extent of osteogenesis and autophagy. We found that melatonin improved the bone microstructure in our rat diabetes model and reduced the level of autophagy(50 mg/kg was better than 100 mg/kg). Melatonin also enhanced osteogenesis and suppressed autophagy in osteoblasts cultured at high glucose levels (10 µM was better than 1 mM). This suggests melatonin may reduce the level of autophagy in osteoblasts and delay diabetes-induced osteoporosis by inhibiting the ERK signaling pathway.


Sujet(s)
Autophagie/effets des médicaments et des substances chimiques , Diabète de type 2/complications , Mélatonine/pharmacologie , Ostéoporose/prévention et contrôle , Animaux , Diabète expérimental/complications , Humains , Système de signalisation des MAP kinases/effets des médicaments et des substances chimiques , Mâle , Ostéoblastes/effets des médicaments et des substances chimiques , Ostéogenèse/effets des médicaments et des substances chimiques , Rats , Rat Sprague-Dawley , Transduction du signal/effets des médicaments et des substances chimiques
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